Effects of cocaine on basal and pulsatile prolactin levels in rhesus monkeys

Gerard M. Honoré, Thomas S. King, Mary Samuels, Arturo Moreno, Theresa M. Siler-Khodr, Carlton A. Eddy, Robert S. Schenken

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Abstract

Objectives: Cocaine abuse is often associated with reproductive cycle dysfunction including altered menstrual cyclicity and decreased ovulation rates. Cocaine might also alter prolactin (PRL) secretion, presumably through the effects of this drug on hypothalamic dopamine, the primary factor regulating pituitary PRL secretion. We assessed basal and pulsatile PRL levels to determine whether hyperprolactinemia is associated with cocaine-induced disruption of menstrual cyclicity in rhesus monkeys. Methods: Normally cycling, drug-naïve monkeys were studied. Cocaine-treated animals were pair-fed with controls to minimize cocaine-related differences in caloric intake. Twenty-eight monkeys were randomized to receive daily intravenous (iv) infusion of saline or cocaine (1, 2, or 4 mg/kg) on cycle days 2-14. Daily blood samples were obtained through indwelling catheters for measurement of ovarian steroids, gonadotropins, and PRL. Laparoscopy was performed 2 days after the midcycle estradiol surge to document ovulation. Sixteen other monkeys were randomized to receive daily iv infusion of saline or cocaine (4 mg/kg). Blood samples were obtained every 15 minutes for 8 hours in the early (cycle day 1-5), mid- (cycle day 6-10), and late (cycle day 11-15) follicular phase. Plasma was assayed for PRL, and pulses were identified by cluster analysis. Results: All seven control monkeys had laparoscopically confirmed ovulation compared to two of seven monkeys receiving 1 mg/kg, three of seven monkeys receiving 2 mg/kg, and one of seven receiving 4 mg/kg of cocaine hydrochloride. Cycle length was normal in six of seven controls, and in one of seven, two of seven, and two of seven monkeys receiving the 1, 2, and 4 mg/kg of cocaine, respectively. Estradiol levels were significantly higher in controls versus cocaine-treated monkeys, but there was no difference in basal gonadotropin levels during treatment. Mean PRL levels during treatment were significantly lower (P <.05) in controls (4.6 ± 0.2 ng/mL) as compared to monkeys receiving 1 (6.5 ± 0.6 ng/mL), 2 (6.1 ± 0.4 ng/mL), and 4 mg/kg (7.2 ± 0.6 ng/mL) of cocaine. There was no significant difference in PRL pulse amplitude or frequency between controls and cocaine-treated monkeys during each cycle phase. Conclusions: Circulating PRL levels were slightly higher in monkeys receiving cocaine during the follicular phase. Although this increase was statistically significant, PRL levels remained well within the euprolactinemic range in cocaine-treated monkeys.

Original languageEnglish (US)
Pages (from-to)351-357
Number of pages7
JournalJournal of the Society for Gynecologic Investigation
Volume8
Issue number6
DOIs
StatePublished - 2001

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Macaca mulatta
Cocaine
Prolactin
Haplorhini
Ovulation
Follicular Phase
Periodicity
Gonadotropins
Intravenous Infusions
Estradiol
Cocaine-Related Disorders
Hyperprolactinemia
Indwelling Catheters
Energy Intake
Pharmaceutical Preparations
Laparoscopy
Cluster Analysis
Dopamine
Steroids

Keywords

  • Cocaine
  • Prolactin
  • Rhesus monkey

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Effects of cocaine on basal and pulsatile prolactin levels in rhesus monkeys. / Honoré, Gerard M.; King, Thomas S.; Samuels, Mary; Moreno, Arturo; Siler-Khodr, Theresa M.; Eddy, Carlton A.; Schenken, Robert S.

In: Journal of the Society for Gynecologic Investigation, Vol. 8, No. 6, 2001, p. 351-357.

Research output: Contribution to journalArticle

Honoré, Gerard M. ; King, Thomas S. ; Samuels, Mary ; Moreno, Arturo ; Siler-Khodr, Theresa M. ; Eddy, Carlton A. ; Schenken, Robert S. / Effects of cocaine on basal and pulsatile prolactin levels in rhesus monkeys. In: Journal of the Society for Gynecologic Investigation. 2001 ; Vol. 8, No. 6. pp. 351-357.
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abstract = "Objectives: Cocaine abuse is often associated with reproductive cycle dysfunction including altered menstrual cyclicity and decreased ovulation rates. Cocaine might also alter prolactin (PRL) secretion, presumably through the effects of this drug on hypothalamic dopamine, the primary factor regulating pituitary PRL secretion. We assessed basal and pulsatile PRL levels to determine whether hyperprolactinemia is associated with cocaine-induced disruption of menstrual cyclicity in rhesus monkeys. Methods: Normally cycling, drug-na{\"i}ve monkeys were studied. Cocaine-treated animals were pair-fed with controls to minimize cocaine-related differences in caloric intake. Twenty-eight monkeys were randomized to receive daily intravenous (iv) infusion of saline or cocaine (1, 2, or 4 mg/kg) on cycle days 2-14. Daily blood samples were obtained through indwelling catheters for measurement of ovarian steroids, gonadotropins, and PRL. Laparoscopy was performed 2 days after the midcycle estradiol surge to document ovulation. Sixteen other monkeys were randomized to receive daily iv infusion of saline or cocaine (4 mg/kg). Blood samples were obtained every 15 minutes for 8 hours in the early (cycle day 1-5), mid- (cycle day 6-10), and late (cycle day 11-15) follicular phase. Plasma was assayed for PRL, and pulses were identified by cluster analysis. Results: All seven control monkeys had laparoscopically confirmed ovulation compared to two of seven monkeys receiving 1 mg/kg, three of seven monkeys receiving 2 mg/kg, and one of seven receiving 4 mg/kg of cocaine hydrochloride. Cycle length was normal in six of seven controls, and in one of seven, two of seven, and two of seven monkeys receiving the 1, 2, and 4 mg/kg of cocaine, respectively. Estradiol levels were significantly higher in controls versus cocaine-treated monkeys, but there was no difference in basal gonadotropin levels during treatment. Mean PRL levels during treatment were significantly lower (P <.05) in controls (4.6 ± 0.2 ng/mL) as compared to monkeys receiving 1 (6.5 ± 0.6 ng/mL), 2 (6.1 ± 0.4 ng/mL), and 4 mg/kg (7.2 ± 0.6 ng/mL) of cocaine. There was no significant difference in PRL pulse amplitude or frequency between controls and cocaine-treated monkeys during each cycle phase. Conclusions: Circulating PRL levels were slightly higher in monkeys receiving cocaine during the follicular phase. Although this increase was statistically significant, PRL levels remained well within the euprolactinemic range in cocaine-treated monkeys.",
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T1 - Effects of cocaine on basal and pulsatile prolactin levels in rhesus monkeys

AU - Honoré, Gerard M.

AU - King, Thomas S.

AU - Samuels, Mary

AU - Moreno, Arturo

AU - Siler-Khodr, Theresa M.

AU - Eddy, Carlton A.

AU - Schenken, Robert S.

PY - 2001

Y1 - 2001

N2 - Objectives: Cocaine abuse is often associated with reproductive cycle dysfunction including altered menstrual cyclicity and decreased ovulation rates. Cocaine might also alter prolactin (PRL) secretion, presumably through the effects of this drug on hypothalamic dopamine, the primary factor regulating pituitary PRL secretion. We assessed basal and pulsatile PRL levels to determine whether hyperprolactinemia is associated with cocaine-induced disruption of menstrual cyclicity in rhesus monkeys. Methods: Normally cycling, drug-naïve monkeys were studied. Cocaine-treated animals were pair-fed with controls to minimize cocaine-related differences in caloric intake. Twenty-eight monkeys were randomized to receive daily intravenous (iv) infusion of saline or cocaine (1, 2, or 4 mg/kg) on cycle days 2-14. Daily blood samples were obtained through indwelling catheters for measurement of ovarian steroids, gonadotropins, and PRL. Laparoscopy was performed 2 days after the midcycle estradiol surge to document ovulation. Sixteen other monkeys were randomized to receive daily iv infusion of saline or cocaine (4 mg/kg). Blood samples were obtained every 15 minutes for 8 hours in the early (cycle day 1-5), mid- (cycle day 6-10), and late (cycle day 11-15) follicular phase. Plasma was assayed for PRL, and pulses were identified by cluster analysis. Results: All seven control monkeys had laparoscopically confirmed ovulation compared to two of seven monkeys receiving 1 mg/kg, three of seven monkeys receiving 2 mg/kg, and one of seven receiving 4 mg/kg of cocaine hydrochloride. Cycle length was normal in six of seven controls, and in one of seven, two of seven, and two of seven monkeys receiving the 1, 2, and 4 mg/kg of cocaine, respectively. Estradiol levels were significantly higher in controls versus cocaine-treated monkeys, but there was no difference in basal gonadotropin levels during treatment. Mean PRL levels during treatment were significantly lower (P <.05) in controls (4.6 ± 0.2 ng/mL) as compared to monkeys receiving 1 (6.5 ± 0.6 ng/mL), 2 (6.1 ± 0.4 ng/mL), and 4 mg/kg (7.2 ± 0.6 ng/mL) of cocaine. There was no significant difference in PRL pulse amplitude or frequency between controls and cocaine-treated monkeys during each cycle phase. Conclusions: Circulating PRL levels were slightly higher in monkeys receiving cocaine during the follicular phase. Although this increase was statistically significant, PRL levels remained well within the euprolactinemic range in cocaine-treated monkeys.

AB - Objectives: Cocaine abuse is often associated with reproductive cycle dysfunction including altered menstrual cyclicity and decreased ovulation rates. Cocaine might also alter prolactin (PRL) secretion, presumably through the effects of this drug on hypothalamic dopamine, the primary factor regulating pituitary PRL secretion. We assessed basal and pulsatile PRL levels to determine whether hyperprolactinemia is associated with cocaine-induced disruption of menstrual cyclicity in rhesus monkeys. Methods: Normally cycling, drug-naïve monkeys were studied. Cocaine-treated animals were pair-fed with controls to minimize cocaine-related differences in caloric intake. Twenty-eight monkeys were randomized to receive daily intravenous (iv) infusion of saline or cocaine (1, 2, or 4 mg/kg) on cycle days 2-14. Daily blood samples were obtained through indwelling catheters for measurement of ovarian steroids, gonadotropins, and PRL. Laparoscopy was performed 2 days after the midcycle estradiol surge to document ovulation. Sixteen other monkeys were randomized to receive daily iv infusion of saline or cocaine (4 mg/kg). Blood samples were obtained every 15 minutes for 8 hours in the early (cycle day 1-5), mid- (cycle day 6-10), and late (cycle day 11-15) follicular phase. Plasma was assayed for PRL, and pulses were identified by cluster analysis. Results: All seven control monkeys had laparoscopically confirmed ovulation compared to two of seven monkeys receiving 1 mg/kg, three of seven monkeys receiving 2 mg/kg, and one of seven receiving 4 mg/kg of cocaine hydrochloride. Cycle length was normal in six of seven controls, and in one of seven, two of seven, and two of seven monkeys receiving the 1, 2, and 4 mg/kg of cocaine, respectively. Estradiol levels were significantly higher in controls versus cocaine-treated monkeys, but there was no difference in basal gonadotropin levels during treatment. Mean PRL levels during treatment were significantly lower (P <.05) in controls (4.6 ± 0.2 ng/mL) as compared to monkeys receiving 1 (6.5 ± 0.6 ng/mL), 2 (6.1 ± 0.4 ng/mL), and 4 mg/kg (7.2 ± 0.6 ng/mL) of cocaine. There was no significant difference in PRL pulse amplitude or frequency between controls and cocaine-treated monkeys during each cycle phase. Conclusions: Circulating PRL levels were slightly higher in monkeys receiving cocaine during the follicular phase. Although this increase was statistically significant, PRL levels remained well within the euprolactinemic range in cocaine-treated monkeys.

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