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.
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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