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© Christelle Durand
Microscopie d'un neurone. Le marquage jaune montre les synapses.
Publication : European journal of pharmacology

Effects of stress on the functional properties of pre- and postsynaptic 5-HT1B receptors in the rat brain

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in European journal of pharmacology - 29 Dec 1995

Bolanos-Jimenez F, Manhaes de Castro RM, Seguin L, Cloez-Tayarani I, Monneret V, Drieu K, Fillion G

Link to Pubmed [PMID] – 8750715

Eur. J. Pharmacol. 1995 Dec;294(2-3):531-40

Numerous studies have clearly shown that the turnover and release of serotonin (5-hydroxytryptamine, 5-HT) are increased under acute stressful conditions. Inasmuch as this latter process is under the control of a feedback mechanism involving the stimulation of presynaptic 5-HT1B autoreceptors, we have investigated the possible effects of acute restraint (40 min) on the functional properties of 5-HT1B receptors. The efficacy of the selective 5-HT1B receptor agonist 3-[1,2,5,6-tetrahydropyrid-4-yl]pyrrolo-[3,2-b]pyrid-5-one (CP-93,129) in inhibiting in vitro the K+-evoked release of [3H]5-HT, was significantly reduced in stressed rats as compared to naive animals. Similarly, the responsiveness of 5-HT1B receptors inhibiting the release of [3H]acetylcholine (presynaptic 5-HT1B heteroreceptors), was reduced by restraint. These effects were observed in the hippocampus, but using the inhibitory effect of CP-93,129 on forskolin-stimulated adenylyl cyclase activity as an index of 5-HT1B receptor function, it could be shown that the 5-HT1B receptors located in the substantia nigra are also desensitized by stress. The number as well as the apparent affinity constant of 5-HT1B binding sites labelled by [125I]iodocyanopindolol, as measured by quantitative autoradiography and membrane binding, were similar in naive and restraint-stressed rats suggesting that the stress-induced desensitization of 5-HT1B receptors is not due to a reduced number of 5-HT1B binding sites. As stress is thought to be a causal factor for the etiology of anxiety and depression, these results support the potential involvement of 5-HT1B receptor dysfunction in the development of these neurological disorders.

https://www.ncbi.nlm.nih.gov/pubmed/8750715