The DOI matches its Crossref record; 148 of the 148 references it cites were found in a registry or an index; 7 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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
75 Not checked yet · 15 Own interpretation · 5 No basis given · 2 Supported · 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.
- 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
“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.
- 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.
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.
- 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. 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
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
- Not checked yetcites [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
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.
None of the sources cited for this claim have been checked 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
- Not checked yetcites [122] Konradi C, Heckers S. Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment. Pharm Ther. 2003;97:153–79. source
- 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
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.
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
Verret, L., Mann, E. O., Hang, G. B., Barth, A. M. I., Cobos, I., Ho, K., Devidze, N., Masliah, E., Kreitzer, A. C., Mody, I., et al. (2012) · Cell · doi:10.1016/j.cell.2012.02.046 · Cited by 1,216
Fast-spiking, parvalbumin + GABAergic interneurons: From cellular design to microcircuit function
Hu, H., Gan, J., & Jonas, P. (2014) · Science · doi:10.1126/science.1255263 · Cited by 1,197
Interneuron dysfunction in psychiatric disorders
Marín, O. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3155 · Cited by 1,190
Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes
Chao, H.-T., Chen, H., Samaco, R. C., Xue, M., Chahrour, M., Yoo, J., Neul, J. L., Gong, S., Lu, H.-C., Heintz, N., et al. (2010) · Nature · doi:10.1038/nature09582 · Cited by 1,168
Peñagarikano, O., Abrahams, B. S., Herman, E. I., Winden, K. D., Gdalyahu, A., Dong, H., Sonnenblick, L. I., Gruver, R., Almajano, J., Bragin, A., et al. (2011) · Cell · doi:10.1016/j.cell.2011.08.040 · Cited by 1,075
Cortical parvalbumin interneurons and cognitive dysfunction in schizophrenia
Lewis, D. A., Curley, A. A., Glausier, J. R., & Volk, D. W. (2012) · Trends in Neurosciences · doi:10.1016/j.tins.2011.10.004 · Cited by 1,071
High rates of schizophrenia in adults with velo-cardio-facial syndrome
Murphy, K. C., Jones, L. A., & Owen, M. J. (1999) · Archives of General Psychiatry · doi:10.1001/archpsyc.56.10.940 · Cited by 1,024
Zhou, J., Greicius, M. D., Gennatas, E. D., Growdon, M. E., Jang, J. Y., Rabinovici, G. D., Kramer, J. H., Weiner, M., Miller, B. L., & Seeley, W. W. (2010) · Brain · doi:10.1093/brain/awq075 · Cited by 1,016
Function of Mitochondrial Stat3 in Cellular Respiration
Wegrzyn, J., Potla, R., Chwae, Y.-J., Sepuri, N. B. V., Zhang, Q., Koeck, T., Derecka, M., Szczepanek, K., Szelag, M., Gornicka, A., et al. (2009) · Science · doi:10.1126/science.1164551 · Cited by 1,014
Lisman, J. E., Coyle, J. T., Green, R. W., Javitt, D. C., Benes, F. M., Heckers, S., & Grace, A. A. (2008) · Trends in Neurosciences · doi:10.1016/j.tins.2008.02.005 · Cited by 1,010
The origin and specification of cortical interneurons
Wonders, C. P., & Anderson, S. A. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1954 · Cited by 980
Ogiwara, I., Miyamoto, H., Morita, N., Atapour, N., Mazaki, E., Inoue, I., Takeuchi, T., Itohara, S., Yanagawa, Y., Obata, K., et al. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.5270-06.2007 · Cited by 879
Gamma Oscillations Correlate with Working Memory Load in Humans
Howard, M. W. (2003) · Cerebral Cortex · doi:10.1093/cercor/bhg084 · Cited by 766
Buhl, E. H., Halasy, K., & Somogyi, P. (1994) · Nature · doi:10.1038/368823a0 · Cited by 728
Mitochondrial STAT3 Supports Ras-Dependent Oncogenic Transformation
Gough, D. J., Corlett, A., Schlessinger, K., Wegrzyn, J., Larner, A. C., & Levy, D. E. (2009) · Science · doi:10.1126/science.1171721 · Cited by 716
Development and Functional Diversification of Cortical Interneurons
Lim, L., Mi, D., Llorca, A., & Marín, O. (2018) · Neuron · doi:10.1016/j.neuron.2018.10.009 · Cited by 714
Parvalbumin-expressing basket-cell network plasticity induced by experience regulates adult learning
Donato, F., Rompani, S. B., & Caroni, P. (2013) · Nature · doi:10.1038/nature12866 · Cited by 703
Akbarian, S. (1993) · Archives of General Psychiatry · doi:10.1001/archpsyc.1993.01820150007001 · Cited by 680
Hippocampal CA1 interneurons: an in vivo intracellular labeling study
Sik, A., Penttonen, M., Ylinen, A., & Buzsaki, G. (1995) · The Journal of Neuroscience · doi:10.1523/jneurosci.15-10-06651.1995 · Cited by 669
Carlén, M., Meletis, K., Siegle, J. H., Cardin, J. A., Futai, K., Vierling-Claassen, D., Rühlmann, C., Jones, S. R., Deisseroth, K., Sheng, M., et al. (2012) · Molecular Psychiatry · doi:10.1038/mp.2011.31 · Cited by 669
Altered brain microRNA biogenesis contributes to phenotypic deficits in a 22q11-deletion mouse model
Stark, K. L., Xu, B., Bagchi, A., Lai, W.-S., Liu, H., Hsu, R., Wan, X., Pavlidis, P., Mills, A. A., Karayiorgou, M., et al. (2008) · Nature Genetics · doi:10.1038/ng.138 · Cited by 648
Ketamine-Induced Loss of Phenotype of Fast-Spiking Interneurons Is Mediated by NADPH-Oxidase
Behrens, M. M., Ali, S. S., Dao, D. N., Lucero, J., Shekhtman, G., Quick, K. L., & Dugan, L. L. (2007) · Science · doi:10.1126/science.1148045 · Cited by 585
Self-citationMutations in the SHANK2 synaptic scaffolding gene in autism spectrum disorder and mental retardation
Berkel, S., Marshall, C. R., Weiss, B., Howe, J., Roeth, R., Moog, U., Endris, V., Roberts, W., Szatmari, P., Pinto, D., et al. (2010) · Nature Genetics · doi:10.1038/ng.589 · Cited by 563
Fuchs, E. C., Zivkovic, A. R., Cunningham, M. O., Middleton, S., LeBeau, F. E. N., Bannerman, D. M., Rozov, A., Whittington, M. A., Traub, R. D., Rawlins, J. N. P., et al. (2007) · Neuron · doi:10.1016/j.neuron.2007.01.031 · Cited by 532
Behavioral phenotypes of Disc1 missense mutations in mice
Clapcote, S. J., Lipina, T. V., Millar, J. K., Mackie, S., Christie, S., Ogawa, F., Lerch, J. P., Trimble, K., Uchiyama, M., Sakuraba, Y., et al. (2007) · Neuron · doi:10.1016/j.neuron.2007.04.015 · Cited by 526
Packer, A. M., & Yuste, R. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.3131-11.2011 · Cited by 506
Alterations in Cortical Network Oscillations and Parvalbumin Neurons in Schizophrenia
Gonzalez-Burgos, G., Cho, R. Y., & Lewis, D. A. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.03.010 · Cited by 497
Lodge, D. J., Behrens, M. M., & Grace, A. A. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.5419-08.2009 · Cited by 488
Gulyás, A. I., Megı́as, M., Emri, Z., & Freund, T. F. (1999) · The Journal of Neuroscience · doi:10.1523/jneurosci.19-22-10082.1999 · Cited by 476
SHANK3 and IGF1 restore synaptic deficits in neurons from 22q13 deletion syndrome patients
Shcheglovitov, A., Shcheglovitova, O., Yazawa, M., Portmann, T., Shu, R., Sebastiano, V., Krawisz, A., Froehlich, W., Bernstein, J. A., Hallmayer, J. F., et al. (2013) · Nature · doi:10.1038/nature12618 · Cited by 470
Nuclear and mitochondrial conversations in cell death: PARP-1 and AIF signaling
Hong, S. J., Dawson, T. M., & Dawson, V. L. (2004) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2004.03.005 · Cited by 463
A Twin Study of Genetic Relationships Between Psychotic Symptoms
Cardno, A. G., Rijsdijk, F. V., Sham, P. C., Murray, R. M., & McGuffin, P. (2002) · American Journal of Psychiatry · doi:10.1176/appi.ajp.159.4.539 · Cited by 460
Akbarian, S. (1993) · Archives of General Psychiatry · doi:10.1001/archpsyc.1993.01820150016002 · Cited by 452
Guiding Neuronal Cell Migrations
Marin, O., Valiente, M., Ge, X., & Tsai, L.-H. (2010) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a001834 · Cited by 417
A disinhibitory microcircuit initiates critical-period plasticity in the visual cortex
Kuhlman, S. J., Olivas, N. D., Tring, E., Ikrar, T., Xu, X., & Trachtenberg, J. T. (2013) · Nature · doi:10.1038/nature12485 · Cited by 412
Sensi, S. L., Yin, H. Z., Carriedo, S. G., Rao, S. S., & Weiss, J. H. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.5.2414 · Cited by 408
Role of the calcium-binding protein parvalbumin in short-term synaptic plasticity
Caillard, O., Moreno, H., Schwaller, B., Llano, I., Celio, M. R., & Marty, A. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.230362997 · Cited by 406
Akbarian, S. (1996) · Archives of General Psychiatry · doi:10.1001/archpsyc.1996.01830050061010 · Cited by 397
Galarreta, M., & Hestrin, S. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.192159599 · Cited by 387
Age-related changes in the default mode network are more advanced in Alzheimer disease
Jones, D. T., Machulda, M. M., Vemuri, P., McDade, E. M., Zeng, G., Senjem, M. L., Gunter, J. L., Przybelski, S. A., Avula, R. T., Knopman, D. S., et al. (2011) · Neurology · doi:10.1212/wnl.0b013e318233b33d · Cited by 370
Mitochondria: The calcium connection
Contreras, L., Drago, I., Zampese, E., & Pozzan, T. (2010) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2010.05.005 · Cited by 363
Steullet, P., Cabungcal, J.-H., Coyle, J., Didriksen, M., Gill, K., Grace, A. A., Hensch, T. K., LaMantia, A.-S., Lindemann, L., Maynard, T. M., et al. (2017) · Molecular Psychiatry · doi:10.1038/mp.2017.47 · Cited by 360 · cited 2×
“In rodent models that recapitulate aspects of brain disorders, higher oxidative stress consistently correlates with decreased PV-positive cortical interneurons [92, 93].”
BackgroundSloviter, R. S., Sollas, A. L., Barbaro, N. M., & Laxer, K. D. (1991) · Journal of Comparative Neurology · doi:10.1002/cne.903080306 · Cited by 349
Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment
Konradi, C., & Heckers, S. (2003) · Pharmacology & Therapeutics · doi:10.1016/s0163-7258(02)00328-5 · Cited by 336
Self-citationKinney, J. W., Davis, C. N., Tabarean, I., Conti, B., Bartfai, T., & Behrens, M. M. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.4722-05.2006 · Cited by 329
Selimbeyoglu, A., Kim, C. K., Inoue, M., Lee, S. Y., Hong, A. S. O., Kauvar, I., Ramakrishnan, C., Fenno, L. E., Davidson, T. J., Wright, M., et al. (2017) · Science Translational Medicine · doi:10.1126/scitranslmed.aah6733 · Cited by 326
Heckers, S., Stone, D., Walsh, J., Shick, J., Koul, P., & Benes, F. M. (2002) · Archives of General Psychiatry · doi:10.1001/archpsyc.59.6.521 · Cited by 322
Resting Brain Connectivity: Changes during the Progress of Alzheimer Disease
Zhang, H.-Y., Wang, S.-J., Liu, B., Ma, Z.-L., Yang, M., Zhang, Z.-J., & Teng, G.-J. (2010) · Radiology · doi:10.1148/radiol.10091701 · Cited by 320
Dikalov, S., Nazarewicz, R. R., Bikineyeva, A. T., Hilenski, L. L., Lassegue, B. P., Griendling, K. K., Harrison, D. G., & Dikalova, A. (2013) · Antioxidants and Redox Signaling · doi:10.1089/ars.2012.4918 · Cited by 312
Kann, O., Papageorgiou, I. E., & Draguhn, A. (2014) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2014.104 · Cited by 295
A Blueprint for the Spatiotemporal Origins of Mouse Hippocampal Interneuron Diversity
Tricoire, L., Pelkey, K. A., Erkkila, B. E., Jeffries, B. W., Yuan, X., & McBain, C. J. (2011) · Journal of Neuroscience · doi:10.1523/jneurosci.0323-11.2011 · Cited by 292
Hippocampal interneurons are abnormal in schizophrenia
Konradi, C., Yang, C. K., Zimmerman, E. I., Lohmann, K. M., Gresch, P., Pantazopoulos, H., Berretta, S., & Heckers, S. (2011) · Schizophrenia Research · doi:10.1016/j.schres.2011.06.007 · Cited by 288
Self-citationGABAergic mechanisms of hippocampal hyperactivity in schizophrenia
Heckers, S., & Konradi, C. (2015) · Schizophrenia Research · doi:10.1016/j.schres.2014.09.041 · Cited by 277
Self-citationJiang, D., Sullivan, P. G., Sensi, S. L., Steward, O., & Weiss, J. H. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m108834200 · Cited by 265
Wöhr, M., Orduz, D., Gregory, P., Moreno, H., Khan, U., Vörckel, K. J., Wolfer, D. P., Welzl, H., Gall, D., Schiffmann, S. N., et al. (2015) · Translational Psychiatry · doi:10.1038/tp.2015.19 · Cited by 258
Schizophrenia-Related Neural and Behavioral Phenotypes in Transgenic Mice Expressing TruncatedDisc1
Shen, S., Lang, B., Nakamoto, C., Zhang, F., Pu, J., Kuan, S. L., Chatzi, C. A., He, S., Mackie, I., Brandon, N. J., et al. (2008) · Journal of Neuroscience · doi:10.1523/jneurosci.3299-08.2008 · Cited by 257
Calcium-permeable AMPA channels in neurodegenerative disease and ischemia
Kwak, S., & Weiss, J. H. (2006) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2006.05.004 · Cited by 256
Kim, Y.-M., Kim, S.-J., Tatsunami, R., Yamamura, H., Fukai, T., & Ushio-Fukai, M. (2017) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00346.2016 · Cited by 251
Interleukin-6 Mediates the Increase in NADPH-Oxidase in the Ketamine Model of Schizophrenia
Behrens, M. M., Ali, S. S., & Dugan, L. L. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.4457-08.2008 · Cited by 241
Self-citationFilice, F., Vörckel, K. J., Sungur, A. Ö., Wöhr, M., & Schwaller, B. (2016) · Molecular Brain · doi:10.1186/s13041-016-0192-8 · Cited by 240
Enwright, J. F., Sanapala, S., Foglio, A., Berry, R., Fish, K. N., & Lewis, D. A. (2016) · Neuropsychopharmacology · doi:10.1038/npp.2016.24 · Cited by 223
Steullet, P., Cabungcal, J.-H., Kulak, A., Kraftsik, R., Chen, Y., Dalton, T. P., Cuenod, M., & Do, K. Q. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.3857-09.2010 · Cited by 202
Bidirectional plasticity in fast-spiking GABA circuits by visual experience
Yazaki-Sugiyama, Y., Kang, S., Câteau, H., Fukai, T., & Hensch, T. K. (2009) · Nature · doi:10.1038/nature08485 · Cited by 200
Sahara, S., Yanagawa, Y., O'Leary, D. D. M., & Stevens, C. F. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.6412-11.2012 · Cited by 198
Kisvárday, Z. F., Beaulieu, C., & Eysel, U. T. (1993) · Journal of Comparative Neurology · doi:10.1002/cne.903270307 · Cited by 195
Harrington, A. J., Raissi, A., Rajkovich, K., Berto, S., Kumar, J., Molinaro, G., Raduazzo, J., Guo, Y., Loerwald, K., Konopka, G., et al. (2016) · eLife · doi:10.7554/elife.20059 · Cited by 193
Kann, O., Huchzermeyer, C., Kovács, R., Wirtz, S., & Schuelke, M. (2011) · Brain · doi:10.1093/brain/awq333 · Cited by 189
Cortical interneuron development: a tale of time and space
Hu, J. S., Vogt, D., Sandberg, M., & Rubenstein, J. L. (2017) · Development · doi:10.1242/dev.132852 · Cited by 189
Piskorowski, R. A., Nasrallah, K., Diamantopoulou, A., Mukai, J., Hassan, S. I., Siegelbaum, S. A., Gogos, J. A., & Chevaleyre, V. (2016) · Neuron · doi:10.1016/j.neuron.2015.11.036 · Cited by 180
Altered Cortical Ensembles in Mouse Models of Schizophrenia
Hamm, J. P., Peterka, D. S., Gogos, J. A., & Yuste, R. (2017) · Neuron · doi:10.1016/j.neuron.2017.03.019 · Cited by 175
Hackos, D. H., Lupardus, P. J., Grand, T., Chen, Y., Wang, T.-M., Reynen, P., Gustafson, A. E., Wallweber, H. J. A., Volgraf, M., Sellers, B. D., et al. (2016) · Neuron · doi:10.1016/j.neuron.2016.01.016 · Cited by 174
Long-Lasting Rescue of Network and Cognitive Dysfunction in a Genetic Schizophrenia Model
Mukherjee, A., Carvalho, F., Eliez, S., & Caroni, P. (2019) · Cell · doi:10.1016/j.cell.2019.07.023 · Cited by 169
Dugan, L. L., Ali, S. S., Shekhtman, G., Roberts, A. J., Lucero, J., Quick, K. L., & Behrens, M. M. (2009) · PLoS ONE · doi:10.1371/journal.pone.0005518 · Cited by 165
Self-citationDownregulation of Parvalbumin at Cortical GABA Synapses Reduces Network Gamma Oscillatory Activity
Volman, V., Behrens, M. M., & Sejnowski, T. J. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.3041-11.2011 · Cited by 164
Powell, S. B., Sejnowski, T. J., & Behrens, M. M. (2012) · Neuropharmacology · doi:10.1016/j.neuropharm.2011.01.049 · Cited by 164
Kim, Y.-H., & Koh, J.-Y. (2002) · Experimental Neurology · doi:10.1006/exnr.2002.7990 · Cited by 163
Huntley, G., Vickers, J., Janssen, W., Brose, N., Heinemann, S., & Morrison, J. (1994) · The Journal of Neuroscience · doi:10.1523/jneurosci.14-06-03603.1994 · Cited by 161
Deficits in Transcriptional Regulators of Cortical Parvalbumin Neurons in Schizophrenia
Volk, D. W., Matsubara, T., Li, S., Sengupta, E. J., Georgiev, D. D., Minabe, Y., Sampson, A. R., Hashimoto, T., & Lewis, D. A. (2012) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2012.12030305 · Cited by 161
Kocsis, B. (2012) · Biological Psychiatry · doi:10.1016/j.biopsych.2011.10.002 · Cited by 159
Chung, D. W., Fish, K. N., & Lewis, D. A. (2016) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2016.16010025 · Cited by 148 · cited 2×
“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].”
BackgroundAutistic Symptoms in Schizophrenia Spectrum Disorders: A Systematic Review and Meta-Analysis
De Crescenzo, F., Postorino, V., Siracusano, M., Riccioni, A., Armando, M., Curatolo, P., & Mazzone, L. (2019) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2019.00078 · Cited by 143
Yin, H. Z., Sensi, S. L., Ogoshi, F., & Weiss, J. H. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-04-01273.2002 · Cited by 143
Populations of hippocampal inhibitory neurons express different levels of cytochrome c
Gulyás, A. I., Buzsáki, G., Freund, T. F., & Hirase, H. (2006) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2006.04814.x · Cited by 142
Goldberg, J. H., Yuste, R., & Tamas, G. (2003) · The Journal of Physiology · doi:10.1113/jphysiol.2003.042598 · Cited by 141
Bitanihirwe, B., Lim, M., Kelley, J., Kaneko, T., & Woo, T. (2009) · BMC Psychiatry · doi:10.1186/1471-244x-9-71 · Cited by 137
Wang, A. Y., Lohmann, K. M., Yang, C. K., Zimmerman, E. I., Pantazopoulos, H., Herring, N., Berretta, S., Heckers, S., & Konradi, C. (2011) · Acta Neuropathologica · doi:10.1007/s00401-011-0881-4 · Cited by 135
Self-citationCueva Vargas, J. L., Osswald, I. K., Unsain, N., Aurousseau, M. R., Barker, P. A., Bowie, D., & Di Polo, A. (2015) · The Journal of Neuroscience · doi:10.1523/jneurosci.1273-15.2015 · Cited by 132
Barr, M. S., Farzan, F., Tran, L. C., Chen, R., Fitzgerald, P. B., & Daskalakis, Z. J. (2010) · Schizophrenia Research · doi:10.1016/j.schres.2010.05.023 · Cited by 125
Cortical interneuron specification: the juncture of genes, time and geometry
Bandler, R. C., Mayer, C., & Fishell, G. (2017) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2016.10.003 · Cited by 125
Hippocampal interneuron loss in an APP/PS1 double mutant mouse and in Alzheimer’s disease
Takahashi, H., Brasnjevic, I., Rutten, B. P. F., Van Der Kolk, N., Perl, D. P., Bouras, C., Steinbusch, H. W. M., Schmitz, C., Hof, P. R., & Dickstein, D. L. (2010) · Brain Structure and Function · doi:10.1007/s00429-010-0242-4 · Cited by 124
Laminar fate of cortical GABAergic interneurons is dependent on both birthdate and phenotype
Rymar, V. V., & Sadikot, A. F. (2007) · The Journal of Comparative Neurology · doi:10.1002/cne.21250 · Cited by 122
Jia, Y., Jeng, J., Sensi, S. L., & Weiss, J. H. (2002) · The Journal of Physiology · doi:10.1113/jphysiol.2002.020172 · Cited by 118
Inan, M., Zhao, M., Manuszak, M., Karakaya, C., Rajadhyaksha, A. M., Pickel, V. M., Schwartz, T. H., Goldstein, P. A., & Manfredi, G. (2016) · Neurobiology of Disease · doi:10.1016/j.nbd.2016.04.004 · Cited by 118
Hippocampal Interneurons in Bipolar Disorder
Konradi, C., Zimmerman, E. I., Yang, C. K., Lohmann, K. M., Gresch, P., Pantazopoulos, H., Berretta, S., & Heckers, S. (2010) · Archives of General Psychiatry · doi:10.1001/archgenpsychiatry.2010.175 · Cited by 115
Self-citationLoss of perineuronal net N-acetylgalactosamine in Alzheimer’s disease
Baig, S., Wilcock, G. K., & Love, S. (2005) · Acta Neuropathologica · doi:10.1007/s00401-005-1060-2 · Cited by 112
Spaethling, J. M., Klein, D. M., Singh, P., & Meaney, D. F. (2008) · Journal of Neurotrauma · doi:10.1089/neu.2008.0532 · Cited by 112
Nissen, W., Szabo, A., Somogyi, J., Somogyi, P., & Lamsa, K. P. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.3481-09.2010 · Cited by 112
Volgraf, M., Sellers, B. D., Jiang, Y., Wu, G., Ly, C. Q., Villemure, E., Pastor, R. M., Yuen, P., Lu, A., Luo, X., et al. (2016) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.5b02010 · Cited by 105
Decision making during interneuron migration in the developing cerebral cortex
Guo, J., & Anton, E. S. (2014) · Trends in Cell Biology · doi:10.1016/j.tcb.2013.12.001 · Cited by 104
Joseph, L. C., Barca, E., Subramanyam, P., Komrowski, M., Pajvani, U., Colecraft, H. M., Hirano, M., & Morrow, J. P. (2016) · PLOS ONE · doi:10.1371/journal.pone.0145750 · Cited by 99
Ahnaou, A., Moechars, D., Raeymaekers, L., Biermans, R., Manyakov, N. V., Bottelbergs, A., Wintmolders, C., Van Kolen, K., Van De Casteele, T., Kemp, J. A., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-13839-6 · Cited by 98
Rubio, S. E., Vega‐Flores, G., Martínez, A., Bosch, C., Pérez‐Mediavilla, A., Río, J. D., Gruart, A., Delgado‐García, J. M., Soriano, E., & Pascual, M. (2012) · The FASEB Journal · doi:10.1096/fj.12-208413 · Cited by 98
MS, M. G., HAINFELLNER, J. A., TRABATTONI, G. R., & BUDKA, H. (1997) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/00005072-199710000-00005 · Cited by 97
Cabungcal, J.-H., Nicolas, D., Kraftsik, R., Cuénod, M., Do, K. Q., & Hornung, J.-P. (2006) · Neurobiology of Disease · doi:10.1016/j.nbd.2006.01.003 · Cited by 96
Dysregulation of Parvalbumin Expression in the Cntnap2−/− Mouse Model of Autism Spectrum Disorder
Lauber, E., Filice, F., & Schwaller, B. (2018) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2018.00262 · Cited by 94
Dysregulated ErbB4 Splicing in Schizophrenia: Selective Effects on Parvalbumin Expression
Chung, D. W., Volk, D. W., Arion, D., Zhang, Y., Sampson, A. R., & Lewis, D. A. (2016) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2015.15020150 · Cited by 86
Huchzermeyer, C., Berndt, N., Holzhütter, H.-G., & Kann, O. (2013) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2012.165 · Cited by 81
McQuail, J. A., Beas, B. S., Kelly, K. B., Simpson, K. L., Frazier, C. J., Setlow, B., & Bizon, J. L. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.2332-16.2016 · Cited by 80
Interneurons, tau and amyloid-β in the piriform cortex in Alzheimer’s disease
Saiz-Sanchez, D., De la Rosa-Prieto, C., Ubeda-Banon, I., & Martinez-Marcos, A. (2015) · Brain Structure and Function · doi:10.1007/s00429-014-0771-3 · Cited by 79
Kaplan, E. S., Cooke, S. F., Komorowski, R. W., Chubykin, A. A., Thomazeau, A., Khibnik, L. A., Gavornik, J. P., & Bear, M. F. (2016) · eLife · doi:10.7554/elife.11450 · Cited by 77
Basal forebrain contributes to default mode network regulation
Nair, J., Klaassen, A.-L., Arato, J., Vyssotski, A. L., Harvey, M., & Rainer, G. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1712431115 · Cited by 77
Cha, J., Jo, H. J., Kim, H. J., Seo, S. W., Kim, H., Yoon, U., Park, H., Na, D. L., & Lee, J. (2013) · European Journal of Neuroscience · doi:10.1111/ejn.12177 · Cited by 76
Timofeeva, O. A., & Levin, E. D. (2011) · Neuroscience · doi:10.1016/j.neuroscience.2011.08.038 · Cited by 74
Whittaker, R. G., Turnbull, D. M., Whittington, M. A., & Cunningham, M. O. (2011) · Brain · doi:10.1093/brain/awr018 · Cited by 74
Szabo, A., Somogyi, J., Cauli, B., Lambolez, B., Somogyi, P., & Lamsa, K. P. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.0206-12.2012 · Cited by 71
Albuquerque, M. S., Mahar, I., Davoli, M. A., Chabot, J.-G., Mechawar, N., Quirion, R., & Krantic, S. (2015) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2015.00030 · Cited by 71
Parvalbumin gene transfer corrects diastolic dysfunction in diseased cardiac myocytes
Wahr, P. A., Michele, D. E., & Metzger, J. M. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.21.11982 · Cited by 66
Nakamura, T., Matsumoto, J., Takamura, Y., Ishii, Y., Sasahara, M., Ono, T., & Nishijo, H. (2015) · PLoS ONE · doi:10.1371/journal.pone.0119258 · Cited by 65
Mahar, I., Albuquerque, M. S., Mondragon-Rodriguez, S., Cavanagh, C., Davoli, M. A., Chabot, J.-G., Williams, S., Mechawar, N., Quirion, R., & Krantic, S. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2016.00327 · Cited by 63
Gill, K. M., & Grace, A. A. (2014) · The International Journal of Neuropsychopharmacology · doi:10.1017/s146114571400056x · Cited by 60
Mao, W., Watanabe, T., Cho, S., Frost, J. L., Truong, T., Zhao, X., & Futai, K. (2015) · European Journal of Neuroscience · doi:10.1111/ejn.12877 · Cited by 59
Nguyen, P. T., Nakamura, T., Hori, E., Urakawa, S., Uwano, T., Zhao, J., Li, R., Bac, N. D., Hamashima, T., Ishii, Y., et al. (2011) · PLoS ONE · doi:10.1371/journal.pone.0018004 · Cited by 56
Transgenic labeling of parvalbumin-expressing neurons with tdTomato
Kaiser, T., Ting, J. T., Monteiro, P., & Feng, G. (2015) · Neuroscience · doi:10.1016/j.neuroscience.2015.08.036 · Cited by 55
Peyre, E., Silva, C. G., & Nguyen, L. (2015) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2015.00129 · Cited by 51
Koh, M. T., Shao, Y., Sherwood, A., & Smith, D. R. (2016) · Schizophrenia Research · doi:10.1016/j.schres.2016.01.023 · Cited by 51
Abnormal interneuron development in disrupted-in-schizophrenia-1 L100P mutant mice
Lee, F. H., Zai, C. C., Cordes, S. P., Roder, J. C., & Wong, A. H. (2013) · Molecular Brain · doi:10.1186/1756-6606-6-20 · Cited by 49
The developmental changes of Nav1.1 and Nav1.2 expression in the human hippocampus and temporal lobe
Wang, W., Takashima, S., Segawa, Y., Itoh, M., Shi, X., Hwang, S.-K., Nabeshima, K., Takeshita, M., & Hirose, S. (2011) · Brain Research · doi:10.1016/j.brainres.2011.02.083 · Cited by 47
Garbelli, R., Meroni, A., Magnaghi, G., Beolchi, M. S., Ferrario, A., Tassi, L., Bramerio, M., & Spreafico, R. (2006) · Epilepsia · doi:10.1111/j.1528-1167.2006.00577.x · Cited by 47
Huntley, G. W., Vickers, J. C., & Morrison, J. H. (1997) · Brain Research · doi:10.1016/s0006-8993(96)00847-5 · Cited by 47
Du, Y., & Grace, A. A. (2016) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyw065 · Cited by 43
Parvalbumin Promoter Hypermethylation in Postmortem Brain in Schizophrenia
Fachim, H. A., Srisawat, U., Dalton, C. F., & Reynolds, G. P. (2018) · Epigenomics · doi:10.2217/epi-2017-0159 · Cited by 41
Verdaguer, E., Brox, S., Petrov, D., Olloquequi, J., Romero, R., de Lemos, M. L., Camins, A., & Auladell, C. (2015) · Experimental Gerontology · doi:10.1016/j.exger.2015.06.013 · Cited by 38
Input-specific maturation of synaptic dynamics of parvalbumin interneurons in primary visual cortex
Lu, J., Tucciarone, J., Lin, Y., & Huang, Z. J. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1400694111 · Cited by 35
Wang, L., Shen, M., Jiang, C., Ma, L., & Wang, F. (2016) · International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyw060 · Cited by 29
Delevich, K. M., Jaaro-Peled, H., Penzo, M. A., Sawa, A., & Li, B. (2020) · eNeuro · doi:10.1523/eneuro.0496-19.2020 · Cited by 25
Jones, N. C., Hudson, M., Foreman, J., Rind, G., Hill, R., Manning, E. E., & van den Buuse, M. (2018) · European Journal of Neuroscience · doi:10.1111/ejn.13722 · Cited by 20
Jaaro-Peled, H., Kumar, S., Hughes, D. N., Sumitomo, A., Kim, S.-H., Zoubovsky, S. P., Hirota-Tsuyada, Y., Zala, D., Bruyère, J., Katz, B. M., et al. (2022) · Molecular Psychiatry · doi:10.1038/s41380-021-01389-3 · Cited by 19
Jaaro-Peled, H., Kumar, S., Hughes, D. N., Kim, S.-H., Zoubovsky, S. P., Hirota-Tsuyada, Y., Zala, D., Sumitomo, A., Bruyère, J., Katz, B. M., et al. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/497446 · Cited by 4
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).”
Background
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-07, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-07 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
