TY - JOUR
T1 - Pindolol pretreatment blocks stimulation by meta-chlorophenylpiperazine of prolactin but not cortisol secretion in normal men
AU - Meltzer, Herbert Y.
AU - Maes, Michael
N1 - Funding Information:
The researchre portedw ass upportedin part by U.S. Public Health Service grant MH-41684, GCRC MO1R R00080f rom theN ational Institute of MentalH ealtha ndb y grantsf rom theE lisabeth SeverancPer entissa ndJohn PascalS awyerF oun-dations, and the Michael Kaplen Investigator Award to M. Maes. H.Y.M. is the recipiento f a U.S. Public HealthS erviceR esearchC areerS cien-tist Award MH-47808f rom the National Institute of Mental Health. The secretariala ssistanceo f Mrs. M. Maes and Ms. Lee Mason is greatly appreciated.
PY - 1995/9/29
Y1 - 1995/9/29
N2 - Previous reports from this laboratory have shown that pindolol, a partial serotonin1A receptor agonist, inhibited prolactin, but not cortisol secretion induced by administration of the serotonin (5-HT) precursor l-5-hydroxytryptophan or the direct-acting 5-HT2A 5HT2C receptor agonist MK-212. The findings suggest additive or interactive effects of 5-HT1A and 5-HT2A 5-HT2C receptors in modulating 5-HT-related prolactin, but not cortisol, responsivity. To examine further the role of 5-HT1A and 5-HT2A 5-HT2C receptors in prolactin and cortisol secretion in healthy men, the effects of meta-chlorophenylpiperazine (mCPP), a potent 5-HT receptor agonist, on the above hormones were studied in eight healthy men with and without pindolol pretreatment. It has previously been demonstrated that ketanserin, a 5-HT2A antagonist, and ritanserin, a 5-HT2A 5-HT2C antagonist, block the prolactin and attenuate the hypothalamic-pituitary-adrenal axis responses to mCPP in man or rodents. Administration of mCPP induced a significant increase in plasma concentrations of prolactin and cortisol. The mCPP-induced prolactin concentrations were significantly blocked by pretreatment with pindolol, whereas mCPP-stimulated cortisol levels were not diminished by pindolol pretreatment. Thus, mCPP-induced prolactin secretion appears to require the availability of both 5-HT2C and 5-HT1A receptor activation, since blockade of either of these receptors may diminish the mCPP-induced prolactin response. Cortisol secretion stimulated by mCPP may occur following 5-HT2C receptor stimulation in the presence of 5-HT1A receptor blockade.
AB - Previous reports from this laboratory have shown that pindolol, a partial serotonin1A receptor agonist, inhibited prolactin, but not cortisol secretion induced by administration of the serotonin (5-HT) precursor l-5-hydroxytryptophan or the direct-acting 5-HT2A 5HT2C receptor agonist MK-212. The findings suggest additive or interactive effects of 5-HT1A and 5-HT2A 5-HT2C receptors in modulating 5-HT-related prolactin, but not cortisol, responsivity. To examine further the role of 5-HT1A and 5-HT2A 5-HT2C receptors in prolactin and cortisol secretion in healthy men, the effects of meta-chlorophenylpiperazine (mCPP), a potent 5-HT receptor agonist, on the above hormones were studied in eight healthy men with and without pindolol pretreatment. It has previously been demonstrated that ketanserin, a 5-HT2A antagonist, and ritanserin, a 5-HT2A 5-HT2C antagonist, block the prolactin and attenuate the hypothalamic-pituitary-adrenal axis responses to mCPP in man or rodents. Administration of mCPP induced a significant increase in plasma concentrations of prolactin and cortisol. The mCPP-induced prolactin concentrations were significantly blocked by pretreatment with pindolol, whereas mCPP-stimulated cortisol levels were not diminished by pindolol pretreatment. Thus, mCPP-induced prolactin secretion appears to require the availability of both 5-HT2C and 5-HT1A receptor activation, since blockade of either of these receptors may diminish the mCPP-induced prolactin response. Cortisol secretion stimulated by mCPP may occur following 5-HT2C receptor stimulation in the presence of 5-HT1A receptor blockade.
KW - Hormones
KW - Hypothalamic-pituitary-adrenal axis
KW - Serotonin receptor subtypes
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U2 - 10.1016/0165-1781(95)02701-W
DO - 10.1016/0165-1781(95)02701-W
M3 - Article
C2 - 8570772
AN - SCOPUS:0028856757
VL - 58
SP - 89
EP - 98
JO - Psychiatry Research
JF - Psychiatry Research
SN - 0165-1781
IS - 2
ER -
