Nk. Mello et al., DOPAMINE INFUSION DOES NOT ALTER LH LEVELS BEFORE OR AFTER CHRONIC COCAINE EXPOSURE IN FEMALE RHESUS-MONKEYS, Pharmacology, biochemistry and behavior, 58(3), 1997, pp. 819-828
Cocaine stimulates release of luteinizing hormone (LH) in preclinical
and clinical studies but the contribution of the indirect dopamine ago
nist actions of cocaine to its effects on LH are unclear. In the prese
nt study, we examined the effects of exogenous dopamine infusions on L
H release in drug-naive, normally cycling, female rhesus monkeys. All
studies were conducted during the mid-follicular phase (cycle days 6-8
). Three successive 80-min dopamine infusions (10 mu g/kg/min, intrave
nous) were alternated with 20-or 40-min interruptions of dopamine infu
sions. There were no significant changes in LH during or following dop
amine infusions. Predopamine baseline LH levels averaged 30 +/- 5.4 ng
/ml. LH aver aged 31.7 +/- 1.3 ng/ml during dopamine infusions and 31.
4 +/- 1.3 ng/ml after dopamine infusions stopped. To determine whether
chronic cocaine exposure influenced the effect of dopamine on LH, rhe
sus females were studied after more than 2 years of cocaine self-admin
istration at an average dose of 6.5 +/- 0.2 mg/kg/day. LH averaged 27.
3 +/- 3.3 ng/ml during baseline and 26.9 +/- 0.7 ng/ml and 26.1 +/- 0.
7 ng/ml during dopamine infusions and interruptions, respectively. Sim
ilarly, during withdrawal from cocaine, baseline LH levels averaged 32
.1 +/- 4.5 ng/ml, and LH did not change significantly during dopamine
infusions (31.2 +/- 1.1 ng/ml) and infusion interruptions (32.1 +/- 1.
1 ng/ml). Under the conditions of the present study, dopamine administ
ration did not change LH levels in gonadally intact rhesus monkeys, an
d these findings are consistent with previous studies in ovariectomize
d rhesus females. However, these data are not consistent with clinical
reports, and some possible implications of this species difference ar
e discussed. Moreover, these data suggest that the stimulation of LH b
y cocaine may not be explained by its indirect dopamine agonist action
s. (C) 1997 Elsevier Science Inc.