Cortical parvalbumin interneurons and cognitive dysfunction in schizophrenia
Open accessAbstract
Deficits in cognitive control, a core disturbance of schizophrenia, appear to emerge from impaired prefrontal gamma oscillations. Cortical gamma oscillations require strong inhibitory inputs to pyramidal neurons from the parvalbumin basket cell (PVBC) class of GABAergic neurons. Recent findings indicate that schizophrenia is associated with multiple pre- and postsynaptic abnormalities in PVBCs, each of which weakens their inhibitory control of pyramidal cells. These findings suggest a new model of cortical dysfunction in schizophrenia in which PVBC inhibition is decreased to compensate for an upstream deficit in pyramidal cell excitation. This compensation is thought to rebalance cortical excitation and inhibition, but at a level insufficient to generate the gamma oscillation power required for high levels of cognitive control.
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Reduced expression of GAD67, the main GABA-synthesizing enzyme in the brain, appears to contribute to altered interneuron activity in psychosis.
“Reduced expression of GAD67, the main GABA-synthesizing enzyme in the brain, appears to contribute to altered interneuron activity in psychosis [86,87] .”
From The traumagenic neurodevelopmental model of psychosis revisited (2014) · cites this paper as [87]
Interneuron function is disrupted in schizophrenia.
“and multiple lines of evidence suggest that interneuron function is disrupted in schizophrenia 49 .”
From Developmental timing and critical windows for the treatment of psychiatric disorders (2016) · cites this paper as [49]
Disruption of PV+ fast spiking interneurons is a core feature of schizophrenia.
“In addition, several lines of evidence suggest that disruption of PV+ fast spiking interneurons is a core feature of schizophrenia 49 .”
From Developmental timing and critical windows for the treatment of psychiatric disorders (2016) · cites this paper as [49]
The levels of GAD67 are consistently lower in the cortex of subjects with schizophrenia, and these defects are more prominent in PV+ interneurons.
“For instance, the levels of one of the enzymes that contributes to the synthesis of GABA, GAD67, are consistently lower in the cortex of subjects with schizophrenia, and these defects are more prominent in PV+ interneurons 49 .”
From Developmental timing and critical windows for the treatment of psychiatric disorders (2016) · cites this paper as [49]
Lewis et al. have associated cognitive dysfunction in schizophrenia with altered inputs on FS-PV interneurons.
“Lewis et al.32, 33 have also associated cognitive dysfunction in schizophrenia with altered inputs on FS-PV interneurons.”
From Cortical fast-spiking parvalbumin interneurons enwrapped in the perineuronal net express the metallopeptidases Adamts8, Adamts15 and Neprilysin (2015) · cites this paper as [33]
Anomalies associated with parvalbumin interneurons are a hallmark of schizophrenia, including reduced density of parvalbumin-immunoreactive cells in the hippocampal formation and alterations in basket and chandelier cells in the dorsolateral prefrontal cortex of post-mortem brains.
“Anomalies associated with PVI constitute a hallmark of the disease, including reduced density of parvalbumin-immunoreactive cells in the hippocampal formation (Wang et al., 2011; Zhang and Reynolds, 2002) and alterations at the level of basket and chandelier cells in the dorsolateral prefrontal cortex (DLPFC) of post-mortem brains (Lewis et al., 2012).”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Lewis et al., 2012
Many reports describe PV-IN-related changes in people with schizophrenia, and animal models that reproduce aspects of the disease support this finding.
“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).”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [2]
PV-expressing interneurons are highly vulnerable to stressors and have been linked to several neuropsychiatric diseases, including schizophrenia, Alzheimer's disease, autism spectrum disorder, and bipolar disorder.
“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.”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [2]
PVI circuits are altered in schizophrenia and autism spectrum disorder despite heterogeneity in etiology.
“Despite heterogeneity in the etiology across schizophrenia and autism spectrum disorder, PVI circuits are altered in these psychiatric disorders.”
From Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia (2017) · cites this paper as [7]
Alterations of GABAergic interneurons found in postmortem studies of schizophrenia patients could be a consequence of NMDA-receptor hypofunctioning.
“suggesting that the alterations of GABAergic interneurons found in postmortem studies of schizophrenia patients (Lewis et al., 2012”
From Neuronal Dynamics and Neuropsychiatric Disorders: Toward a Translational Paradigm for Dysfunctional Large-Scale Networks (2012) · cites this paper as Lewis et al., 2012
Deficits in GABAergic parvalbumin-positive interneurons contribute to schizophrenia pathophysiology through alterations in the brain's excitation-inhibition balance that result in impaired behaviour and cognition.
“Molecular, genetic and pathological evidence suggests that deficits in GABAergic parvalbumin-positive interneurons contribute to schizophrenia pathophysiology through alterations in the brain's excitation-inhibition balance that result in impaired behaviour and cognition.”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [2]
Many diverse causes of schizophrenia and schizophrenia-like behaviours converge on aberrant function of fast-spiking parvalbumin-positive interneurons, which leads to altered excitation-inhibition balance.
“Pathologically, many diverse causes of schizophrenia and schizophrenia-like behaviours appear to converge on a similar deficit: the aberrant function of fast-spiking parvalbumin-positive interneurons (PVIs) 2 , which leads to altered excitation-inhibition balance 3 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [2]
A milder NMDAR antagonism regime caused long-lasting behavioural changes and a specific long-lasting decrease in cortical PVI numbers, mimicking a key pathological feature of schizophrenia.
“A milder antagonism regime caused long-lasting behavioural changes and a specific longlasting decrease in cortical PVI numbers 29 , mimicking a key pathological feature of schizophrenia 2 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [2]
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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 · see citing works
Juvenile stress induces behavioral change and affects perineuronal net formation in juvenile mice
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Oxygen levels regulate the development of human cortical radial glia cells
Ortega, J. A., Sirois, C. L., Memi, F., Glidden, N., & Zecevic, N. (2016) · Cerebral Cortex · doi:10.1093/cercor/bhw194 · Cited by 37 · see citing works
The Cytokine CXCL12 Promotes Basket Interneuron Inhibitory Synapses in the Medial Prefrontal Cortex
Wu, P.-R., Cho, K. K. A., Vogt, D., Sohal, V. S., & Rubenstein, J. L. R. (2017) · Cerebral Cortex · doi:10.1093/cercor/bhw230 · Cited by 32 · see citing works
Tan, T., Wang, W., Williams, J., Ma, K., Cao, Q., & Yan, Z. (2019) · Schizophrenia Bulletin · doi:10.1093/schbul/sby163 · Cited by 29 · see citing works
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- Authors
- Lewis, D. A., Curley, A. A., Glausier, J. R., & Volk, D. W.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Lewis, David A.
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2012-01
- Volume
- 35
- Issue
- 1
- Pages
- 57-67
- ISSN
- 0166-2236 (ISSN-L)
- PMC
- PMC3253230
- OpenAlex
- W2103592460
- Cited by
- 1,071
- References
- 18
- Citations by year
- 2026: 55 · 2025: 64 · 2024: 57 · 2023: 57 · 2022: 72 · 2021: 74 · 2020: 80 · 2019: 73 · 2018: 81 · 2017: 91 · 2016: 86 · 2015: 98 · 2014: 75 · 2013: 77 · 2012: 29
- FWCI
- 7.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Mental Health (P50MH084053, MH084053, R01MH043784, K08MH084016, R37MH043784, MH043784)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- parvalbumin basket cells, schizophrenia, cognitive control, cortical inhibition, pyramidal neurons, GABAergic interneurons, prefrontal cortex
- MeSH terms
- Cognition Disorders, gamma-Aminobutyric Acid, Humans, Interneurons, Parvalbumins, Schizophrenia, Prefrontal Cortex, Pyramidal Cells, GABAergic Neurons
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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.
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