MATING-RELATED STIMULATION INDUCES PHOSPHORYLATION OF DOPAMINE-REGULATED AND CYCLIC-AMP-REGULATED PHOSPHOPROTEIN-32 IN PROGESTIN RECEPTOR-CONTAINING AREAS IN THE FEMALE RAT-BRAIN

Vaginal-cervical stimulation induces a number of physiological and beh avioral events, including the facilitation of mating behavior. Althoug h the facilitation of one component of mating behavior, lordosis, by v aginal-cervical stimulation does not require the presence of progester one, it appears to be mediated by neural progestin receptors. Abundant evidence suggests that dopamine may play a role in the neural circuit ry activated by vaginal-cervical stimulation, including the mating-ind uced release of dopamine in progestin receptor-containing areas of the brain, changes in the activational state of progestin receptors becau se of dopamine D-1 receptor stimulation, facilitation of lordosis by D -1 receptor stimulation in estradiol-primed rats via progesterone-inde pendent events, and D-1 agonist-induced neuronal responses in progesti n receptor-containing areas and cells. We tested the hypothesis that v aginal-cervical stimulation induces phosphorylation of dopamine- and c yclic AMP-regulated phosphoprotein (DARPP-32; M-r = 32,000), a protein phosphorylated predominantly in response to the stimulation of D-1 re ceptors. At 9 d after ovariectomy, female rats were injected subcutane ously with a behaviorally effective dose of estradiol benzoate. At 48 hr later they received vaginal-cervical or control (perineal) stimulat ion, and they were perfused 1 hr later. Vaginal-cervical stimulation i ncreased the number of cells expressing pDARPP-32 immunoreactivity by 92% in the medial preoptic nucleus, 134% in the caudal ventromedial hy pothalamic nucleus, 123% in the posterodorsal medial amygdala, and 103 % in the bed nucleus of the stria terminalis. These results suggest th at some of the neuronal effects of vaginal-cervical stimulation, and p erhaps other social or environmental stimuli, are mediated by phosphor ylation of DARPP-32, perhaps via stimulation of D-1 receptors, within progestin receptor-containing areas.