Within the medial basal hypothalamus (MBH), serotonin (5-HT) can both inhibit and facilitate female rat sexual receptivity. We have suggested that this dual regulation is important in allowing the female to coordinate her reproductive behavior with the external environment. Even if the female were optimally sexually receptive, under life-threatening conditions, mating would be an inappropriate behavioral choice for the female to make. However, should the threat be minimal, increased vulnerability to stress might unnecessarily reduce reproductive success. Our emphasis is on the interplay among 5-HT1A, 5-HT2C and 5-HT1B receptors. Our working model is that mild stress (5 min restraint) increases the release of 5-HT in the MBH. The increased extracellular 5-HT activates 5-HT1A, 5-HT1B and, 5-HT2C receptors. Activation of 5-HT1A receptors leads to inhibition of lordosis behavior while activation of 5-HT2C receptors limits the duration of this inhibition and allows recovery to occur. Progesterone enhances the function of terminal 5-HT1B autoreceptors so that a smaller increase in extracellular 5-HT occurs in response to stress. As a result, the occupation of 5-HT1A receptors is insufficient for inhibition of lordosis behavior. The proposed experiments are designed to test each element of this proposed model. Although the proposed studies are focused on the role of 5-HT receptor subtypes in the control of lordosis behavior, they can provide valuable information about hormonal modulation of 5-HT function and how these hormones influence the female's response to an acute environmental challenge.
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