Genomic regulation of sexual behavior

Estrogen receptors are distributed in discrete areas of the hypothalamus, preoptic area and amygdala of the rat brain, and in some of these areas estrogens induce progestin receptor sites. Estradiol (E), followed by progesterone (P), induce feminine sexual behavior in female, but not in male, rats. This induction takes time (on the order of hours, not minutes, so that the hormone may be cleared from the body) and is dependent on RNA and protein synthesis. Within the hypothalamic ventromedial nuclei (VMN), E and P induce changes in RNA and protein synthesis and also induce morphological changes indicative of cellular growth, genomic activation, and either new synapse formation or morphological rearrangement of existing synapses. Neurochemically, a number of neurotransmitter systems are implicated in the control of feminine sexual behavior, including acetylcholine, serotonin, GABA, and the neuropeptides, oxytocin and CCK. One of the means by which E and P may exert their influence on sexual behavior, aside from the morphological alterations, is by regulating levels of receptors for certain of these neurotransmitters. The critical differences which underlie the inability of male rats to display high levels of feminine sexual behavior after E plus P priming may depend on sex differences in the ability of E to induce particular neurochemical products as well as P receptors and upon differences in neural circuitry in the VMN.