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Regulation of the release of 5‐hydroxytryptamine in the median raphe nucleus of the rat by catecholaminergic afferents
Author(s) -
Adell Albert,
Artigas Francesc
Publication year - 1999
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1999.00642.x
Subject(s) - chemistry , idazoxan , raclopride , raphe nuclei , endocrinology , prazosin , medicine , agonist , dorsal raphe nucleus , serotonin , dopamine , dopaminergic , pharmacology , serotonergic , antagonist , receptor , biology , biochemistry
The present study was conducted in order to examine the influence of catecholaminergic afferents on the release of serotonin in the median raphe nucleus in vivo. To this aim, selective dopamine D 1 and D 2 , and α 1 ‐ and α 2 ‐adrenergic agonists and antagonists were administered locally (1, 10 and 100 μ m ) through a dialysis probe implanted in the median raphe nucleus of freely moving rats. The D 1 and D 2 agonists, (±)‐1‐phenyl‐2,3,4,5‐tetrahydro‐(1H)‐3‐benzazepine‐7,8‐diol (SKF‐38393) and quinpirole, respectively, and the D 1 and D 2 antagonists, r ‐(+)‐7‐chloro‐8‐hydroxy‐3‐methyl‐1‐phenyl‐2,3,4,5‐tetrahydro‐1H‐3‐benzazepine (SCH‐23390) and raclopride, respectively, did not alter the release of serotonin in the median raphe nucleus. The α 1 ‐adrenoceptor agonist phenylephrine did not modify the release of serotonin in this nucleus, although an increased release was observed when the more potent α 1 ‐adrenoceptor agonist cirazoline was used. In contrast, the α 1 ‐adrenoceptor antagonist prazosin reduced the release of 5‐hydroxytryptamine (5‐HT) in a concentration‐dependent manner. The release of 5‐HT was also reduced by the α 2 ‐adrenoceptor agonist clonidine and increased by the α 2 ‐adrenoceptor antagonist 2‐methoxy‐idazoxan (RX821002). These results indicate that the release of serotonin in the median raphe nucleus does not appear to be regulated by dopaminergic afferents through the activation of dopamine D 1 or D 2 receptors. On the contrary, it is suggested that endogenous noradrenaline exerts a direct tonic stimulatory control on the release of serotonin through α 1 ‐adrenoceptors, and an indirect tonic inhibitory influence through α 2 ‐adrenoceptors located probably in noradrenergic nerve terminals within the median raphe nucleus.