Cortical Parvalbumin Neurons and Cognitive Deficits in Schizophrenia

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  • Hashimoto Takanori
    Department of Psychiatry and Behavioral Science, Graduate School of Medical Sciences, Kanazawa University
  • Kaneda Reizo
    Department of Psychiatry and Behavioral Science, Graduate School of Medical Sciences, Kanazawa University
  • Tsubomoto Makoto
    Department of Psychiatry and Behavioral Science, Graduate School of Medical Sciences, Kanazawa University

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  • 大脳皮質パルブアルブミン陽性ニューロンと統合失調症の認知機能障害
  • ダイノウ ヒシツ パルブアルブミン ヨウセイ ニューロン ト トウゴウ シッチョウショウ ノ ニンチ キノウ ショウガイ

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Abstract

Patients with schizophrenia exhibit impairments in diverse cognitive functions, such as sensory processing, memory, attention, learning, reasoning, and executive function. These functions depend on neural networks formed by multiple brain regions, including areas of the cerebral cortex. Parvalbumin (PV) -expressing neurons represent one of the three separate subsets of cortical inhibitory neurons. Each PV neuron makes powerful, divergent inhibitory innervations on nearby pyramidal neurons and receives convergent excitatory inputs from pyramidal neurons. PV neurons are mutually connected through inhibitory synapses, forming homogenous interneuron networks. Recently developed optogenetics enabled targeted manipulations of PV neuron activities and successfully revealed roles of PV neurons. PV neurons are essential for the generation of neuronal oscillations, which enhance information processing within and between cortical areas in neural networks. During development and learning, PV neurons regulate neuronal plasticity through attenuation of their activities and resultant disinhibition of neural network. In the cortex of subjects with schizophrenia, lower expression levels of molecules that regulate excitability and neurotransmission of PV neurons have been observed in postmortem studies, indicating that alterations of PV neurons contribute to the cognitive deficits in schizophrenia, an idea supported by aberrant neuronal oscillations commonly observed in patients during various cognitive tasks. In order to test the involvement of PV neurons in the pathophysiology of cognitive deficits in schizophrenia, several mouse models, in which PV neurons were genetically manipulated to mimic their alterations in schizophrenia, has been created for analyses of their molecular, electrophysiological and behavioral phenotypes.

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