INTRATESTICULAR SEROTONIN AFFECTS STEROIDOGENESIS IN THE RAT TESTIS

Citation
Z. Csaba et al., INTRATESTICULAR SEROTONIN AFFECTS STEROIDOGENESIS IN THE RAT TESTIS, Journal of neuroendocrinology, 10(5), 1998, pp. 371-376
Citations number
29
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism
ISSN journal
09538194
Volume
10
Issue
5
Year of publication
1998
Pages
371 - 376
Database
ISI
SICI code
0953-8194(1998)10:5<371:ISASIT>2.0.ZU;2-H
Abstract
The effect of intratesticular administration of serotonin (5-HT), keta nserin (5-HT2 receptor antagonist), and 5,7-dihydroxytryptamine (5,7-D HT) (the neurotoxin that destroys serotoninergic neural elements) on s teroidogenesis was studied in immature and adult rats. In adults, bila teral intratesticular injection of 5-HT resulted in a significant decr ease in basal but not in hCG-stimulated testosterone secretion and in serum testosterone concentration, whereas ketanserin induced a signifi cant rise in steroidogenesis 1 h post-treatment. There was no effect 1 day after administration of 5-HT or ketanserin, and 7 days after the injection of 5,7-DHT. In immature rats 1 day after bilateral testicula r administration of ketanserin, basal testosterone secretion in vitro was significantly suppressed. In immature hemicastrates, local injecti on of 5-HT resulted (1 day post-treatment) in a significant rise in st eroidogenesis while administration of 5,7-DHT decreased testosterone s ecretion 7 days after the injection of the neurotoxin. The results ind icate that in adult rats 5-HT exerts a suppressive, whereas in immatur e rats, a stimulatory action on steroidogenesis occurs, Data also sugg est that, in both age groups, the effect of 5-HT is mediated through 5 -HT2 receptors, The observation that in immatures administration of th e neurotoxin resulted in an effect similar to that found following the treatment with the receptor antagonist suggests that, in this age gro up, 5-HT derived from local neural elements might also be involved in the control of 5-HT on Leydig cell steroidogenesis.