The DOI matches its Crossref record; 148 of the 148 references it cites were found in a registry or an index; 10 of the 143 sources its claims cite were checked for support.
Parvalbumin interneuron vulnerability and brain disorders
Open accessAbstract
Parvalbumin-expressing interneurons (PV-INs) are highly vulnerable to stressors and have been implicated in many neuro-psychiatric diseases such as schizophrenia, Alzheimer's disease, autism spectrum disorder, and bipolar disorder. We examined the literature about the current knowledge of the physiological properties of PV-INs and gathered results from diverse research areas to provide insight into their vulnerability to stressors. Among the factors that confer heightened vulnerability are the substantial energy requirements, a strong excitatory drive, and a unique developmental trajectory. Understanding these stressors and elaborating on their impact on PV-IN health is a step toward developing therapies to protect these neurons in various disease states and to retain critical brain functions.
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Claims the paper makes
73 Not checked yet · 15 Own interpretation · 5 No basis given · 3 Supported · 1 Supported so far · 1 Partly supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Mouse models relevant for both disorders, including the disrupted in schizophrenia 1 gene (Disc1) [57][58][59][60][61], or brain derived neurotrophic factor (Bdnf) [62], show abnormal PV-IN function ranging from migration deficits to reduction in IN number.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Partly supportedcites [57] Lee FH, Zai CC, Cordes SP, Roder JC, Wong AH. Abnormal interneuron development in disrupted-in-schizophrenia-1 L100P mutant mice. Mol Brain. 2013;6:20. sourceExperimental — accuracy not yet measured
The Results sections on embryonic tangential position, adult cortical PV-interneuron distribution, and mPFC cell numbers report migration-related abnormalities and fewer PV-positive interneurons in Disc1-L100P mice. The paper describes this model as relevant to schizophrenia and refers generally to other mental disorders, but does not establish its relevance to bipolar disorder. Bdnf has a separate citation in the citing sentence and is not attributed to this source. (LLM, conf=0.83)
- Partly supportedcites [62] Jones NC, Hudson M, Foreman J, Rind G, Hill R, Manning EE, et al. Brain-derived neurotrophic factor haploinsufficiency impairs high-frequency cortical oscillations in mice. Eur J Neurosci. 2018;48:2816–25. sourceExperimental — accuracy not yet measured
The Results section (‘Effects of BDNF genotype on parvalbumin levels’; page unavailable) reports reduced cortical PV immunoreactivity in BDNF-deficient mice, supporting an abnormality associated with PV interneurons. It measures protein expression, not interneuron number or migration, and the paper frames the model as relevant to schizophrenia rather than establishing relevance to bipolar disorder. The Disc1 models are attached to other citations in the sentence. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
In the paper
“Furthermore, individuals with schizophrenia have a lower density of excitatory synapses on PV-INs [12] and exhibit alterations in gamma oscillations during a working memory task [13].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [12] Chung DW, Fish KN, Lewis DA. Pathological basis for deficient excitatory drive to cortical parvalbumin interneurons in schizophrenia. Am J Psychiatry. 2016;173:1131–9. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Injury to, or dysfunction of, parvalbumin inhibitory interneurons (PV-INs) has been proposed to contribute to the pathophysiology of several important neuro-psychiatric disorders, including schizophrenia, autism spectrum disorder (ASD), bipolar disorder (BPD), various neurodegenerative diseases, and even aging-related cognitive changes.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Furthermore, individuals with schizophrenia have a lower density of excitatory synapses on PV-INs [12] and exhibit alterations in gamma oscillations during a working memory task [13].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [13] Barr MS, Farzan F, Tran LC, Chen R, Fitzgerald PB, Daskalakis ZJ. Evidence for excessive frontal evoked gamma oscillatory activity in schizophrenia during working memory. Schizophr Res. 2010;121:146–52. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“Animal models that mimic schizophrenia replicate the loss of PV-INs in the hippocampus [6,14,15], and show a loss of PV fluorescence per cell in prelimbic regions [16].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [6] Lodge DJ, Behrens MM, Grace AA. A loss of parvalbumin-containing interneurons is associated with diminished oscillatory activity in an animal model of schizophrenia. J Neurosci. 2009;29:2344–54. source
- Not checked yetcites [14] Koh MT, Shao Y, Sherwood A, Smith DR. Impaired hippocampal-dependent memory and reduced parvalbumin-positive interneurons in a ketamine mouse model of schizophrenia. Schizophr Res. 2016;171:187–94. source
- Not checked yetcites [15] Harrington AJ, Raissi A, Rajkovich K, Berto S, Kumar J, Molinaro G, et al. MEF2C regulates cortical inhibitory and excitatory synapses and behaviors relevant to neurodevelopmental disorders. eLife 2016;5:e20059. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Interestingly, early intervention during the prepubertal period might prevent loss of PV-INs, as shown in the methylazoxymethanol acetate (MAM) rat model of PV-IN loss in the ventral hippocampus [17].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [17] Du Y, Grace AA. Loss of parvalbumin in the hippocampus of MAM schizophrenia model rats is attenuated by peripubertal diazepam. Int J Neuropsychopharmacol. 2016;19:pyw060. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Reductions in the number of PV-INs were reported in the hippocampus, entorhinal cortex, and subicular areas [1,[9][10][11].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [1] Konradi C, Yang CK, Zimmerman EI, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons are abnormal in schizophrenia. Schizophr Res. 2011;131:165–73. source
- Not checked yetcites [9] Wang AY, Lohmann KM, Yang CK, Zimmerman EI, Pantazopoulos H, Herring N, et al. Bipolar disorder type 1 and schizophrenia are accompanied by decreased density of parvalbumin- and somatostatin-positive interneurons in the parahippocampal region. Acta Neuropathol. 2011;122:615–26. source
- Not checked yetcites [10] Chung DW, Volk DW, Arion D, Zhang Y, Sampson AR, Lewis DA. Dysregulated ErbB4 splicing in schizophrenia: selective effects on parvalbumin expression. Am J Psychiatry. 2016;173:60–8. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“While these findings point to a pathology in PV-INs, they cannot differentiate between loss of neurons or loss of PV expression.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Animal models that mimic schizophrenia replicate the loss of PV-INs in the hippocampus [6,14,15], and show a loss of PV fluorescence per cell in prelimbic regions [16].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [16] Behrens MM, Ali SS, Dao DN, Lucero J, Shekhtman G, Quick KL, et al. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science. 2007;318:1645–7. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, decreases in the number of PV-INs in the hippocampus were observed in two mouse models of AD [33,34], while an increase in hippocampal PV immunoreactivity was observed in another [35], and no change in the number of hippocampal PV-positive interneurons was observed in yet another model [36].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [33] Mahar I, Albuquerque MS, Mondragon-Rodriguez S, Cavanagh C, Davoli MA, Chabot JG, et al. Phenotypic alterations in hippocampal NPY- and PV-expressing interneurons in a presymptomatic transgenic mouse model of Alzheimer’s disease. Front Aging Neurosci. 2016;8:327.
- Not checked yetcites [34] Takahashi H, Brasnjevic I, Rutten BP, Van Der Kolk N, Perl DP, Bouras C, et al. Hippocampal interneuron loss in an APP/PS1 double mutant mouse and in Alzheimer’s disease. Brain Struct Funct. 2010;214:145–60. source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 34
- Probably not a substantial claim. 9
Every source the paper cites for this claim was checked and supports it.
In the paper
“STAT3 can directly regulate mitochondrial function [97,98], and Nox2 can modulate mitochondrial activity [99][100][101]”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Supportedcites [97] Gough DJ, Corlett A, Schlessinger K, Wegrzyn J, Larner AC, Levy DE. Mitochondrial STAT3 supports Ras-dependent oncogenic transformation. Science. 2009;324:1713–6. source
The paper’s Abstract states that STAT3 regulates a metabolic function in mitochondria. Its experimental account reports that mitochondrial function was impaired without STAT3, including reduced activity of electron-transport-chain complexes II and V. The Nox2 clause has separate citations and is not attributed to this source. (LLM, conf=0.93)
- Supportedcites [98] Wegrzyn J, Potla R, Chwae YJ, Sepuri NB, Zhang Q, Koeck T, et al. Function of mitochondrial Stat3 in cellular respiration. Science. 2009;323:793–7. source
This source is cited for the STAT3 portion of the sentence, not the separately cited Nox2 portion. In the supplied passages (section labeled Abstract; no page given), mitochondria-targeted STAT3 restored electron transport chain activity in STAT3-deficient cells, supporting a direct role in mitochondrial function. (LLM, conf=0.94)
- Supportedcites [99] Kim YM, Kim SJ, Tatsunami R, Yamamura H, Fukai T, Ushio-Fukai M. ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis. Am J Physiol Cell Physiol. 2017;312:C749–64. source
The citation to this paper is attached to the Nox2 clause, not the STAT3 clause. The paper’s conclusion states that Nox2 promotes mitochondrial ROS production in endothelial cells, supporting the claim that Nox2 can modulate mitochondrial activity. (LLM, conf=0.90)
- Supportedcites [100] Joseph LC, Barca E, Subramanyam P, Komrowski M, Pajvani U, Colecraft HM, et al. Inhibition of NAPDH oxidase 2 (NOX2) prevents oxidative stress and mitochondrial abnormalities caused by saturated fat in cardiomyocytes. PLoS ONE. 2016;11:e0145750. source
The citation to this paper is attached to the Nox2 clause, not the STAT3 clause. In the Results section, NOX2 inhibition prevented palmitate-induced mitochondrial ROS, depolarization, and calcium overload in cardiomyocytes, supporting the claim that Nox2 can modulate mitochondrial activity. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These receptors activate intraneuronal signaling cascades that dynamically remodel microtubule and actin cytoskeletal components to extend and retract processes that move the cells toward their destination [133].”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
What the sources say
- Supportedcites [133] Peyre E, Silva CG, Nguyen L. Crosstalk between intracellular and extracellular signals regulating interneuron production, migration and integration into the cortex. Front Cell Neurosci. 2015;9:129. source
In “Migration of cINs: extracellular cues guide cINs movement” (page not provided), the paper says extracellular cues are transduced at the cytoskeleton, causing extension or retraction of leading processes. “Molecular regulation of the cytoskeleton in migrating cINs” describes receptor-triggered intracellular signaling that changes both actin and microtubule organization during branching and migration. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“In schizophrenia, NMDA receptors are believed to be hypo-functioning, and the inhibition of NMDA receptors recapitulates many of the symptoms of schizophrenia [104, 122, 123].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [104] Timofeeva OA, Levin ED. Glutamate and nicotinic receptor interactions in working memory: importance for the cognitive impairment of schizophrenia. Neuroscience. 2011;195:21–36. source
- Supportedcites [122] Konradi C, Heckers S. Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment. Pharm Ther. 2003;97:153–79. source
The Introduction describes decreased NMDA receptor activity as a hypothesis of schizophrenia, and Section 2.3 says NMDA receptor hypofunction seems central to its pathology. Section 2.3 also reports that NMDA receptor inhibition with PCP or ketamine causes schizophrenia-like psychoses and mimics both positive and negative symptoms. (LLM, conf=0.94)
- Supportedcites [123] Lisman JE, Coyle JT, Green RW, Javitt DC, Benes FM, Heckers S, et al. Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia. Trends Neurosci. 2008;31:234–42. source
The Introduction’s “NMDA hypofunction” section describes reduced NMDA receptor function as a theory of schizophrenia. It also states that NMDA antagonists reproduce positive and negative symptoms and many associated cognitive deficits. The cited paper therefore supports both parts of the paraphrase. (LLM, conf=0.94)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“During migration, cellintrinsic programs and external cues must be coordinated in a time-and location-sensitive manner [131].”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
What the sources say
- Supportedcites [131] Guo J, Anton ES. Decision making during interneuron migration in the developing cerebral cortex. Trends Cell Biol. 2014;24:342–51. source
The section on choices of migratory streams says intrinsic characteristics combine with regionally localized extracellular cues to determine interneuron routes. The intracortical-dispersion section adds that interneurons and their environment may mature in a stage-dependent, synchronized way, supporting the claim’s time-sensitive aspect. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
None of the sources cited for this claim have been checked yet.
In the paper
“Parvalbumin-expressing interneurons (PV-INs) are highly vulnerable to stressors and have been implicated in many neuropsychiatric diseases such as schizophrenia, Alzheimer's disease, autism spectrum disorder, and bipolar disorder.”
§ Parvalbumin interneuron vulnerability and brain disorders > Abstract
What the sources say
- Not checked yetcites [1] Konradi C, Yang CK, Zimmerman EI, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons are abnormal in schizophrenia. Schizophr Res. 2011;131:165–73. source
- Not checked yetcites [2] Lewis DA, Curley AA, Glausier JR, Volk DW. Cortical parvalbumin interneurons and cognitive dysfunction in schizophrenia. Trends Neurosci. 2012;35:57–67. source
- Not checked yetcites [3] Marin O. Interneuron dysfunction in psychiatric disorders. Nat Rev Neurosci. 2012;13:107–20. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Among the factors that confer heightened vulnerability are the substantial energy requirements, a strong excitatory drive, and a unique developmental trajectory.”
§ Parvalbumin interneuron vulnerability and brain disorders > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In schizophrenia, lower levels of PVALB mRNA, the gene coding for PV, were seen in the hippocampus and layer 4 of the dorsolateral prefrontal cortex, which might be partially explained by DNA hypermethylation [1,8].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [1] Konradi C, Yang CK, Zimmerman EI, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons are abnormal in schizophrenia. Schizophr Res. 2011;131:165–73. source
- Not checked yetcites [8] Fachim HA, Srisawat U, Dalton CF, Reynolds GP. Parvalbumin promoter hypermethylation in postmortem brain in schizophrenia. Epigenomics. 2018;10:519–24. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Extensive accounts in the literature point to PV-IN-related changes in individuals with schizophrenia [1][2][3][4], a finding that is supported by various animal models that recapitulate aspects of the disease [5][6][7] (Table 1).”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [1] Konradi C, Yang CK, Zimmerman EI, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons are abnormal in schizophrenia. Schizophr Res. 2011;131:165–73. source
- Not checked yetcites [2] Lewis DA, Curley AA, Glausier JR, Volk DW. Cortical parvalbumin interneurons and cognitive dysfunction in schizophrenia. Trends Neurosci. 2012;35:57–67. source
- Not checked yetcites [3] Marin O. Interneuron dysfunction in psychiatric disorders. Nat Rev Neurosci. 2012;13:107–20. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Some human and animal model data suggest that formerly PV-INs are still present but cease to express PV, though a definitive conclusion cannot be drawn at this point [7,[18][19][20].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [7] Gill KM, Grace AA. Corresponding decrease in neuronal markers signals progressive parvalbumin neuron loss in MAM schizophrenia model. Int J Neuropsychopharmacol. 2014;17:1609–19. source
- Not checked yetcites [18] Powell SB, Sejnowski TJ, Behrens MM. Behavioral and neurochemical consequences of cortical oxidative stress on parvalbumin-interneuron maturation in rodent models of schizophrenia. Neuropharmacology. 2012;62:1322–31. source
- Not checked yetcites [19] Enwright JF, Sanapala S, Foglio A, Berry R, Fish KN, Lewis DA. Reduced labeling of parvalbumin neurons and perineuronal nets in the dorsolateral prefrontal cortex of subjects with schizophrenia. Neuropsychopharmacology. 2016;41:2206–14. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Stimulation of PV-INs leads to an increase in gamma oscillation patterns, while inhibition of PV-INs or downregulation of PV at cortical synapses reduces gamma oscillations [76][77][78].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [76] Cardin JA, Carlen M, Meletis K, Knoblich U, Zhang F, Deisseroth K, et al. Driving fast-spiking cells induces gamma rhythm and controls sensory responses. Nature. 2009;459:663–7. source
- Not checked yetcites [77] Sohal VS, Zhang F, Yizhar O, Deisseroth K. Parvalbumin neurons and gamma rhythms enhance cortical circuit performance. Nature. 2009;459:698–702. source
- Not checked yetcites [78] Volman V, Behrens MM, Sejnowski TJ. Downregulation of parvalbumin at cortical GABA synapses reduces network gamma oscillatory activity. J Neurosci. 2011;31:18137–48. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Transgenic mice with AD-like pathology were found to have reduced gamma power that, in one model, precedes cognitive impairment and amyloid plaque formation [21,22].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [21] Iaccarino HF, Singer AC, Martorell AJ, Rudenko A, Gao F, Gillingham TZ, et al. Gamma frequency entrainment attenuates amyloid load and modifies microglia. Nature. 2016;540:230–5. source
- Not checked yetcites [22] Rubio SE, Vega-Flores G, Martinez A, Bosch C, Perez-Mediavilla A, del Rio J, et al. Accelerated aging of the GABAergic septohippocampal pathway and decreased hippocampal rhythms in a mouse model of Alzheimer’s disease. FASEB J. 2012;26:4458–67. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Since PV rapidly sequesters Ca 2+ , it strongly attenuates the Ca 2+ -activated potassium conductance responsible for postspike hyperpolarization, which explains in part why PV-INs repolarize faster and fire faster than other neurons.”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Individual PV-INs contact nearly every local pyramidal neuron which enables them to synchronize networks [74].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [74] Packer AM, Yuste R. Dense, unspecific connectivity of neocortical parvalbumin-positive interneurons: a canonical microcircuit for inhibition? J Neurosci. 2011;31:13260–71. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“PV-INs have roles in both feedforward and feedback inhibition, regulation of sensory responses, and in learning and plasticity [66].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [66] Hu H, Gan J, Jonas P. Interneurons. Fast-spiking, parvalbumin(+) GABAergic interneurons: from cellular design to microcircuit function. Science. 2014;345:1255263. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There is therefore ample evidence that PV-INs are vital for brain function and intricately linked to brain malfunction.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Epilepsy [63,64] and prion disease [65] are among other disorders that are associated with alterations in PV-INs.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [63] Sloviter RS, Sollas AL, Barbaro NM, Laxer KD. Calcium-binding protein (calbindin-D28K) and parvalbumin immunocytochemistry in the normal and epileptic human hippocampus. J Comp Neurol. 1991;308:381–96. source
- Not checked yetcites [64] Garbelli R, Meroni A, Magnaghi G, Beolchi MS, Ferrario A, Tassi L, et al. Architectural (Type IA) focal cortical dysplasia and parvalbumin immunostaining in temporal lobe epilepsy. Epilepsia. 2006;47:1074–8. source
- Not checked yetcites [65] Guentchev M, Hainfellner JA, Trabattoni GR, Budka H. Distribution of parvalbumin-immunoreactive neurons in brain correlates with hippocampal and temporal cortical pathology in Creutzfeldt-Jakob disease. J Neuropathol Exp Neurol. 1997;56:1119–24. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Schizophrenia also shares significant overlap with BPD [55,56], including PV-IN pathology.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [55] Consortium C-DGotPG, Lee SH, Ripke S, Neale BM, Faraone SV, Purcell SM, et al. Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs. Nat Genet. 2013;45:984–94. source
- Not checked yetcites [56] Cardno AG, Rijsdijk FV, Sham PC, Murray RM, McGuffin P. A twin study of genetic relationships between psychotic symptoms. Am J Psychiatry. 2002;159:539–45. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PV increases the rate of Ca 2+ sequestration, reduces presynaptic Ca 2+ levels, modulates short-term synaptic plasticity, and prevents cumulative facilitation (Fig. 1), [67,68].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [67] Caillard O, Moreno H, Schwaller B, Llano I, Celio MR, Marty A. Role of the calcium-binding protein parvalbumin in short-term synaptic plasticity. Proc Natl Acad Sci USA. 2000;97:13372–7. source
- Not checked yetcites [68] Wahr PA, Michele DE, Metzger JM. Parvalbumin gene transfer corrects diastolic dysfunction in diseased cardiac myocytes. Proc Natl Acad Sci USA. 1999;96:11982–5. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Separately, a voltage-gated sodium channel (Na v 1.1) that is largely found on axons of PV-INs was decreased in a mouse model with amyloid pathology, and in AD patients [24][25][26].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [24] Ogiwara I, Miyamoto H, Morita N, Atapour N, Mazaki E, Inoue I, et al. Nav1.1 localizes to axons of parvalbumin-positive inhibitory interneurons: a circuit basis for epileptic seizures in mice carrying an Scn1a gene mutation. J Neurosci. 2007;27:5903–14. source
- Not checked yetcites [25] Wang W, Takashima S, Segawa Y, Itoh M, Shi X, Hwang SK, et al. The developmental changes of Na(v)1.1 and Na(v)1.2 expression in the human hippocampus and temporal lobe. Brain Res. 2011;1389:61–70. source
- Not checked yetcites [26] Verret L, Mann EO, Hang GB, Barth AM, Cobos I, Ho K, et al. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model. Cell. 2012;149:708–21. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
In the paper
“ASD shares many overlaps with schizophrenia, not just on a clinical scale, but also with similar PV-IN abnormalities [39].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [39] De Crescenzo F, Postorino V, Siracusano M, Riccioni A, Armando M, Curatolo P, et al. Autistic symptoms in schizophrenia spectrum disorders: a systematic review and meta-analysis. Front Psychiatry. 2019;10:78. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Gamma oscillations in humans are also associated with increased working memory load [79].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [79] Howard MW, Rizzuto DS, Caplan JB, Madsen JR, Lisman J, Aschenbrenner-Scheibe R, et al. Gamma oscillations correlate with working memory load in humans. Cereb Cortex. 2003;13:1369–74. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Indeed, it would be surprising to find that PV-IN densities in disease are uniform across every brain region given that fast-spiking interneurons have different functions in different brain areas.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Restoration of the levels of this voltage-gated sodium channel increased gamma oscillations, while memory deficits and premature deaths decreased [26].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [26] Verret L, Mann EO, Hang GB, Barth AM, Cobos I, Ho K, et al. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model. Cell. 2012;149:708–21. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PV-INs have extraordinary energy requirements to support a high metabolic activity and to protect against significant glutamatergic stress [16,80,81].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [16] Behrens MM, Ali SS, Dao DN, Lucero J, Shekhtman G, Quick KL, et al. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science. 2007;318:1645–7. source
- Not checked yetcites [80] Gulyas AI, Megias M, Emri Z, Freund TF. Total number and ratio of excitatory and inhibitory synapses converging onto single interneurons of different types in the CA1 area of the rat hippocampus. J Neurosci. 1999;19:10082–97. source
- Not checked yetcites [81] Kann O, Papageorgiou IE, Draguhn A. Highly energized inhibitory interneurons are a central element for information processing in cortical networks. J Cereb Blood Flow Metab. 2014;34:1270–82. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“A substantial quantity of cytochrome c and cytochrome c oxidase supports the high bioenergetic needs of PV-INs [81,85], but comes at a price as cytochrome c is also central to the induction of apoptosis [86].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [81] Kann O, Papageorgiou IE, Draguhn A. Highly energized inhibitory interneurons are a central element for information processing in cortical networks. J Cereb Blood Flow Metab. 2014;34:1270–82. source
- Not checked yetcites [85] Gulyas AI, Buzsaki G, Freund TF, Hirase H. Populations of hippocampal inhibitory neurons express different levels of cytochrome c. Eur J Neurosci. 2006;23:2581–94. source
- Not checked yetcites [86] Liu X, Kim CN, Yang J, Jemmerson R, Wang X. Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c. Cell. 1996;86:147–57. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The energy requirements of PV-INs make them highly susceptible to the loss of mitochondrial membrane potential (a component of, and a proxy for, a decrease in mitochondrial function), and to metabolic and oxidative stress that accompanies disease states [81,91].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [81] Kann O, Papageorgiou IE, Draguhn A. Highly energized inhibitory interneurons are a central element for information processing in cortical networks. J Cereb Blood Flow Metab. 2014;34:1270–82. source
- Not checked yetcites [91] Whittaker RG, Turnbull DM, Whittington MA, Cunningham MO. Impaired mitochondrial function abolishes gamma oscillations in the hippocampus through an effect on fast-spiking interneurons. Brain. 2011;134:e180. author reply e81 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“If the pathological threshold is crossed, the electron transfer chain is disrupted, reactive oxygen species accumulate, the permeability transition pore opens, the outer mitochondrial membrane ruptures, cytochrome c is released, and an apoptotic cell death program is activated [86,109].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [86] Liu X, Kim CN, Yang J, Jemmerson R, Wang X. Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c. Cell. 1996;86:147–57. source
- Not checked yetcites [109] Kwak S, Weiss JH. Calcium-permeable AMPA channels in neurodegenerative disease and ischemia. Curr Opin Neurobiol. 2006;16:281–7. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“PV-INs have a higher density of inputs, more excitatory and inhibitory synapses, and a higher ratio of inhibitory to excitatory inputs than calbindin-and calretinin-positive interneurons [80].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [80] Gulyas AI, Megias M, Emri Z, Freund TF. Total number and ratio of excitatory and inhibitory synapses converging onto single interneurons of different types in the CA1 area of the rat hippocampus. J Neurosci. 1999;19:10082–97. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Consistent with the notion that the presence of Ca 2+ -permeable AMPA receptors contributes to the vulnerability of PV-INs, blocking of these receptors attenuates cortical neuron death in an in vitro model of traumatic brain injury; attenuates hippocampal pyramidal neuron loss in a mouse hippocampal slice model of oxygen-glucose deprivation; and attenuates retinal ganglion cells loss in a rat”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [111] Yin HZ, Sensi SL, Ogoshi F, Weiss JH. Blockade of Ca2+-permeable AMPA/kainate channels decreases oxygen-glucose deprivation-induced Zn2+ accumulation and neuronal loss in hippocampal pyramidal neurons. J Neurosci. 2002;22:1273–9. source
- Not checked yetcites [116] Cueva Vargas JL, Osswald IK, Unsain N, Aurousseau MR, Barker PA, Bowie D, et al. Soluble tumor necrosis factor alpha promotes retinal ganglion cell death in glaucoma via calcium-permeable AMPA receptor activation. J Neurosci. 2015;35:12088–102. source
- Not checked yetcites [117] Spaethling JM, Klein DM, Singh P, Meaney DF. Calcium-permeable AMPA receptors appear in cortical neurons after traumatic mechanical injury and contribute to neuronal fate. J Neurotrauma. 2008;25:1207–16. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the hippocampus, oxidative stress was associated with a decrease in PV-INs as well as a reduction in gamma oscillations [94].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [94] Steullet P, Cabungcal JH, Kulak A, Kraftsik R, Chen Y, Dalton TP, et al. Redox dysregulation affects the ventral but not dorsal hippocampus: impairment of parvalbumin neurons, gamma oscillations, and related behaviors. J Neurosci. 2010;30:2547–58. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Animal studies suggest that a key mechanism of neural oscillations is through glutamatergic regulation.”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Importantly, NMDA receptors in PV-INs are regulating gamma rhythms and cognitive behaviors [121].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [121] Carlen M, Meletis K, Siegle JH, Cardin JA, Futai K, Vierling-Claassen D, et al. A critical role for NMDA receptors in parvalbumin interneurons for gamma rhythm induction and behavior. Mol Psychiatry. 2012;17:537–48. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Indeed, PV-INs receive the greatest excitatory input of any population of inhibitory neurons in the cortex, which puts them under intense stress [16,80].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [16] Behrens MM, Ali SS, Dao DN, Lucero J, Shekhtman G, Quick KL, et al. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science. 2007;318:1645–7. source
- Not checked yetcites [80] Gulyas AI, Megias M, Emri Z, Freund TF. Total number and ratio of excitatory and inhibitory synapses converging onto single interneurons of different types in the CA1 area of the rat hippocampus. J Neurosci. 1999;19:10082–97. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, the NMDA receptor antagonist ketamine, a pro-inflammatory stimulus, injures PV-INs in vitro and in vivo [16,95].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [16] Behrens MM, Ali SS, Dao DN, Lucero J, Shekhtman G, Quick KL, et al. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science. 2007;318:1645–7. source
- Not checked yetcites [95] Behrens MM, Ali SS, Dugan LL. Interleukin-6 mediates the increase in NADPH-oxidase in the ketamine model of schizophrenia. J Neurosci. 2008;28:13957–66. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Like Ca 2+ influx, zinc influx into neurons leads to the generation of nitric oxide and subsequent activation of PARP-1 and cell death [114].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [114] Kim YH, Koh JY. The role of NADPH oxidase and neuronal nitric oxide synthase in zinc-induced poly(ADP-ribose) polymerase activation and cell death in cortical culture. Exp Neurol. 2002;177:407–18. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Working memory is notably impaired in schizophrenia and in other neuro-psychiatric diseases likely due to the expected change in gamma oscillation power resulting from disinhibition”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Like other interneurons, PV-INs are derived from progenitor cells in the embryonic ganglionic eminences of the ventral telencephalon of the developing brain (Fig. 2).”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“PV-INs are implicated in neurodevelopmental diseases such as early-onset psychiatric disorders and in neurodegenerative diseases such as AD, demonstrating the vulnerability of this interneuron subset throughout life.”
§ Parvalbumin interneuron vulnerability and brain disorders > CONCLUSION AND FUTURE DIRECTIONS
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Externally, an exquisite coordination of attractant and repellant guidance factors transmitted from various brain regions guide migrating neurons to their ultimate destination [132].”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
What the sources say
- Not checked yetcites [132] Marin O, Valiente M, Ge X, Tsai LH. Guiding neuronal cell migrations. Cold Spring Harb Perspect Biol. 2010;2:a001834. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“PV-INs are important for proper brain function.”
§ Parvalbumin interneuron vulnerability and brain disorders > CONCLUSION AND FUTURE DIRECTIONS
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“NMDA receptor antagonists, such as ketamine and phencyclidine, can transiently reproduce key clinical features of schizophrenia, and are believed to reduce PV-IN excitation [123].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [123] Lisman JE, Coyle JT, Green RW, Javitt DC, Benes FM, Heckers S, et al. Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia. Trends Neurosci. 2008;31:234–42. source
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The authors state this as an assumption.
The developmental process by which interneurons migrate and integrate into cortical networks has vulnerabilities.
“While there likely is some space to correct for minor variabilities, it seems reasonable to assume that the process also has some vulnerabilities.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Dysfunction and/or deficient inhibitory output from PV interneurons may be a common mechanism of multiple psychiatric disorders, such as schizophrenia (SCZ) (Lewis et al. 2005), autism spectrum disorders (ASD) (Gao and Penzes 2015) and bipolar disorder (BD) (Ruden et al. 2021).”
From Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration (2022) · cites this paper as Ruden et al. 2021
Citations
Cites
1 retracted
Chen, L. Y., Jiang, M., Zhang, B., Gökçe, Ö., & Südhof, T. C. (2017) · Neuron · doi:10.1016/j.neuron.2017.04.011 · Cited by 209
RetractedShrestha, S., & Offer, S. M. (2016) · Medical Epigenetics · doi:10.1159/000444713 · Cited by 8,951
Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome c
Liu, X., Kim, C. N., Yang, J., Jemmerson, R., & Wang, X. (1996) · Cell · doi:10.1016/s0092-8674(00)80085-9 · Cited by 5,167
Greicius, M. D., Srivastava, G., Reiss, A. L., & Menon, V. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0308627101 · Cited by 3,684
Mechanisms of Gamma Oscillations
Buzsáki, G., & Wang, X.-J. (2012) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-062111-150444 · Cited by 2,796
Parvalbumin neurons and gamma rhythms enhance cortical circuit performance
Sohal, V. S., Zhang, F., Yizhar, O., & Deisseroth, K. (2009) · Nature · doi:10.1038/nature07991 · Cited by 2,606
Driving fast-spiking cells induces gamma rhythm and controls sensory responses
Cardin, J. A., Carlén, M., Meletis, K., Knoblich, U., Zhang, F., Deisseroth, K., Tsai, L.-H., & Moore, C. I. (2009) · Nature · doi:10.1038/nature08002 · Cited by 2,603
Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs
Cross-Disorder Group of the Psychiatric Genomics Consortium (2013) · Nature Genetics · doi:10.1038/ng.2711 · Cited by 2,263
GABAergic Interneurons in the Neocortex: From Cellular Properties to Circuits
Tremblay, R., Lee, S., & Rudy, B. (2016) · Neuron · doi:10.1016/j.neuron.2016.06.033 · Cited by 2,033
Gamma frequency entrainment attenuates amyloid load and modifies microglia
Iaccarino, H. F., Singer, A. C., Martorell, A. J., Rudenko, A., Gao, F., Gillingham, T. Z., Mathys, H., Seo, J., Kritskiy, O., Abdurrob, F., et al. (2016) · Nature · doi:10.1038/nature20587 · Cited by 1,328
Cited by
Sorted by citations
Cognitive impairment in schizophrenia: aetiology, pathophysiology, and treatment
McCutcheon, R. A., Keefe, R. S. E., & McGuire, P. K. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-01949-9 · Cited by 861
“For example, because parvalbumin interneurons have extremely high energy requirements, oxidative and metabolic stressors can have a disproportionate impact on these neurons, and their effects may be greatest in regions where they are present at high densities [265].”
BackgroundCortical interneurons in autism
Contractor, A., Ethell, I. M., & Portera‐Cailliau, C. (2021) · Nature Neuroscience · doi:10.1038/s41593-021-00967-6 · Cited by 186
Gómez de San José, N., Massa, F., Halbgebauer, S., Oeckl, P., Steinacker, P., & Otto, M. (2022) · Journal of Neural Transmission · doi:10.1007/s00702-021-02411-2 · Cited by 112
Brown, D. A., Altermatt, M., Dobreva, T., Chen, S., Wang, A. Z., Thomson, M. W., & Gradinaru, V. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.730825 · Cited by 61
Canetta, S. E., Holt, E. S., Benoit, L. J., Teboul, E., Sahyoun, G. M., Ogden, R. T., Harris, A. Z., & Kellendonk, C. (2022) · eLife · doi:10.7554/elife.80324 · Cited by 59
“The importance of this cell population for cortical development is underscored by the fact that they show histological abnormalities in multiple neurological and psychiatric disorders with a presumed neurodevelopmental origin, most classically schizophrenia (Lewis, 2014, Ruden et al., 2021).”
BackgroundSpoleti, E., Barbera, L. L., Cauzzi, E., Paolis, M. L. D., Saba, L., Marino, R., Sciamanna, G., Lazzaro, V. D., Keller, F., Nobili, A., et al. (2024) · Molecular Psychiatry · doi:10.1038/s41380-024-02408-9 · Cited by 63
Integrated platform for multiscale molecular imaging and phenotyping of the human brain
Park, J., Wang, J., Guan, W., Gjesteby, L., Pollack, D., Kamentsky, L. D., Evans, N. B., Stirman, J., Gu, X., Zhao, C., et al. (2024) · Science · doi:10.1126/science.adh9979 · Cited by 70
“CR+ (in layers I to III), PV+ (in layers III to V), and CR+/PV+ (in layers I to III) interneurons displayed lower density in AD, a pattern potentially associated with neurodegeneration, impaired homeostasis, and calcium-based signaling, consistent with the literature ( 47 , 48 ).”
Tabassum, S., Misrani, A., Huang, H., Zhang, Z.-Y., Li, Q.-W., & Long, C. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03395-8 · Cited by 58
Kumar, P., Goettemoeller, A. M., Espinosa‐García, C., Tobin, B. R., Tfaily, A., Nelson, R. S., Natu, A., Dammer, E. B., Santiago, J. V., Malepati, S., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-47028-7 · Cited by 53
“Among neuronal subtypes, PV-INs represent a unique class of inhibitory interneurons with fast-fi ring properties and high metabolic activity 13,98 .”
The fate of interneurons, GABA A receptor sub‐types and perineuronal nets in Alzheimer's disease
Ali, A. B., Islam, A., & Constanti, A. (2022) · Brain Pathology · doi:10.1111/bpa.13129 · Cited by 49
“PV-expressing interneurons are known to be highly vulnerable to stressors [128].”
BackgroundKang, Y., Clement, E. M., Park, I., Greenfield, L. J., Smith, B. N., & Lee, S.-H. (2021) · Experimental Neurology · doi:10.1016/j.expneurol.2021.113724 · Cited by 31
Jeong, N., & Singer, A. C. (2022) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2022.102604 · Cited by 46
The 40-Hz auditory steady-state response in bipolar disorder: A meta-analysis
Jefsen, O. H., Юрьевич, Ш. Ю., Larsen, K. M., & Dietz, M. J. (2022) · Clinical Neurophysiology · doi:10.1016/j.clinph.2022.06.014 · Cited by 42
“These NMDA-receptor and interneuron dysfunctions are, however, not specific to schizophrenia, but have also been reported in patients with bipolar disorder (Beneyto and Meador-Woodruff, 2008, Clinton and Meador-Woodruff, 2004, Ruden et al., 2021, Scarr et al., 2003, Toker et al., 2018).”
Parvalbumin - Positive Neurons in the Neocortex: A Review
Druga, R., Salaj, M., & Al‐Redouan, A. (2023) · Physiological Research · doi:10.33549/physiolres.935005 · Cited by 47
“Tremendous number of new data and concepts were collected in recent years describing the phenotypic characteristics of PV+ GABAergic interneurons and their operations in cortical microcircuits and larger neocortical assemblies acting as substrate in neurodegenerative processes [23].”
Santos‐Silva, T., Fabris, D. D. S., de Oliveira, C. L., Guimarães, F. S., & Gomes, F. V. (2023) · Schizophrenia Bulletin · doi:10.1093/schbul/sbad123 · Cited by 45
Dannenhoffer, C. A., Gómez‐A, A., Macht, V. A., Jawad, R., Sutherland, E. B., Vetreno, R. P., Crews, F. T., Boettiger, C. A., & Robinson, D. L. (2022) · Alcoholism Clinical and Experimental Research · doi:10.1111/acer.14810 · Cited by 36
Santos‐Silva, T., Colodete, D. A. E., Lisboa, J. R., Freitas, I. D. S., Lopes, C. F. B., Hadera, V., Lima, T. S. A., Souza, A. J., & Gomes, F. V. (2024) · Basic & Clinical Pharmacology & Toxicology · doi:10.1111/bcpt.13994 · Cited by 39
“13 Removing its pro-domain leads to MMP activation, which can occur via the action of other MMPs, serine proteinases, nitric oxide and ROS.”
BackgroundInfluentialKlocke, B., Krone, K., Tornes, J., Moore, C., Ott, H., & Pitychoutis, P. M. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1093099 · Cited by 35
“Taken together, these studies suggest that the impaired Ca2+ buffering brought about by the absence of PVALB may result in a compensatory proliferation and subplasmalemmal relocation of mitochondria to maintain the rapid Ca2+ dynamics these neurons rely on (Janickova and Schwaller, 2020; Ruden et al., 2021).”
BackgroundInfluentialOláh, V. J., Goettemoeller, A. M., Rayaprolu, S., Dammer, E. B., Seyfried, N. T., Rangaraju, S., Dimidschstein, J., & Rowan, M. J. (2022) · eLife · doi:10.7554/elife.75316 · Cited by 34
“PV-specific vulnerability could manifest as a result of their high metabolic demand ( Ruden et al., 2021 ) or through abnormal regulation of ion channel subunits necessary for maintaining their fast-spiking nature ( Martinez-Losa et al., 2018 ).”
Wu, X., Ji, M., Yin, X., Gu, H., Zhu, T., Wang, R.-Z., Yang, J., & Shen, J.-C. (2022) · International Immunopharmacology · doi:10.1016/j.intimp.2022.108724 · Cited by 31
Bucher, E., Collins, J. M., King, A. E., Vickers, J. C., & Kirkcaldie, M. (2021) · Brain Structure and Function · doi:10.1007/s00429-021-02327-3 · Cited by 31
The Engram’s Dark Horse: How Interneurons Regulate State-Dependent Memory Processing and Plasticity
Raven, F., & Aton, S. J. (2021) · Frontiers in Neural Circuits · doi:10.3389/fncir.2021.750541 · Cited by 29
Development, Diversity, and Death of MGE-Derived Cortical Interneurons
Williams, R. H., & Riedemann, T. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22179297 · Cited by 25
The neural hierarchy of consciousness: A theoretical model and review on neurophysiology and NCCs
Almeida, V. N. (2022) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2022.108202 · Cited by 29
Pinna, A., & Colasanti, A. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.689473 · Cited by 28
Altered neural oscillations and behavior in a genetic mouse model of NMDA receptor hypofunction
Aguilar, D. D., Radzik, L. K., Schiffino, F. L., Folorunso, O. O., Zielinski, M. R., Coyle, J. T., Balu, D. T., & McNally, J. M. (2021) · Scientific Reports · doi:10.1038/s41598-021-88428-9 · Cited by 27
Bíró, L., Miskolczi, C., Szebik, H., Bruzsik, B., Varga, Z. K., Szente, L., Tóth, M., Halász, J., & Mikics, É. (2023) · Neurobiology of Stress · doi:10.1016/j.ynstr.2023.100546 · Cited by 28
“Disturbances in glutamatergic drive of PV+ INs and the associated abnormal gamma oscillations have been implicated in various neuropsychiatric disorders, including schizophrenia (Ruden et al., 2021).”
Region-Specific Alterations of Perineuronal Net Expression in Postmortem Autism Brain Tissue
Brandenburg, C., & Blatt, G. J. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.838918 · Cited by 25
Tan, Z., Garduño, B. M., Fernández‐Aburto, P., Chen, L., Ha, N. M.-L., Cogram, P., Holmes, T. C., & Xu, X. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01481-x · Cited by 30
“Neurodegeneration is one of the main neuropathological features in the human AD brain and accounts for the significant brain atrophy seen in these patients [33, 34].”
BackgroundMarichal, N., Péron, S., Beltrán-Arranz, A., Galante, C., Scarante, F. F., Wiffen, R., Schuurmans, C., Karow, M., Gascón, S., & Berninger, B. (2024) · Science Advances · doi:10.1126/sciadv.adl5935 · Cited by 28
The Role of Perineuronal Nets in Physiology and Disease: Insights from Recent Studies
Auer, S., Schicht, M., Hoffmann, L., Budday, S., Frischknecht, R., Blümcke, I., & Paulsen, F. P. (2025) · Cells · doi:10.3390/cells14050321 · Cited by 32
“…an interneuron dysfunction was shown to be implicated in a variety of psychiatric disorders, including schizophrenia (SZ), autism spectrum disorder (ASD), and bipolar disorder (BPD), and in neurodegenerative disorders, like Alzheimer’s disease (AD), and aging (for a detailed review, see [99]).”
Armenta-Reséndiz, M., Assali, A., Tsvetkov, E., Cowan, C. W., & Lavín, A. (2022) · Neuropsychopharmacology · doi:10.1038/s41386-022-01371-9 · Cited by 25
Dufour, B. D., McBride, E., Bartley, T., Juárez, P., & Martínez‐Cerdeño, V. (2023) · Autism · doi:10.1177/13623613231154053 · Cited by 23
NADPH-oxidases as potential pharmacological targets for thrombosis and depression comorbidity
Amadio, P., Sandrini, L., Zarà, M., Barbieri, S. S., & Ieraci, A. (2024) · Redox Biology · doi:10.1016/j.redox.2024.103060 · Cited by 25
“Dysfunction of parvalbumin-positive GABAergic interneurons were correlated with various psychiatric disorders such as depression, schizophrenia, post-traumatic stress disorder and Alzheimer ’ s disease [229].”
BackgroundZahedi, E., Sadr, S. S., Sanaeierad, A., & Roghani, M. (2023) · Metabolic Brain Disease · doi:10.1007/s11011-023-01227-1 · Cited by 21
Kim, E.-G., Chang, W., Shin, S., Adhikari, A. S., Seol, G. H., Song, D., & Min, S. S. (2022) · Korean Journal of Physiology and Pharmacology · doi:10.4196/kjpp.2023.27.1.113 · Cited by 23
“The long-lasting changes in brain interneuron populations have been proposed to contribute to the pathophysiology of many important neuro-psychiatric disorders [73] since it causes E-I imbalance.”
Ghirardini, E., Sagona, G., Márquez-Galera, Á., Calugi, F., Navarrón, C. M., Cacciante, F., Chen, S., Vetta, F. D., Dadà, L., Mazziotti, R. M., et al. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01533-w · Cited by 16
Li, X., Sun, H., Zhu, Y., Wang, F., Wang, X., Han, L., Cui, D., Luo, D., Zhai, Y., Zhuo, L., et al. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.1010152 · Cited by 25
Parvalbumin interneuron-derived tissue-type plasminogen activator shapes perineuronal net structure
Lépine, M., Douceau, S., Devienne, G. F., Prunotto, P., Lenoir, S., Regnauld, C., Pouettre, E., Piquet, J., Lebouvier, L., Hommet, Y., et al. (2022) · BMC Biology · doi:10.1186/s12915-022-01419-8 · Cited by 21
“These FS-PV interneurons are fundamental for several behavioral responses and their dysfunction participates in several diseases, including schizophrenia and autism [35, 73].”
BackgroundZhang, B., Chen, K., Dai, Y., Luo, X., Xiong, Z., Zhang, W., Huang, X., So, K., & Zhang, L. (2024) · Communications Biology · doi:10.1038/s42003-024-06896-x · Cited by 17
“…degenerationincorticalregions 32 ,afewmodelshavebeendiscussedtoexplain the vulnerability of GABAergic neurons under proteinopathy, including the relatively higher energy requirement 33 , or the preference of microglial phagocytosis targeting the extracellular matrix of PV-INs 34 .”
BackgroundImaging high-frequency voltage dynamics in multiple neuron classes of behaving mammals
Haziza, S., Chrapkiewicz, R., Zhang, Y., Kruzhilin, V., Li, J., Li, J., Delamare, G., Swanson, R. A., Buzsáki, G., Kannan, M., et al. (2025) · Cell · doi:10.1016/j.cell.2025.06.028 · Cited by 20
Maternal P7C3-A20 Treatment Protects Offspring from Neuropsychiatric Sequelae of Prenatal Stress
Schroeder, R. E., Sridharan, P. S., Nguyen, L. T., Loren, A., Williams, N. S., Kettimuthu, K. P., Cintrón-Pérez, C. J., Vázquez‐Rosa, E., Pieper, A. A., & Stevens, H. E. (2021) · Antioxidants and Redox Signaling · doi:10.1089/ars.2020.8227 · Cited by 17
Wei, J., Liu, L., Song, X., Lin, B., Cui, J., Luo, L., Liu, Y., Li, S., Li, X., So, K., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112240 · Cited by 18
Parvalbumin as a sex-specific target in Alzheimer’s disease research – A mini-review
Terstege, D. J., & Epp, J. R. (2023) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2023.105370 · Cited by 14
“However, it appears that markers of altered metabolism, sex hormones, and inflammation each seem better suited as predictors of PV neuron loss (Cabungcal et al., 2006; Filice et al., 2018; Ruden et al., 2021; Steullet et al., 2017).”
Colodete, D. A. E., Grace, A. A., Guimarães, F. S., & Gomes, F. V. (2024) · Biological Psychiatry Global Open Science · doi:10.1016/j.bpsgos.2024.100338 · Cited by 16
“This imbalance can generate reactive oxygen species, mitochondrial membrane rupture, and subsequent activation of apoptotic pathways (13,47).”
Schreiber, C. S., Ramil, L. N., Bieligk, J., Meineke, R., Rimmelzwaan, G. F., Käufer, C., & Richter, F. (2025) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2025.05.021 · Cited by 15
Krajčíková, K., Semančíková, E., Zakuťanská, K., Kondrakhova, D., Mašlanková, J., Stupák, M., Talian, I., Tomašovičová, N., Kimáková, T., Komanický, V., et al. (2021) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2021.03.038 · Cited by 15
Santos‐Silva, T., Lopes, C. F. B., Ülgen, D. H., Guimarães, D. A., Guimarães, F. S., Alberici, L. C., Sandi, C., & Gomes, F. V. (2024) · Schizophrenia Bulletin · doi:10.1093/schbul/sbae033 · Cited by 20
Yu, H., Shao, M., Luo, X., Pang, C., So, K., Yu, J., & Zhang, L. (2023) · Neural Regeneration Research · doi:10.4103/1673-5374.377771 · Cited by 14
“(i) The relatively high energy requirement (Ruden et al., 2021): Under normal physiological conditions, the fast-spiking feature of PV-interneurons confers a high energy demand (Kann et al., 2014), making them the primary target when cellular metabolism is disrupted, as it is by pilocarpine (Lee et…”
BackgroundSantos‐Silva, T., Souza, B. K., Colodete, D. A. E., Campos, L. R., Lima, T. S. A., Guimarães, F. S., & Gomes, F. V. (2024) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyae042 · Cited by 15
Loss of KCC2 in GABAergic Neurons Causes Seizures and an Imbalance of Cortical Interneurons
Zavalin, K. A., Hassan, A., Fu, C., Delpire, E. J., & Lagrange, A. H. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.826427 · Cited by 14
Hameed, M. Q., Hodgson, N., Lee, H. H. C., Pascual-Leone, A., MacMullin, P., Jannati, A., Dhamne, S. C., Hensch, T. K., & Rotenberg, A. (2022) · Cerebral Cortex · doi:10.1093/cercor/bhac327 · Cited by 14
The metabolic engine of cognition: microglia–neuron interactions in health, ageing and disease
Asimakidou, E., Pluchino, S., Silva, B. A., & Peruzzotti‐Jametti, L. (2025) · Nature Metabolism · doi:10.1038/s42255-025-01409-4 · Cited by 24
Wang, S. H., Lee, D.-S., Kim, T.-H., Kim, J.-E., & Kang, T. (2024) · Cell Death and Disease · doi:10.1038/s41419-024-07050-5 · Cited by 13
“These fi ndings indicate that both CDK5-DRP1-mediated mitochondrial fi ssion and impaired GPx1-mediated NF-κ B inhibition may diminish PV expression, which may lead to PV neuronal degeneration following SE.”
InfluentialKang, J.-B., Park, D.-J., Shah, M.-A., & Koh, P. (2022) · Journal of Veterinary Science · doi:10.4142/jvs.21273 · Cited by 13
“Parvalbumin protects the mitochondria from calcium overload by inhibiting a depolarization-induced calcium increase and buffering calcium in an intracellular environment [15].”
BackgroundIntegrated platform for multi-scale molecular imaging and phenotyping of the human brainPreprint
Park, J., Wang, J., Guan, W., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.03.13.484171 · Cited by 12
Calcium-binding protein parvalbumin in the spinal cord and dorsal root ganglia
Veshchitskii, A. A., & Merkulyeva, N. S. (2023) · Neurochemistry International · doi:10.1016/j.neuint.2023.105634 · Cited by 12
Morphett, J., Whittaker, A. L., Reichelt, A. C., & Hutchinson, M. R. (2024) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2024.105568 · Cited by 14
“PV neurons are fast-spiking GABAergic interneurons which are vulnerable to the environment and are implicated in various neurodevelopmental disorders (Ruden et al., 2021).”
BackgroundAn, D., You, Y., Ma, Q., Xu, Z., Liu, Z., Liao, R., Chen, H., Wang, Y., Wang, Y., Dai, H., et al. (2025) · Neuron · doi:10.1016/j.neuron.2024.12.002 · Cited by 13
Linking Social Cognition, Parvalbumin Interneurons, and Oxytocin in Alzheimer’s Disease: An Update
Černotová, D., Hrůzová, K., Levčík, D., Svoboda, J., & Stuchlı́k, A. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230333 · Cited by 12
“Although the AD pathology was studied primarily in terms of dysfunction of glutamatergic and cholinergic systems, there is growing evidence that GABAergic, i.e., inhibitory signaling is affected in the early stages of this disorder, leaving a negative impact on the E/I balance [27, 55–60].”
BackgroundAllami, P., Yazdanpanah, N., & Rezaei, N. (2025) · Reviews in the Neurosciences · doi:10.1515/revneuro-2024-0153 · Cited by 11
Possible Role of Parvalbumin Interneurons in Meditation and Psychiatric Illness
Thippaiah, S. M., Pradhan, B., Voyiaziakis, E., Shetty, R., Iyengar, S., Olson, C., & Tang, Y. (2022) · Journal of Neuropsychiatry · doi:10.1176/appi.neuropsych.21050136 · Cited by 12
Huang, T.-H., Lin, Y.-S., Hsiao, C., Wang, L.-Y., Ajibola, M. I., Abdulmajeed, W. I., Lin, Y., Li, Y., Chen, C.-Y., Lien, C., et al. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1146278 · Cited by 12
“Consequently, dysfunction of inhibition is associated with various brain disorders (Belelli et al., 2009; Baroncelli et al., 2011; Ruden et al., 2021; Song et al., 2021; Yang et al., 2022).”
Brown, D. A., Altermatt, M., Dobreva, T., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.06.25.449955 · Cited by 11
Zhang, X., Wu, M., Cheng, L., Cao, W., Liu, Z., Yang, S., & Kim, M. S. (2024) · Molecular Psychiatry · doi:10.1038/s41380-024-02756-6 · Cited by 13
“Consequently, the de fi ning phenotype of PV-INs is an FS action potential associated with high-energy consumption [24, 85].”
Fin, N. A. S. H., Yip, A., Scott, J. T., Teo, L., Homman‐Ludiye, J., & Bourne, J. A. (2025) · Development · doi:10.1242/dev.204254 · Cited by 14
Age-related inflammatory changes and perineuronal net dynamics: implications for aging
Colon, Z. A., Chan, S. C., & Maguire‐Zeiss, K. A. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03568-3 · Cited by 13
“Dysfunction of these cells has previously been linked to epilepsy, schizophrenia, and autism [21, 22], as well as PD [23] and AD [24].”
Haikonen, J., Szrinivasan, R., Ojanen, S., Rhee, J. K., Ryazantseva, M., Sulku, J., Zumaraite, G., & Lauri, S. E. (2024) · Molecular Psychiatry · doi:10.1038/s41380-024-02641-2 · Cited by 9
“The existing research linking PV IN dysfunction to neuropsychiatric conditions, especially schizophrenia is extensive, comprising both of human and animal model studies 46,47,69–72 .”
BackgroundForebrain expression of serine racemase during postnatal development
Folorunso, O. O., Harvey, T. L., Brown, S. E., Cruz, C., Shahbo, E., Ajjawi, I., & Balu, D. T. (2021) · Neurochemistry International · doi:10.1016/j.neuint.2021.104990 · Cited by 12
Fournier, L. A., Phadke, R. A., Salgado, M., Brack, A., Nocon, J. C., Bolshakova, S., Grant, J. R., Padró-Luna, N. M., Sen, K., & Cruz‐Martín, A. (2024) · iScience · doi:10.1016/j.isci.2024.110800 · Cited by 8
Minetti, A., Montagni, E., Meneghetti, N., Macchi, F., Coulomb, É., Martello, A., Tiberi, A., Capsoni, S., Mazzoni, A., Mascaro, A. L. A., et al. (2025) · npj Parkinson s Disease · doi:10.1038/s41531-025-01052-6 · Cited by 10
Gamma Activity in Sensory and Cognitive Processing
Strüber, D., & Herrmann, C. S. (2022) · Oxford University Press eBooks · doi:10.1093/oxfordhb/9780192898340.013.8 · Cited by 8
Prepubertal ovariectomy confers resilience to stress-induced anxiety in adult female mice
Woodward, E. M., Ringland, A., Ackerman, J., & Coutellier, L. D. (2022) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2022.105997 · Cited by 8
Defects of parvalbumin-positive interneurons are implicated in psychiatric disorders
Zhao, F., & Guan, W. (2024) · Biochemical Pharmacology · doi:10.1016/j.bcp.2024.116599 · Cited by 9
Song, C., Zhao, Y. G., Zhang, J., Dong, Z., Kang, X., Pan, Y., Du, J., Gao, Y., Zhang, H., Ye, X., et al. (2023) · Neuroscience Bulletin · doi:10.1007/s12264-023-01083-0 · Cited by 8
“PV interneurons are vulnerable under pathological conditions [14].”
BackgroundKlimczak, P., Alcaide, J., Gramuntell, Y., Castillo-Gómez, E., Varea, E., Pérez-Rando, M., & Nácher, J. (2024) · Translational Psychiatry · doi:10.1038/s41398-024-03166-6 · Cited by 7
“Consequently, it is unsurprising that alterations in their density, connectivity, and physiology have been found in different psychiatric disorders with a neurodevelopmental origin, such as schizophrenia [5, 6].”
Kang, J.-B., Park, D.-J., & Koh, P. (2022) · Neurochemical Research · doi:10.1007/s11064-022-03769-9 · Cited by 7
“It is interconnected with electrical and chemical synapses in the cerebral cortex, regulating sensory response, learning, and synaptic plasticity [17].”
BackgroundDOT1L deletion impairs the development of cortical parvalbumin-expressing interneurons
Cheffer, A., Garcia‐Miralles, M., Maier, E., Akol, I., Franz, H., Srinivasan, V. S. V., & Vogel, T. (2023) · Cerebral Cortex · doi:10.1093/cercor/bhad281 · Cited by 7
“Indeed, impairments in GABAergic neurotransmission and consequently altered E-I balance are implicated in many neurological and psychiatric conditions, including Alzheimer’s disease, epilepsy, schizophrenia, autism, depression and mood disorders (reviewed in Nahar et al. 2021; Prévot and Sibille 2021; Ruden et al. 202…”
BackgroundHuang, D., Li, M., Qiao, Z., Zhou, H., Cai, Y., Li, X., Zhang, Z., & Zhou, J. (2024) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2024.06.006 · Cited by 7
“Notably, alterations in cognitive function have been closely linked to impaired PV + interneurons (Ruden et al., 2021).”
BackgroundSullivan, E. D. K., Dannenhoffer, C. A., Sutherland, E. B., Vidrascu, E. M., Gómez‐A, A., Boettiger, C. A., & Robinson, D. L. (2024) · Alcoholism Clinical and Experimental Research · doi:10.1111/acer.15395 · Cited by 9
Ratner, M. H., & Farb, D. H. (2022) · Frontiers in Toxicology · doi:10.3389/ftox.2022.836427 · Cited by 7
“The hippocampus is vulnerable to adverse effects of drugs and neurotoxicants (Tsunashima et al., 1998; Campbell et al., 2004; Bowyer and Ali, 2006; Bowyer et al., 2008; Ruden et al., 2021)”
BackgroundCortical interneuron development is affected in 4H leukodystrophy
Dooves, S., Kok, L. M. L., Holmes, D. B., Breeuwsma, N., Breur, M., Bugiani, M., Wolf, N. I., & Heine, V. M. (2023) · Brain · doi:10.1093/brain/awad017 · Cited by 8
“spiking interneurons with a high metabolic demand, which makes them vulnerable for injury.(64) Interestingly, the development of SST and PV interneurons is depending on SHH levels,(65,66) and deletion of Arx in PV neurons led to increased neuronal activity and altered synaptic properties in a mouse model.”
Dang, T. N., Tien, S. N., Ochi, R., Le, D. T., Nishio, K., Kuwamura, H., Kurose, T., Fujita, N., Nishijo, H., Nakamura, Y., et al. (2023) · Behavioural Brain Research · doi:10.1016/j.bbr.2023.114786 · Cited by 6
Hippocampal parvalbumin and perineuronal nets: Possible involvement in anxiety‐like behavior in rats
Fan, Z., Gong, X., Xu, H., Qu, Y., Li, B., Li, L., Yan, Y., Wu, L., & Yan, C. (2023) · Hippocampus · doi:10.1002/hipo.23595 · Cited by 7
“autism spectrum disorder, and bipolar disorder (Ruden et al., 2021; Song et al., 2021).”
Emerging Perspectives on Neuroprotection
Hasler, G., & Inta, D. (2024) · Psychotherapy and Psychosomatics · doi:10.1159/000540032 · Cited by 6
“Vulnerability is conferred mainly by their very high energy demand, re-fl ected by unique enrichment with mitochondria and are highly vulnerable to stressors [12].”
Zheng, Y., Wang, W., Xia, S., et al. (2025) · Neuroscience · doi:10.1016/j.neuroscience.2025.09.012 · Cited by 6
Rethinking parvalbumin: From passive marker to active modulator of hippocampal circuits
Zhang, N., Hu, B., Li, X., & Huang, H. (2025) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2025.10.005 · Cited by 7
“Their high metabolic demands, extensive connectivity, and constant high-frequency activity make them exquisitely sensitive to a wide range of insults (Kann et al., 2014; Ruden et al., 2021; Yao et al., 2020).”
InfluentialOkuzono, S., Fujii, F., Matsushita, Y., Setoyama, D., Shinmyo, Y., Taira, R., Yonemoto, K., Akamine, S., Motomura, Y., Sanefuji, M., et al. (2023) · Neuroscience Research · doi:10.1016/j.neures.2023.03.001 · Cited by 6
Brandt, M. J. V., Kosmeijer, C. M., Achterberg, E. J. M., de Theije, C. G. M., & Nijboer, C. H. A. (2024) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2024.100817 · Cited by 8
“…2020; Desfeux et al., 2010; Roux et al., 2015), and hypomyelination (Lim et al., 2018; Hafner et al., 2019; Wamsley and Fishell, 2017), due to their energy requirements, excitatory inputs and developmental trajectory (Zhang et al., 2016; Ruden et al., 2021; Juarez and Martínez-Cerde ˜ no, 2022).”
Long‐range inputome of prefrontal GABAergic interneurons in the Alzheimer's disease mouse
Ren, M., Li, Y., Jiang, T., Liu, B., Li, X., Jia, X., Li, A., Luo, Q., Gong, H., & Li, X. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14552 · Cited by 5
Olfactory deficits in aging and Alzheimer’s—spotlight on inhibitory interneurons
Elhabbari, K., Sireci, S., Rothermel, M., & Brunert, D. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1503069 · Cited by 7
“Significant reductions in the densities of SST and CR interneurons were observed in the LEC of an AD mouse model compared to wild-type (WT) mice (Figure 2A; Klein et al., 2016) while fast-spiking PV-expressing interneurons do not show a significant decline (Ruden et al., 2021).”
Human mutations in SLITRK3 implicated in GABAergic synapse development in mice
Efthymiou, S., Han, W., Ilyas, M., Li, J., Yu, Y., Scala, M., Malintan, N. T., Vavouraki, N., Mankad, K., Maroofian, R., et al. (2022) · bioRxiv · doi:10.3389/fnmol.2024.1222935 · Cited by 4
“Parvalbumin (PV) interneurons in the hippocampus are mostly basket cells with fast-spiking actions at a high energy cost, are highly vulnerable to stressors, and have been implicated in many neuropsychiatric disorders (Ruden et al., 2020).”
BackgroundBanerjee, T., Pati, S., Tiwari, P., & Vaidya, V. A. (2022) · Journal of Biosciences · doi:10.1007/s12038-022-00308-0 · Cited by 6
“In this regard, our approach to chemogenetically manipulate PV-positive interneurons during postnatal development across diverse circuits bears relevance to both models of early adversity and neurodevelopmental disorders, which impact PV-positive interneurons across several limbic brain regions (Ruden et al. 2021).”
BackgroundInfluentialChalatsi, T., Fernandez, L. M. J., Scholler, J., Batti, L., Kolaxi, A., Restivo, L., Lüthi, A., Mameli, M., & Nikoletopoulou, V. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.10.10.511533 · Cited by 4
Kumar, P., Goettemoeller, A. M., Espinosa‐García, C., Tobin, B. R., Tfaily, A., Nelson, R. S., Natu, A., Dammer, E. B., Santiago, J. V., Malepati, S., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.05.17.541038 · Cited by 4
Fin, N. A. S. H., Yip, A., Teo, L., Homman‐Ludiye, J., & Bourne, J. A. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.07.10.602904 · Cited by 3
Bakos, E., Tiszlavicz, Á., Szegedi, V., Douida, A., Furdan, S., Welter, D. K., Landry, J. J. M., Bende, B., Hutóczki, G., Barzó, P., et al. (2025) · PLoS Biology · doi:10.1371/journal.pbio.3003549 · Cited by 7
“Slowed inhibitory signaling in the human neocortex would be detrimental, as theoretical models and in vivo animal studies have linked such changes to reduced cortical computation speed and cognitive impairment [40,72–75].”
Manns, M., Juckel, G., & Freund, N. (2025) · Brain Sciences · doi:10.3390/brainsci15020169 · Cited by 5
Zhang, X.-R., Cheng, L., Yang, S.-B., jin, M., Piao, Q.-Y., Kim, D.-W., & Kim, M.-S. (2025) · Current Neuropharmacology · doi:10.2174/011570159x356939250306075324 · Cited by 3
“The energy requirements of PV-INs make them highly susceptible to oxidative stress and the loss of mitochondrial membrane potential in neurodegenerative diseases [24, 29].”
Metadata
- Authors
- Ruden, J. B., Dugan, L. L., & Konradi, C.
- Affiliations
- Vanderbilt University (US)
- Corresponding author
- Konradi, Christine
- Venue
- Neuropsychopharmacology
- Published
- 2020-07-28
- Volume
- 46
- Issue
- 2
- Pages
- 279-287
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC7852528
- OpenAlex
- W3044343625
- Semantic Scholar
- 2c4e5394f3b88323dda4206c07141d738c058a9c
- Cited by
- 194
- References
- 148
- Citations by year
- 2026: 33 · 2025: 50 · 2024: 36 · 2023: 31 · 2022: 28 · 2021: 16
- FWCI
- 2.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX004321)
- Vanderbilt University
- Vanderbilt Institute for Clinical and Translational Research
- Geriatric Research Education and Clinical Center
- National Institute on Aging (R01AG058856)
- National Center for Research Resources (KL2RR024977)
- NIH Clinical Center
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- parvalbumin interneurons, neuronal vulnerability, stressors, schizophrenia, Alzheimer's disease, autism spectrum disorder, bipolar disorder, excitatory drive, energy requirements, interneuron development, neuroprotection
- MeSH terms
- Autism Spectrum Disorder, Alzheimer Disease, Humans, Interneurons, Neurons, Parvalbumins
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