Possible role of inhibitory glycinergic neurons in the regulation of lordosis behavior in the rat

Abstract

Strychnine sulfate (3, 9 or 27 μg in 0.5 μl saline) was bilaterally infused into the ventromedial hypothalamic nucleus (VMH) of ovariectomized sexually inexperienced rats primed 40 hr earlier with 4 μg of estradiol benzoate (EB). This dose of EB induced only weak lordosis behavior in 25% of the subjects (Ss). Strychnine at the 3 and 9 μg dosages, but not at 27 μg, induced intense lordosis behavior, but no proceptivity, in most estrogen-primed Ss (69% in 3 μg, 94% in 9 μg). Ovariectomized adrenalectomized EB-primed Ss also displayed significant lordosis behavior (59%) following infusion of 9 μg of strychnine into the VMH. Strychnine (9 μg) failed to stimulate lordosis in ovariectomized Ss that were not estrogen-primed. Administration of 5 μg EB followed 40 hr later by 2 mg of progesterone (P) elicited intense lordosis behavior in most Ss. Bilateral injections into the VMH of glycine (100 μg), β-alanine (100 μg) or taurine (50 μg) to rats that were already displaying estrous behavior (80 LQ) in response to the sequential administration of EB and P failed to depress lordosis when tested between 5 min and 60 min postinjection. Similarly, glycine (20 or 100 μg) injected into the VMH of estrogen-primed, ovariectomized rats within 15 minutes of a 2 mg SC injection of P failed to interfere with the subsequent response to this steroid when tested 2 and 4 hr after P. The results suggest that strychnine injected into the VMH facilitates lordosis behavior in estrogen-primed rats by removing a tonic inhibitory effect exerted by glycinergic neurons on VMH neurons. Failure of glycine or glycine agonists, when injected into the VMH, to inhibit lordosis induced by EB and P may be due to either their rapid removal from the synaptic region or to the inability of the local restricted injections of amino acids to inhibit all the VMH neurons activated by the systemic administration of the steroids.