The aim of this study was to characterize the acute effects of cocaine admi
nistration on pituitary gonadotrophin secretion in adult female rats. Ovari
ectomized, oestradiol-treated rats were infused i.v. with 0.1 ml normal sal
ine or 2 mg cocaine hydrochloride kg(-1). Blood samples were collected imme
diately before cocaine infusion and at 3, 10, 30 and 60 min after cocaine i
nfusion. Circulating LH concentrations were increased by 10 min after cocai
ne administration (P < 0.05 versus saline-treated controls) and decreased t
hereafter. Serum FSH concentrations were not significantly different from t
hose of saline-infused controls at any time. In a second experiment, oestra
diol-treated, ovariectomized rats were infused i.v. with: saline only, 2 mg
cocaine hydrochloride kg(-1) in saline, 200 ng synthetic GnRH in 100 pl PB
S or 200 ng synthetic GnRH plus 2 mg cocaine hydrochloride kg(-1) in PBS. B
lood samples were collected immediately before drug infusions and 20 min la
ter. Cocaine had no effect on either GnRH-stimulated LH or FSH secretion. I
n a third experiment, pituitary cells were obtained from oestradiol-treated
, ovariectomized rats. The cell cultures were exposed to 25 ng cocaine hydr
ochloride ml(-1), 10(-10)-10(-7) mol GnRH l(-1) with and without 25 ng coca
ine hydrochloride ml(-1), or vehicle only. Medium was collected before and
after exposure to GnRH to determine concentrations of secreted LH and FSH.
Similar to the results of the second study, cocaine had no effect on GnRH-s
timulated LH or FSH secretion from pituitary cells in vitro. On the basis o
f these results it is suggested that acutely administered cocaine stimulate
s release of hypothalamic GnRH, which, in turn, stimulates pituitary gonado
trophin secretion. Acute administration of cocaine does not appear to affec
t pituitary gonadotrophin secretion directly.