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統合失調症I
Schizophrenia I

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開催日
2010年09月02日(木)
時 間
11:00 - 12:00
会 場
Poster Room 2

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統合失調症モデルマウスにおける海馬ニューロンの聴覚性応答異常
Abnormal responses of hippocampal neurons to auditory paired-click stimuli in a neurodevelopmental mouse-model of schizophrena

演題番号 : P1-p09

岡本 正博 / Masahiro Okamoto:1 浄土 英一 / Eiichi Jodo:1 片山 規央 / Tadahiro Katayama:1 鈴木 喜明 / Yoshiaki Suzuki:2 星野 研洋 / Ken-Yo Hoshino:2 山田 博 / Hiroshi Yamada:3 松岡 信也 / Shinya Matsuoka:3 香山 雪彦 / Yukihiko Kayama:1 

1:福島医大・医・神経生理 / Depart Neurophysiol, Fukushima Med Univ, Fukushima 2:福島医大・医・神経精神 / Dept Neuropsychiat, Fukushima Med Univ, Fukushima 3:アステラス製薬・薬理研究所・神経科学研究室 / Depart of Neurosci, Pharmacol Res Lab. Drug Discov Res, Astellas Pharma Inc., Tsukuba 

 

Disturbances in sensory gating are commonly found in both patients with schizophrenia and its animal models. The sensory gating function can be assessed by homologous methods in humans and animals, and many studies so far have been made on that function. However, the underlying neural mechanism remains not well understood. In the present study, to investigate neural mechanisms underlying deficits in sensory gating, we recorded unit activity of hippocampal neurons in mice that underwent systemic administration of phencyclidine (PCP) in a neonatal period under an auditory paired click paradigm. Three hundred and forty neurons were recorded in total (n = 144, PCP-treated; n = 196, saline-treated). The hippocampal neurons in the PCP-treated mice exhibited excitatory (33.3%, n = 48) or inhibitory (18.8%, n = 27) responses to both test (the first click) and control stimuli (the second click). Those of the saline-treated mice also exhibited excitatory (19.4%, n = 38) or inhibitory (31.1%, n = 61) responses. However, the proportion of neurons exhibiting excitatory responses to auditory clicks was higher in the PCP-treated mice than that in the saline-treated ones. The duration of neuronal responses to the second click was also significantly different between the PCP-treated and saline-treated mice. The excitatory response in the PCP-treated mice lasted for longer time than that in the saline-treated ones (PCP-treated: 111 msec; saline-treated: 53 msec, p < 0.05). In contrast, the duration of the inhibitory response was significantly shorter in the PCP-treated mice than that in the saline-treated ones (PCP-treated: 93 msec; saline-treated: 165 msec, p < 0.05). These results suggest that systemic administration of PCP in a neonatal period may disturb the normal development of inhibitory neural circuits in the hippocampus, which may result in disturbed sensory gating.

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