Direct evidence for an important species difference in the mechanism of 8-OH-DPAT-induced hypothermia.

摘要: Abstract 1. Parallel series of experiments were carried out in the rat and mouse order to investigate mechanism(s) underlying hypothermia induced rodents by selective 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). 2. In mouse, lesioning central 5-hydroxytryptaminergic neurones (by use neurotoxin, 5,7-dihydroxytryptamine; 5,7-DHT) abolished hypothermic response 8-OH-DPAT, depletion brain 5-hydroxytryptamine (5-HT) levels (with 5-HT synthesis inhibitor, p-chlorophenylalanine) markedly attenuated this species. These pretreatments did not significantly attenuate 8-OH-DPAT-induced rat, except for a significant attenuation 5,7-DHT-lesioned rats at top dose 8-OH-DPAT (1.0 mg kg-1, s.c.). 3. Pharmacological which facilitate release (selective uptake inhibitors, precursor (5-hydroxytryptophan) loading, or fenfluramine), mouse. generally had no effect on rat. 4. The noradrenaline desipramine, either dopamine nomifensin, increased but affect high, motor stimulant doses, when was attenuated. 5. data are consistent with hypothesis that is mediated presynaptic autoreceptors postsynaptic receptors rat.(ABSTRACT TRUNCATED AT 250 WORDS)