当前位置： SCI文献检索 > NEUROSCIENCE LETTERS期刊下所有文献 > The alpha 2-adrenoceptor antagonist idazoxan is an agonist at 5-HT1A autoreceptors modulating serotonin synthesis in the rat brain in vivo.

The alpha 2-adrenoceptor antagonist idazoxan is an agonist at 5-HT1A autoreceptors modulating serotonin synthesis in the rat brain in vivo.

Abstract：

:The in vivo effects of the alpha 2-adrenoceptor idazoxan, rauwolscine and phentolamine on alpha 2-auto/heteroreceptors and 5-HT1A autoreceptors modulating the synthesis of dopa/noradrenaline and 5-HTP/serotonin were assessed in rats, using the accumulation of dopa and 5-HTP after decarboxylase inhibition as a measure of the rate of tyrosine and tryptophan hydroxylation. The acute administration of idazoxan (0.1-40 mg/kg) induced a pronounced dose-dependent increase in the synthesis of dopa in the cerebral cortex (22-86%) and hippocampus (8-80%), as a consequence of the powerful blockade of alpha 2-autoreceptors. However, idazoxan did not increase the synthesis of 5-HTP in these brain regions, as it would have been expected by the concurrent blockade of alpha 2-heteroreceptors on serotonergic terminals. Instead, idazoxan decreased the synthesis of 5-HTP in the cerebral cortex (13-33%) and hippocampus (25-48%), suggesting that these inhibitory effects were mediated through activation of 5-HT1A autoreceptors. Similar results were obtained for rauwolscine. Pre-treatment of rats with the selective 5-HT1A receptor antagonist WAY100135 (10 mg/kg) fully antagonized the inhibitory effects of idazoxan (10 mg/kg) on 5-HTP synthesis, but it did not prevent the stimulatory effects of idazoxan on dopa synthesis. The results indicate that idazoxan is a potent and specific agonist at 5-HT1A autoreceptors modulating brain serotonin synthesis in vivo.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Lladó J,Esteban S,García-Sevilla JA

doi

10.1016/s0304-3940(96)13132-3

subject

Has Abstract

pub_date

1996-11-01 00:00:00

pages

111-4

issue

2

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(96)13132-3

journal_volume

218

pub_type

杂志文章

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