5-HT1A autoreceptor desensitization by chronic ultramild stress in mice

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