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Buspirone Does Not Alter the Reinforcing, Subjective or Physiological Effects of Intranasal Cocaine
Author(s) -
Stoops William,
Bolin B,
Lile Joshua,
Rush Craig
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.930.4
Subject(s) - buspirone , cocaine dependence , placebo , pharmacology , agonist , partial agonist , psychology , dosing , medicine , pharmacodynamics , anesthesia , addiction , psychiatry , pharmacokinetics , receptor , alternative medicine , pathology
Despite extensive research efforts, no effective medications have been identified for managing cocaine use disorder. The purpose of this study was to evaluate buspirone, a dopamine D 3 / D 4 receptor antagonist and serotonin 5‐HT 1A receptor partial agonist, as a candidate cocaine pharmacotherapy using human laboratory methods. To this end, nine current cocaine users completed a repeated measures, inpatient protocol in which they were maintained on placebo and buspirone (30 mg/day) in counterbalanced order for 3 days before completing experimental sessions. The reinforcing, subjective and physiological effects of placebo and intranasal cocaine (15 and 45 mg) were assessed during those sessions. Cocaine functioned as a reinforcer and produced other prototypic effects (i.e., increased ratings of good effects and heart rate in a dose‐ and time‐related manner). Although cocaine was well tolerated during buspirone maintenance, there were no systematic differences observed in these outcome measures as a function of buspirone condition. These data indicate that this dosing regimen of buspirone did not change the pharmacodynamic effects of cocaine, consistent with clinical trial data suggesting that buspirone does not reduce cocaine use. However, longer dosing periods and higher buspirone doses should be tested to more fully determine the potential utility of buspirone for managing cocaine use disorder. Supported by R21DA034095.