Cortical inhibitory neurons and schizophrenia

Lewis, David A.; Hashimoto, Takanori; Volk, David W.

doi:10.1038/nrn1648

Cited by 2,297Schizophrenia research and treatmentNeuroscience and Neuropharmacology ResearchNeurotransmitter Receptor Influence on Behavior

Cortical inhibitory neurons and schizophrenia

Lewis, David A., Hashimoto, Takanori, Volk, David W.·2005·Nature Reviews Neuroscience

DOI 10.1038/nrn1648

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Abstract

Impairments in certain cognitive functions, such as working memory, are core features of schizophrenia. Convergent findings indicate that a deficiency in signalling through the TrkB neurotrophin receptor leads to reduced GABA (gamma-aminobutyric acid) synthesis in the parvalbumin-containing subpopulation of inhibitory GABA neurons in the dorsolateral prefrontal cortex of individuals with schizophrenia. Despite both pre- and postsynaptic compensatory responses, the resulting alteration in perisomatic inhibition of pyramidal neurons contributes to a diminished capacity for the gamma-frequency synchronized neuronal activity that is required for working memory function. These findings reveal specific targets for therapeutic interventions to improve cognitive function in individuals with schizophrenia.

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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 [86]
In individuals with psychosis, certain classes of GABA interneurons are altered, specifically reduced density in the anterior cingulate and reduced activity in the dorsolateral prefrontal cortex in the parvalbumin-expressing subpopulation.
“Certain classes of GABA interneurons are altered in individuals with psychosis, in particular reduced density in the anterior cingulate and reduced activity in the dorsolateral prefrontal cortex in the subpopulation expressing parvalbumin [84-86] .”
From The traumagenic neurodevelopmental model of psychosis revisited (2014) · cites this paper as [86]
The correct balance of inhibition and excitation seems to be critical for normative executive function, and conversely, disturbance of this balance is thought to be a fundamental component of psychiatric illness.
“Thus, the correct balance of inhibition and excitation seems to be critical for normative executive function, and conversely, disturbance of this balance is thought to be a fundamental component of psychiatric illness.69, 70”
From A role for synaptic plasticity in the adolescent development of executive function (2013) · cites this paper as [69]
The expression of several GABA receptors and markers of inhibitory synapses are also altered in schizophrenia.
“Moreover, the expression of several GABA receptors and markers of inhibitory synapses are also altered in schizophrenia 50 .”
From Developmental timing and critical windows for the treatment of psychiatric disorders (2016) · cites this paper as [50]
Schizophrenia is increasingly viewed as a neurodevelopmental disorder involving brain circuit alterations, including dysfunction of parvalbumin-positive fast-spiking GABA neurons.
“Schizophrenia is increasingly recognized as a neurodevelopmental disorder that involves alterations in brain circuits, including dysfunction of parvalbumin (PV)-positive, fast-spiking GABA neurons (1, 2).”
From Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons (2015) · cites this paper as [1]

Schizophrenia onset is linked to disrupted physiological maturation of fast-spiking parvalbumin-positive GABAergic interneurons.
“its onset is linked to a potential disruption of the physiological maturation of inhibitory neural networks consisting of fast-spiking parvalbumin-positive gamma-aminobutric acid (GABAergic) interneurons”
From Perineuronal nets and schizophrenia: The importance of neuronal coatings (2014) · cites this paper as Lewis et al., 2005
Dysfunction and/or deficient inhibitory output from PV interneurons may be a common mechanism of multiple psychiatric disorders, such as schizophrenia, autism spectrum disorders and bipolar disorder.
“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 Lewis et al. 2005
Cortical disinhibition occurs in schizophrenia due to disrupted functioning of inhibitory interneurons, resulting in elevated E/I ratio.
“Specifically, there is growing support for a hypothesis that cortical disinhibition occurs in schizophrenia, due to the disrupted functioning of inhibitory interneurons, which results in elevated E/I ratio (Lewis et al. 2005;Marin 2012).”
From Linking microcircuit dysfunction to cognitive impairment: Effects of disinhibition associated with schizophrenia in a cortical working memory model (2014) · cites this paper as Lewis et al. 2005
Prefrontal cortex exhibits altered inhibitory microcircuitry in schizophrenia.
“The prefrontal cortex is a key node in the distributed cortical network recruited during WM (Owen et al. 2005;Fuster 2008) and exhibits altered inhibitory microcircuitry in schizophrenia (Lewis et al. 2005;Bitanihirwe et al. 2009).”
From Linking microcircuit dysfunction to cognitive impairment: Effects of disinhibition associated with schizophrenia in a cortical working memory model (2014) · cites this paper as Lewis et al. 2005
Elevated prefrontal E/I ratio may result from alterations in multiple pathways implicated in schizophrenia, including GABAergic deficits, increased background input from other areas, or abnormal levels of neuromodulators.
“Elevated prefrontal E/I ratio may result from alterations in multiple pathways that are implicated in schizophrenia.These include GABAergic deficits, such as reduced GAD67 production (Lewis et al. 2005); increased background input from other areas such as the thalamus or hippocampus (Lisman et al. 2008); or abnormal levels of neuromodulators (Laruelle et al. 2003).”
From Linking microcircuit dysfunction to cognitive impairment: Effects of disinhibition associated with schizophrenia in a cortical working memory model (2014) · cites this paper as Lewis et al. 2005
Both interneuron cell classes are altered in schizophrenia.
“Both interneuron cell classes are altered in schizophrenia (Lewis et al. 2005;Morris et al. 2008;Bitanihirwe et al. 2009).”
From Linking microcircuit dysfunction to cognitive impairment: Effects of disinhibition associated with schizophrenia in a cortical working memory model (2014) · cites this paper as Lewis et al. 2005

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GAD1 (2q31.1), which encodes glutamic acid decarboxylase (GAD67), is associated with childhood-onset schizophrenia and cortical gray matter volume loss
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Crair (2001) · doi:10.1002/1096-9861(20010205)430:2
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“In post-mortem brain from patients with schizophrenia, there is an upregulation of the α2 subunit in the axon initial segments of these pyramidal neuron”
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Authors: Lewis, D. A., Hashimoto, T., & Volk, D. W.
Affiliations: University of Pittsburgh (US)
Corresponding author: Lewis, David A.
ORCID: Lewis, David A.
Hashimoto, Takanori
Volk, David W.
Venue: Nature Reviews Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2005-04
Volume: 6
Issue: 4
Pages: 312-324
ISSN: 1471-003X (ISSN-L)
1471-0048
DOI: 10.1038/nrn1648
OpenAlex: W2089912569
Cited by: 2,297
References: 123
Citations by year: 2026: 36 · 2025: 51 · 2024: 63 · 2023: 48 · 2022: 70 · 2021: 86 · 2020: 77 · 2019: 94 · 2018: 102 · 2017: 89 · 2016: 123 · 2015: 148 · 2014: 132 · 2013: 167 · 2012: 151
FWCI: 16.54
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Neuroscience (publishedVersion)
PubMed (publishedVersion)
Funders: National Alliance for Research on Schizophrenia and Depression
National Institutes of Health
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 › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords: schizophrenia, cortical inhibitory neurons, parvalbumin interneurons, GABA synthesis, dorsolateral prefrontal cortex, working memory, perisomatic inhibition, cognitive impairment
MeSH terms: Animals, Cerebral Cortex, Humans, Nerve Net, Neural Inhibition, Neurons, Schizophrenia

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Cortical inhibitory neurons and schizophrenia

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