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dc.contributor.authorFarren, Connor K.
dc.contributor.authorZiedonis, Douglas M.
dc.contributor.authorClare, Anthony W.
dc.contributor.authorHammeedi, Faiq A.
dc.contributor.authorDinan, Timothy G.
dc.date2022-08-11T08:10:26.000
dc.date.accessioned2022-08-23T17:08:40Z
dc.date.available2022-08-23T17:08:40Z
dc.date.issued1995-12-01
dc.date.submitted2010-08-28
dc.identifier.citationAlcohol Clin Exp Res. 1995 Dec;19(6):1578-82.
dc.identifier.issn0145-6008 (Linking)
dc.identifier.pmid8749830
dc.identifier.urihttp://hdl.handle.net/20.500.14038/45633
dc.description.abstractSerum prolactin response to the serotonin agonist D-fenfluramine were measured in 19 DSM-111-R male alcoholics, 2.5 or more weeks postalcohol withdrawal. Prolactin responses were compared with nine healthy nonalcoholic male controls. After an overnight fast, each subject received 30 mg of D-fenfluramine orally, and serial samples of serum prolactin were taken over a 4-hr period. D-fenfluramine caused a significantly attenuated peak delta-prolactin response in the alcoholics relative to the controls (p = 0.05). A repeated-measures ANOVA of delta-prolactin yielded a significant within-subjects effect of time (p < 0.05), a within-subjects effect of group that reached significance (p = 0.05), and a nonsignificant group by time interaction. The delta-prolactin value at time points 60 and 240 min postadministration of the probe was significantly attenuated in the alcoholic group, with p < 0.05. There was also some evidence for a diminished serotonergic response in those alcoholics with a negative family history. The delta-prolactin response did not correlate with subjects' age, duration of alcohol use, duration of abstinence from alcohol, severity of alcohol dependence, or age of onset. Results imply a relative subsensitivity of the serotonin system in postwithdrawal alcoholics, and this may be primarily of the 5-HT2 receptor.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=8749830&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1111/j.1530-0277.1995.tb01027.x
dc.subjectAdult
dc.subjectAlcohol Withdrawal Delirium
dc.subjectAlcoholism
dc.subjectFenfluramine
dc.subjectGenotype
dc.subjectHumans
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectProlactin
dc.subjectReceptors, Serotonin
dc.subjectReference Values
dc.subjectTemperance
dc.subjectPsychiatry
dc.titleD-fenfluramine-induced prolactin responses in postwithdrawal alcoholics and controls
dc.typeJournal Article
dc.source.journaltitleAlcoholism, clinical and experimental research
dc.source.volume19
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/psych_pp/167
dc.identifier.contextkey1482968
html.description.abstract<p>Serum prolactin response to the serotonin agonist D-fenfluramine were measured in 19 DSM-111-R male alcoholics, 2.5 or more weeks postalcohol withdrawal. Prolactin responses were compared with nine healthy nonalcoholic male controls. After an overnight fast, each subject received 30 mg of D-fenfluramine orally, and serial samples of serum prolactin were taken over a 4-hr period. D-fenfluramine caused a significantly attenuated peak delta-prolactin response in the alcoholics relative to the controls (p = 0.05). A repeated-measures ANOVA of delta-prolactin yielded a significant within-subjects effect of time (p < 0.05), a within-subjects effect of group that reached significance (p = 0.05), and a nonsignificant group by time interaction. The delta-prolactin value at time points 60 and 240 min postadministration of the probe was significantly attenuated in the alcoholic group, with p < 0.05. There was also some evidence for a diminished serotonergic response in those alcoholics with a negative family history. The delta-prolactin response did not correlate with subjects' age, duration of alcohol use, duration of abstinence from alcohol, severity of alcohol dependence, or age of onset. Results imply a relative subsensitivity of the serotonin system in postwithdrawal alcoholics, and this may be primarily of the 5-HT2 receptor.</p>
dc.identifier.submissionpathpsych_pp/167
dc.contributor.departmentDepartment of Psychiatry
dc.source.pages1578-82


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