Since some estrogenic effects on lordotic responsiveness are mediated through hypothalamic protein synthesis, we conducted experiments to determine if axoplasmic transport in the hypothalamus is necessary for the induction and maintenance of this reflex by estrogen. Colchicine infusion into the hypothalamus, but not into the dorsal thalamus, of ovariectomized rats 24 h prior to administration of subcutaneous estrogen implants delayed the induction of lordotic responsiveness, as measured by the manual (cutaneous-pressure) method, by 2 days, as compared with vehicle-infused rats. In other experiments, colchicine infusion into the hypothalamus, but not into the dorsal thalamus, of conscious, ovariectomized, estrogen-implanted rats displaying maximal lordotic responsiveness resulted in a bimodal decline in lordotic responsiveness. An initial decline occurred 20-40 min after infusion, and was associated with general behavioral agitation and hyperactivity. A subsequent decline began 4 h after infusion and lasted for several days. Vehicle infusion did not decrease lordotic responsiveness. Colchicine infusion did not alter multiunit electrical activity recorded near hypothalamically directed cannulae tips over a period of several hours. Results suggest that axoplasmic transport within and/or from the hypothalamus is necessary for the estrogenic induction and maintenance of the lordosis reflex in rats.