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.
引用
收藏
页码：3369 / 3374
页数：6
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