Estrogenic maintenance of lordotic responsiveness: requirement for hypothalamic action potentials.

Studies were conducted to determine the requirement for hypothalamic, sodium current-based action potentials in the performance of a stereotypic, estrogen-dependent reflex, the lordosis response. Intrahypothalamic infusion of local anesthetics (50% procaine or 0.5% bupivacaine) into conscious rats had no effect on lordotic responsiveness, and, in a separate group of urethane-anesthetized rats, depressed multiunit electrical activity temporarily. Intrahypothalamic infusion of tetrodotoxin into conscious rats, however, resulted in a dose-dependent, reversible decline in lordotic responsiveness. The first significant drop in lordotic responsiveness occurred 40 min after infusion; the minimum was reached 2-4 h after infusion. Recovery of lordotic responsiveness to preinfusion levels was complete by 12-24 h after infusion. Electrophysiological studies in a separate group of urethane-anesthetized rats revealed that intrahypothalamic tetrodotoxin infusion in most cases suppressed multiunit activity completely usually within 6 min, and this suppression lasted for at least several hours. These data indicate that large, prolonged decreases in electrical activity in the hypothalamus, where estrogenic action is necessary and sufficient to induce lordosis, result in a gradual, reversible decline in lordotic responsiveness. These data are consistent with a 'tonic' rather than a 'mount-by-mount' role of hypothalamic neurons in lordosis. Furthermore, since lordotic responsiveness declined only when hypothalamic electrical activity had been disrupted severely for at least 40 min, it is postulated that the neuroactive products released by lordosis-relevant, hypothalamic neurons may have a duration of action of at least several minutes.