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Morphine (M) treatment has been shown to suppress LH release in rats. These studies were undertaken to determine whether a decrease in the response of LHRH neurons to excitatory neurotransmitters may be responsible for the depressed LH secretion in M-treated rats. Ovariectomized rats bearing permanent cannulae in the third ventricle of the brain were primed with estradiol benzoate and progesterone; 3 days later, they received M (20 mg/kg, sc) or saline (controls). The effects of two intraventricular (Ivt) 2-min pulses delivered 80 min apart of vehicle (artificial cerebrospinal fluid), dopamine, norepinephrine, or epinephrine (E) on LH release were assessed. Basal blood LH levels were undisturbed by Ivt administration of vehicle in saline-treated rats. Intraventricular infusions of dopamine (5.3 micrograms/pulse) also failed to evoke LH release in saline-treated rats. However, similar pulse norepinephrine or E infusions (5.3 micrograms/pulse) readily elicited well defined episodes of LH hypersecretion. The magnitude and temporal pattern of LH responses in the control and M-treated rats were quite similar. In another experiment, the progesterone-induced afternoon LH surge was blocked by M treatment of estradiol benzoate-primed rats. In these blocked rats, Ivt administration of E evoked rapid and substantial LH secretion. Thus, our results failed to demonstrate any evidence of diminution in the response of LHRH neurons to excitatory neurotransmitters in M-treated rats. On the other hand, they lend credence to the view that a decreased influx of adrenergic signals in the vicinity of the LHRH neurons may result in the suppression of LH release after M administration.
Kalra et al. (Fri,) studied this question.