Dispensability of spinal monoaminergic systems in mediating the lordosis reflex of the female rat

Abstract

The possibility that bulbospinal monoaminergic systems are essential for expression of the estrogen-induced lordosis reflex in female rats was tested by studying the effects of reserpine and monoamine antagonists on the lordosis responses to mating and manual stimulation. Lordosis performance of five groups of ovariectomized rats, either treated (groups II through V) or not treated (group I) with estrogen, were measured before and after pharmacological treatments. Immediately after post-treatment measurements, females (except group V) were decapitated and the lumbosacral cord quickly removed, frozen, and later assayed for norepinephrine, dopamine and serotonin. Group I females (n=7) did not show any lordosis before or after a control saline injection, and their spinal monoamine contents were not different from those of group II (n=8), who showed near maximal levels of lordosis both before and after a saline injection. Reserpine at low (2 mg/kg; group III, n=6) or high (10 mg/kg, group IV, n=10) doses depleted spinal monoamines severely but had no significant effect on lordosis, except for a slight decline of lordosis intensity after the high dose treatment. A combination treatment of reserpine (10 mg/kg) and a serotonin receptor blocker, methiothepin (10 mg/kg), did not affect lordosis performance (group V, n=6). Further injection of an α-adrenergic antagonist, phenoxybenzamine (20 mg/kg), in addition to this combination, had no effect on the lordosis reflex in response to manual stimulation, although the response to mating stimulation was reduced. The reduction was probably a result of a drug-induced abnormal posture, which made most of the reflexogenic skin area of the female inaccessible to mating stimuli. These results showed that estrogen treatment sufficient to induce a near maximal level of lordosis performance did not alter spinal monoamine contents, and that the monoamines in the spinal cord are not necessary for mediating the estrogen-stimulated lordosis reflex.