5-HT1A autoreceptor desensitization by chronic ultramild stress in mice

被引：87

作者：

Lanfumey, L

Pardon, MC

Laaris, N

Joubert, C

Hanoun, N

Hamon, M

Cohen-Salmon, C

机构：

[1] CHU Pitie Salpetriere, INSERM, U288, F-75634 Paris 13, France

[2] CHU Pitie Salpetriere, IFR Neurosci, CNRS 7593, F-75634 Paris, France

来源：

NEUROREPORT | 1999年 / 10卷 / 16期

关键词：

chronic ultramild stress; electrophysiology; 5-HT1A autoreceptors; serotonin; slice;

D O I：

10.1097/00001756-199911080-00021

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

ELECTROPHYSIOLOGICAL and biochemical approaches were used to assess possible changes in central 5-HT neurotransmission in mice that had been subjected to chronic ultramild stress for 8 weeks. This treatment produced a significant decrease in the potency of the 5-HT1A agonist ipsapirone to inhibit the electrical activity of serotoninergic neurons in the dorsal raphe nucleus, without modifying 5-HT1A receptor binding in various brain areas. These data demonstrate that chronic ultra-mild stress triggers a long term and durable functional desensitization of somatodendritic 5-HT1A autoreceptors in mice. NeuroReport 10:3369-3374 (C) 1999 Lippincott Williams & Wilkins.

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页码：3369 / 3374

页数：6

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