Blockade of progesterone-activated estrous behavior in rats by intracerebral anisomycin is site specific.

The hypothesis that progesterone (P) activates estrous behavior in estrogen-primed female rats via a protein synthetic mechanism was examined. The protein synthesis inhibitor anisomycin was applied intracerebrally via 28-gauge bilateral implants to neural sites implicated in the mediation of estrous responsiveness. Results showed that anisomycin blockade of P-activated estrous behavior was neural site specific. Animals with anisomycin placed in the ventromedial hypothalamus (VMH) (n = 27) showed low levels of lordosis and solicitation behavior 4 h after the subcutaneous administration of 500 micrograms P, whereas animals with anisomycin implants in the preoptic area (n = 11) or the midbrain area in the region of the interpeduncular nucleus (n = 11) displayed high levels of estrous behavior. No deficits in open-field activity were observed following localized anisomycin treatment, and all animals appeared to be healthy. Results of the present study are consistent with the hypothesis that P acts to promote estrous behavior via a receptor-mediated genomic protein synthetic mechanism, and provide additional evidence that the VMH is the primary site of P action.