Neuroendocrine and hypothermic effects of 5-HT1A receptor stimulation with ipsapirone in healthy men: a placebo-controlled study.
The neuroendocrine effects of 5-hydroxytryptamine-1A (5-HT1A) receptor stimulation remain uncertain in humans, in respect to both anterior and posterior pituitary hormone release. This is important because these endocrine responses are often used as indications of 5-HT1A receptor sensitivity. The link between receptor stimulation and subsequent hormone release is more direct with posterior pituitary hormones because there is no intermediate hypothalamic peptide in the pathway. Theoretically, therefore, posterior pituitary hormones should be more valid indicators of central 5-HT1A receptor sensitivity. We used the 5-HT1A receptor partial agonist ipsapirone (20 mg) as an oral serotonergic challenge drug in a random-order, double-blind placebo-controlled study of 12 healthy men. Blood sampling occurred at 30 min intervals up to 180 min after the administration of drug or placebo. Ipsapirone caused clear and significant elevations in adrenocorticotrophin (ACTH), cortisol (CORT), prolactin (PRL), and growth hormone (GH) release. Peak hormone and ipsapirone blood levels both occurred at 60 min after ipsapirone administration. Release of the posterior pituitary hormone oxytocin was also stimulated, but less robustly and with more baseline variation. Temperature fell significantly more after ipsapirone than placebo. These results contrast with previous studies, which found no effect of ipsapirone on PRL and GH release in humans, but are in accordance with data using other 5-HT1A agonist drugs. The presence of an oxytocin response to ipsapirone suggests that oxytocin is a potential marker for serotonergic function in neuroendocrine challenge studies, but this awaits further study.[1]References
- Neuroendocrine and hypothermic effects of 5-HT1A receptor stimulation with ipsapirone in healthy men: a placebo-controlled study. Cleare, A.J., Forsling, M., Bond, A.J. International clinical psychopharmacology. (1998) [Pubmed]
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