The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.
Pathological Basis for Deficient Excitatory Drive to Cortical Parvalbumin Interneurons in Schizophrenia
Open accessAbstract
OBJECTIVE: Deficient excitatory drive to parvalbumin-containing cortical interneurons is proposed as a key neural substrate for altered gamma oscillations and cognitive dysfunction in schizophrenia. However, a pathological entity producing such a deficit has not been identified. The authors tested the hypothesis that cortical parvalbumin interneurons receive fewer excitatory synaptic inputs in individuals with schizophrenia. METHOD: Fluorescent immunohistochemistry, confocal microscopy, and post-image processing techniques were used to quantify the number of putative excitatory synapses (i.e., the overlap of vesicular glutamate transporter 1-positive [VGlut1+] puncta and postsynaptic density protein 95-positive [PSD95+] puncta) per surface area of parvalbumin-positive (PV+) or calretinin-positive (CR+) neurons in the dorsolateral prefrontal cortex from schizophrenia subjects and matched unaffected comparison subjects. RESULTS: Mean density of VGlut1+/PSD95+ puncta on PV+ neurons was 18% lower in schizophrenia, a significant difference. This deficit was not influenced by methodological confounds or schizophrenia-associated comorbid factors, not present in monkeys chronically exposed to antipsychotic medications, and not present in CR+ neurons. Mean density of VGlut1+/PSD95+ puncta on PV+ neurons predicted the activity-dependent expression levels of parvalbumin and glutamic acid decarboxylase 67 (GAD67) in schizophrenia subjects but not comparison subjects. CONCLUSIONS: To the authors' knowledge, this is the first demonstration that excitatory synapse density is lower selectively on parvalbumin interneurons in schizophrenia and predicts the activity-dependent down-regulation of parvalbumin and GAD67. Because the activity of parvalbumin interneurons is required for generation of cortical gamma oscillations and working memory function, these findings reveal a novel pathological substrate for cortical dysfunction and cognitive deficits in schizophrenia.
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“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].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [12]
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Citations
Cites
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“Edges of PV+ or CR+ cell bodies were segmented by the MATLAB edge function using the Canny edge detector operator(30).”
BackgroundMethodParvalbumin neurons and gamma rhythms enhance cortical circuit performance
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“Because cortical gamma oscillations require the activity of parvalbumin-containing (PV) interneurons(4, 5), deficient cortical PV interneuron activity could provide the neural substrate for altered prefrontal gamma oscillations and consequently impaired working memory in schizophrenia.”
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“Because cortical gamma oscillations require the activity of parvalbumin-containing (PV) interneurons(4, 5), deficient cortical PV interneuron activity could provide the neural substrate for altered prefrontal gamma oscillations and consequently impaired working memory in schizophrenia.”
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“Excitatory synapses on PV interneurons predict PV and GAD67 expression levels in human DLPFC Finally, we assessed whether the density of excitatory synapses on PV+ neurons predicted levels of PV and GAD67, molecular markers of PV interneuron activity.”
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Fremeau, R. T., Troyer, M. D., Pahner, I., Nygaard, G. O., Tran, C. H., Reimer, R. J., Bellocchio, E. E., Fortin, D. L., Storm‐Mathisen, J., & Edwards, R. H. (2001) · Neuron · doi:10.1016/s0896-6273(01)00344-0 · Cited by 1,266 · cited 1×
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“VGlut1+ and PSD95+ puncta were used to identify the pre- and postsynaptic elements, respectively, as these molecular markers have been previously used to define excitatory synapses in PV interneurons(11, 28, 29).”
Method
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Rittweger, N., Ishorst, T., Barmashenko, G., Aliane, V., Winter, C., & Funke, K. (2021) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2021.670699 · Cited by 7
“…(rTMS), have been shown to modulate cortical excitability and plasticity (Huang et al., 2005; Ziemann and Siebner, 2008; Ridding and Ziemann, 2010; Dayan et al., 2013), they may also be considered as alternative therapeutic or possible preventive tools (Post and Keck, 2001; Padberg and George,…”
BackgroundGarcía‐López, R., Pombero, A., Estirado, A., Geijo‐Barrientos, E., & Martı́nez, S. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.693919 · Cited by 7
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“Increases in activity of excitatory neurons in schizophrenia can 375 come about due to decreased excitatory drive on fast-spiking cortical inhibitory interneurons 376 (Chung et al., 2016), or an overactive dopaminergic system (Gracitelli et al.”
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“…by synchronising cortical glutamatergic pyramidal cell firing through a negative feedback inhibition (Whittington et al. 1995; Sohal et al. 2009), and that a disturbance of this interaction is a key feature in the pathophysiology of schizophrenia (Benes 2000; Lewis et al. 2005; Chung et al. 2016).”
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“…et al., 2010; Volk et al., 2012) and reduced PV immunoreactivity (Belforte et al., 2010; Glausier et al., 2014; Enwright et al., 2016) in the soma of PV-expressing GABAergic interneurons (INs), without any change in their density (Hashimoto et al., 2003; Chung et al., 2016; Batiuk et al., 2022).”
Taking a Bleulerian perspective: a role for negative symptoms in the staging model?
Wunderink, L. (2017) · World Psychiatry · doi:10.1002/wps.20449 · Cited by 4
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Insights Into the Genomic Underpinnings of Psychopathology
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“Although results vary, most studies suggest that patients with schizophrenia present with lower PV+ protein expression and PVALB mRNA in comparison with controls, in brain regions including the PFC [91 – 94], hippocampus [95] and entorhinal cortex [96].”
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“It has been reported that layer 4 PV 1 neurons of the PFC receive a lower density of excitatory synapses in schizophrenia, with this predicting reduced messenger RNA expression of PV and the GABA synthesis enzyme GAD67 within these neurons (53).”
Disorganized Inhibitory Dynamics in Hippocampal area CA1 of 22q11.2 Deletion Mutant MicePreprint
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“Studies in mouse models for schizophrenia and human patients have predominantly focused on PV-expressing INs, implicating reduced prevalence and activity of these cells in disorganized network activity 41,86,88,89,97,102,126–129 .”
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“12 Given that ketamine reduced PV expression levels, and the hypothesised role of PV interneuron hypofunction in schizophrenia (37, 38), we aimed to determine if activating”
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“For example, we previously reported fewer E → I synapses in PFC of SZ (Chung et al., 2016a).”
Self-citationChung, Y., Bazmi, H. H., Lewis, D. A., & Chung, D. W. (2026) · Cerebral Cortex · doi:10.1093/cercor/bhag045 · Cited by 2
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Self-citationThe MAM Model to Study the Role of Dopamine in Schizophrenia
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The biology of schizophrenia as a neurodevelopmental disorder
van Berlekom, A. B. (2022) · Utrecht University Repository (Utrecht University) · doi:10.33540/1269 · Cited by 1
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“This is consistent with recent work suggesting that PV interneuron deficits are secondary to reduced excitatory drive (31,44).”
InfluentialQuestioning the Medical Model of Mental Health
Littrell, J. L. (2017) · Journal of Constructivist Psychology · doi:10.1080/10720537.2016.1268080
Role of ErbB4 splicing in parvalbumin interneuron maturation and schizophrenia
Chung, D. W. (2016) · D-Scholarship@Pitt (University of Pittsburgh)
Self-citationDeficient auditory gamma-BOLD coupling in schizophrenia is related to sensory gating deficitsPreprint
Jacob, M., Sargent, K., Roach, B. J., Shamshiri, E., Mathalon, D. H., & Ford, J. M. (2021) · medRxiv · doi:10.1101/2021.08.31.21262929
“Alterations in gamma power in SZ are therefore thought to relate to disturbances in inhibitory transmission and E/I balance (Chung et al., 2016; Grent-’t-Jong et al., 2018; Selten et al., 2018; Sohal et al., 2009).”
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Cellular Mechanisms of Psychotic Disorders
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“reducing their excitation lowers prefrontal gamma power [85, 86].”
BackgroundMetzner, C., Dimulescu, C., Kamp, F., Fromm, S. P., Uhlhaas, P. J., & Obermayer, K. (2023) · medRxiv · doi:10.1101/2023.12.08.23299714
“Excitatory and inhibitory neurotransmission is disturbed, for example a reduced excitatory drive onto GABAergic inhibitory neurons (Chung et al. (2016, 2022)) and a decreased inhibitory output (Hashimoto et al. (2003); Morris et al. (2008); Moyer et al. (2012)).”
BackgroundVolk, D. W., Jenkins, A. K., & Lewis, D. A. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-19176-3.00031-5 · Cited by 2
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Chung, D. W., & Ermentrout, B. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.29.728634
“The density of VGlut1 + /PSD95 + puncta on PVIs provides a direct morphological measure of E → I strength and is lower in PFC of SZ [21], but this measure has not yet been quantified in V1.”
Self-citationLi, Z., Si, T., Wu, Q.-R., Zhao, J.-H., Hua, W.-Z., Zhang, Y., Yang, S., Mao, Y.-Y., Zang, W., & Cao, J. (2026) · iScience · doi:10.1016/j.isci.2026.116454
“64,65 These disruptions can negatively impact cognitive and emotional processing, contributing to the development of depression and other psychiatric symptoms.”
Btbd11 regulates glutamatergic synapse organization in GABAergic inhibitory interneuronsPreprint
Brady, M., Zhang, S., Levy, A. D., Schamber, P., Hartman, H., Blanpied, T. A., & Bygrave, A. M. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.06.22.733761
“Given the link between impaired glutamatergic excitation of INs in psychiatric disease 9–12 , elucidating the unique proteins and mechanisms that govern IN-PSD organization provides an exciting avenue for discovery of potential novel therapeutic targets.”
Hyperexcitable but seizure-free: hippocampal network dysfunction in a Wolfram syndrome modelPreprint
Ahmadi, S., Pinera, J. G., Dokholyan, S., Sauerbeck, A. D., Phan, H. N., Carman, B., Debnath, A., Brunwasser, S., Skinner, G., Rensing, N. R., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.09.27.754840
Gordillo, D., Baradarantohidi, E., Grent-‘t-Jong, T., & Uhlhaas, P. J. (2026) · Biological Psychiatry · doi:10.1016/j.biopsych.2026.09.004
Metadata
- Authors
- Chung, D. W., Fish, K. N., & Lewis, D. A.
- Affiliations
- University of Pittsburgh (US)
- Venue
- American Journal of Psychiatry
- Published
- 2016-11-01
- Volume
- 173
- Issue
- 11
- Pages
- 1131-1139
- ISSN
- 0002-953X (ISSN-L)
- 1535-7228
- PMC
- PMC5089927
- OpenAlex
- W2490214293
- Cited by
- 148
- References
- 55
- Citations by year
- 2026: 11 · 2025: 13 · 2024: 16 · 2023: 11 · 2022: 14 · 2021: 18 · 2020: 14 · 2019: 14 · 2018: 20 · 2017: 16 · 2016: 1
- FWCI
- 15.11
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal of Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (R01MH043784, P50MH103204, R01MH096985, R37MH043784)
- 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, parvalbumin interneurons, glutamatergic synapses, VGLUT1, PSD-95, calretinin interneurons, dorsolateral prefrontal cortex, GAD67, gamma oscillations, working memory, cognitive impairment
- MeSH terms
- Disks Large Homolog 4 Protein, Adult, Animals, Female, Glutamate Decarboxylase, Humans, Interneurons, Macaca fascicularis, Male, Membrane Proteins, Middle Aged, Parvalbumins, Schizophrenia, Antipsychotic Agents, Case-Control Studies, Prefrontal Cortex, Intracellular Signaling Peptides and Proteins, Vesicular Glutamate Transport Protein 1, Calbindin 2
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