Guerrila V wrote:I’m very confused about 5-ht1a receptors, and I think also a lot of people are confused. SSRI desensitizes these receptors, so why 5-ht1a antagonists, like WAY 100 635, are recommended? Receptors antagonist wouldn’t lead to more serotonin production?
Also 5-ht1a agonists are recommended to treat PSSD, like Ginkgo Biloba. In my logic, I think agonists should be more useful, as these recepetors are downregulated. Of course I’m not a specialist.
“With respect to serotonin, this journal states that serotonin exerts a stimulatory effect on sexual functioning when acting on 5-HT1A receptors and an inhibitory effect when it acts on 5-HT2/5-HT1B/5-HT1C receptors.” (I'd post the link but I can't cause I'm new here)
Jay, can you explain to us why this confusion? Thank you!
Serotonin does not stimulate "sexual functioning" with exception of the ejaculation aspect as 5-HT1A activation does decrease 'ejaculation latency'....that's an old journal entry you are quoting... A LOT of research has been conducted and CORRECTED since then.
http://www.ncbi.nlm.nih.gov/pubmed/19435548 http://www.ncbi.nlm.nih.gov/pubmed/1357709 http://www.ncbi.nlm.nih.gov/pubmed/119653591A agonists and activation of serotonin 1A decreases erections and the initiatory aspects of male sexual behavior as well as reducing the testosterone response to female pheromones....so no, 1A agonism is not recommended...it may help with trust and partner bonding but there are other, more plausible ways to add oxytocin than that receptor....
Int J Neuropsychopharmacol. 2009 Sep;12(
:1045-53. doi: 10.1017/S1461145709000406. Epub 2009 May 13.
5-HT(1A) receptor antagonism reverses and prevents fluoxetine-induced sexual dysfunction in rats.
Sukoff Rizzo SJ1, Pulicicchio C, Malberg JE, Andree TH, Stack GP, Hughes ZA, Schechter LE, Rosenzweig-Lipson S.
Author information
Abstract
Sexual dysfunction associated with antidepressant treatment continues to be a major compliance issue for antidepressant therapies. 5-HT(1A) antagonists have been suggested as beneficial adjunctive treatment in respect of antidepressant efficacy; however, the effects of 5-HT(1A) antagonism on antidepressant-induced side-effects has not been fully examined. The present study was conducted to evaluate the ability of acute or chronic treatment with 5-HT(1A) antagonists to alter chronic fluoxetine-induced impairments in sexual function. Chronic 14-d treatment with fluoxetine resulted in a marked reduction in the number of non-contact penile erections in sexually experienced male rats, relative to vehicle-treated controls. Acute administration of the 5-HT(1A) antagonist WAY-101405 resulted in a complete reversal of chronic fluoxetine-induced deficits on non-contact penile erections at doses that did not significantly alter baselines. Chronic co-administration of the 5-HT(1A) antagonists WAY-100635 or WAY-101405 with fluoxetine prevented fluoxetine-induced deficits in non-contact penile erections in sexually experienced male rats. Moreover, withdrawal of WAY-100635 from co-treatment with chonic fluoxetine, resulted in a time-dependent reinstatement of chronic fluoxetine-induced deficits in non-contact penile erections. Additionally, chronic administration of SSA-426, a molecule with dual activity as both a SSRI and 5-HT(1A) antagonist, did not produce deficits in non-contact penile erections at doses demonstrated to have antidepressant-like activity in the olfactory bulbectomy model. Taken together, these data suggest that 5-HT(1A) antagonist treatment may have utility for the management of SSRI-induced sexual dysfunction.
PMID: 19435548 [PubMed - indexed for MEDLINE]