This article is within the scope of WikiProject Pharmacology, a collaborative effort to improve the coverage of Pharmacology on Wikipedia. If you would like to participate, please visit the project page, where you can join the discussion and see a list of open tasks.PharmacologyWikipedia:WikiProject PharmacologyTemplate:WikiProject Pharmacologypharmacology articles
This article is within the scope of WikiProject Chemicals, a daughter project of WikiProject Chemistry, which aims to improve Wikipedia's coverage of chemicals. To participate, help improve this article or visit the project page for details on the project.ChemicalsWikipedia:WikiProject ChemicalsTemplate:WikiProject Chemicalschemicals articles
Latest comment: 12 years ago1 comment1 person in discussion
The sole source cited in this article alleges that SB-649,915 acts as a 5-HT autoreceptor antagonist, thereby inhibiting release of serotonin. Unless someone can find an article stating that 5-HT1 autoreceptors are atypical, then this assertion is entirely erroneous. Caffeine, an adenosine autoreceptor antagonist, works by inhibiting the detection of adenosine (ATP leftovers, in a way) and thereby increasing the homeostatic levels of adenosine, which in turn mildly stimulates most kinds of energetic cellular activity (activity that consumes ATP or any of its relative compounds). Under this well-studied logical paradigm, any typical autoreceptor antagonist would increase the homeostatic levels of the hormone whose autoreceptor is under blockade, not decrease. This is a logical flaw that should be corrected in the interest of correctness. — Preceding unsigned comment added by 70.112.251.139 (talk) 06:51, 23 February 2012 (UTC)Reply
