Estrogen-dependent cholinergic regulation of sexual receptivity in intact cycling female rats
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Description
Manipulations of central cholinergic activity alter the female rodent sexual behavior, lordosis. Agents that enhance cholinergic function, such as the acetylcholinesterase inhibitor physostigmine, activate lordosis in intact cycling female rats during proestrus when endogenous estrogen levels are high and not during diestrus when endogenous estrogen levels are low. In the present experiments, intraventricular administration of physostigmine activated lordosis in intact female rats at Mid-diestrus or Diestrus II only when exogenous estrogen was administered the day before. The degree of activation of lordosis by physostigmine at Mid-diestrus or Diestrus II was related to the priming dose of estrogen. These results indicate that cholinergic mechanisms that regulate sexual receptivity depend upon sufficient estrogen priming. Serum progesterone titers measured in these females were higher at Mid-diestrus than Diestrus II. In the absence of cholinergic manipulations, females were more likely to exhibit lordosis at Mid-diestrus than at Diestrus II, possibly as a consequence of elevated progesterone levels at Mid-Diestrus. Despite dissimilar levels of circulating progesterone, physostigmine activated lordosis equally at Mid-diestrus and Diestrus II following estradiol priming. These results suggest that the level of progesterone did not influence the ability of the cholinergic system to activate lordosis. Muscarinic binding as determined by the muscarinic antagonist ($\sp3$H) QNB varied across the estrous cycle. When compared to muscarinic binding during diestrus, muscarinic binding during Proestrus-Estrus was increased in two brain regions traditionally associated with the activation of lordosis, the medio-basal hypothalamus and central gray, and decreased in a brain region traditionally associated with the inhibition of lordosis, the preoptic area. However, administration of estradiol on the day before decreased muscarinic binding in the septum, preoptic area, and central gray. Estradiol administration did not change muscarinic binding in the medio-basal hypothalamus. Because these changes in binding were complex and unpredicted, a relationship between the estrogen regulation of lordosis and muscarinic binding in these areas was not evident. These results do not support the hypothesis that changes in muscarinic binding in these brain regions are necessary for the cholinergic activation of lordosis