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Buspirone challenge test
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====== Sharpe et al 1996 ====== The [[Michael Sharpe|Sharpe]] 1996 study<ref name=":2">{{Cite journal | last = Sharpe | first = M. | last2 = Clements | first2 = A. | last3 = Hawton | first3 = K. | last4 = Young | first4 = A.H. | last5 = Sargent | first5 = P. | last6 = Cowen | first6 = P.J. | date = 1996-11-04 | title = Increased prolactin response to buspirone in chronic fatigue syndrome | url =https://www.ncbi.nlm.nih.gov/pubmed/8938208 | journal = Journal of Affective Disorders | volume = 41 | issue = 1 | pages = 71–76|issn=0165-0327|pmid=8938208}}</ref> orally administered 0.5 mg/kg of buspirone in a single dose to 11 ME/CFS patients and 11 healthy controls, and then measured their plasma prolactin levels every 30 minutes for the next 4 hours. They found ME/CFS patients exhibited both a significantly higher buspirone-stimulated plasma prolactin peak, as well as a faster time to peak, than healthy controls. ME/CFS patients also experienced more nausea and lightheadedness than controls in response to the buspirone. However, no significant differences in growth hormone secretion after stimulation by buspirone were observed in these two groups. The authors thus question whether ME/CFS patients' exaggerated prolactin response to buspirone is caused by increased hypothalamic serotonin receptor sensitivity, as they point out both prolactin and growth hormone release is elicited by activation of hypothalamic 5-HT1A receptors, and thus one might expect an exaggerated release of both these hormones in ME/CFS patients. But since ME/CFS patients' growth hormone responses to buspirone were not significantly raised compared to controls, the authors suggest this casts a degree of doubt (although with some caveats) on the hypothesis of increased hypothalamic serotonin receptor sensitivity in ME/CFS. As an alternative hypothesis, the authors point out buspirone binds to dopamine D2 receptors, and suggest the ability of buspirone to stimulate prolactin release might instead be primarily mediated by a dopamine receptor blockade.
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