Hippocampal interneurons are abnormal in schizophrenia
Open accessAbstract
Objective The cellular substrate of hippocampal dysfunction in schizophrenia remains unknown. We tested the hypothesis that hippocampal interneurons are abnormal in schizophrenia, but that the total number of hippocampal neurons in the pyramidal cell layer is normal.Methods We collected whole hippocampal specimens of 13 subjects with schizophrenia and 20 matched healthy control subjects to study the number of all neurons, the somal volume of neurons, the number of somatostatin- and parvalbumin-positive interneurons and the messenger RNA levels of somatostatin, parvalbumin and glutamic acid decarboxylase 67.Results The total number of hippocampal neurons in the pyramidal cell layer was normal in schizophrenia, but the number of somatostatin- and parvalbumin-positive interneurons, and the level of somatostatin, parvalbumin and glutamic acid decarboxylase mRNA expression were reduced.Conclusions The study provides strong evidence for a specific defect of hippocampal interneurons in schizophrenia and has implications for emerging models of hippocampal dysfunction in schizophrenia.
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Altered parvalbumin-containing interneuron activity has been reported in several hippocampal subfields.
“Altered parvalbumin-containing interneuron activity has been reported in several subfields [114,115] .”
From The traumagenic neurodevelopmental model of psychosis revisited (2014) · cites this paper as [115]
The Results (§§3.2–3.3; page not provided) report reduced parvalbumin-positive neuron counts and parvalbumin mRNA in different hippocampal sectors in schizophrenia. The Discussion (§4; page not provided) infers abnormal hippocampal firing, but the study did not directly measure parvalbumin-containing interneuron activity. Thus, the subfield abnormalities are supported, while the claim about measured activity is not. (LLM, conf=0.85)
Experimental — accuracy not yet measuredMany 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 [1]
Reduced numbers of PV-INs have been reported in the hippocampus, entorhinal cortex, and subicular areas in schizophrenia.
“Reductions in the number of PV-INs were reported in the hippocampus, entorhinal cortex, and subicular areas [1,[9][10][11].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [1]
In schizophrenia, PVALB mRNA levels are lower in the hippocampus and in layer 4 of the dorsolateral prefrontal cortex, and DNA hypermethylation may partly account for this.
“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].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [1]
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 [1]
The high frequency of interneuron pathologies in the hippocampus and adjacent cortical areas, such as in schizophrenia and bipolar disorder, may partly reflect extended developmental vulnerability.
“The preponderance of interneuron pathologies in the hippocampus and adjacent cortical areas, such as the interneuron pathologies observed in schizophrenia and BPD, might be, at least in part, a reflection of this extended developmental vulnerability [1, 9, 122, 140-142].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [1]
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- Authors
- Konradi, C., Yang, C. K., Zimmerman, E. I., Lohmann, K. M., Gresch, P., Pantazopoulos, H., Berretta, S., & Heckers, S.
- Affiliations
- Vanderbilt University (US)
- McLean Hospital (US)
- Corresponding author
- Konradi, Christine
- ORCID
- Venue
- Schizophrenia Research
- Publisher
- Elsevier BV
- Published
- 2011-09
- Volume
- 131
- Issue
- 1-3
- Pages
- 165-173
- ISSN
- 0920-9964 (ISSN-L)
- PMC
- PMC3159834
- OpenAlex
- W2067274883
- Cited by
- 288
- References
- 46
- Citations by year
- 2026: 7 · 2025: 14 · 2024: 21 · 2023: 23 · 2022: 23 · 2021: 21 · 2020: 23 · 2019: 21 · 2018: 19 · 2017: 16 · 2016: 18 · 2015: 25 · 2014: 32 · 2013: 12 · 2012: 10
- FWCI
- 12.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Schizophrenia Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- McLean Hospital
- National Institute of Mental Health (R01MH067999, R24MH068855, MH74000, MH 068855, R01MH074000, MH67999)
- 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, hippocampal interneurons
- MeSH terms
- Adult, Aged, Aged, 80 and over, Analysis of Variance, Cell Count, Female, Glutamate Decarboxylase, Hippocampus, Humans, Male, Middle Aged, Neurons, Parvalbumins, Schizophrenia, Somatostatin, Antipsychotic Agents, Gene Expression, Case-Control Studies, Young Adult
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