Ovarian estradiol and progesterone activate neurocircuits which regulate rat sexual receptivity (lordosis). Estradiol initially activates an inhibitory lordosis circuit, and subsequent progesterone infused into the arcuate nucleus (ARH) deactivates this circuit and facilitates lordosis within thirty minutes, indicating progesterone is acting through extranuclear signaling mechanisms. I showed that progesterone signals through Src family kinase (Src) in the ARH as does the dopamine D1 receptor (D1) to facilitate lordosis. Antagonism of progesterone receptor (PR), D1, or Src kinase blocks the facilitation of lordosis by agonists for each, indicating that their actions are interdependent. Additionally, I demonstrated that similar to progesterone, facilitation of lordosis by Src and D1 are independent of OFQ-ORL-1 signaling. These studies demonstrate that the rapid facilitation of lordosis by progesterone and D1 is mediated through Src and that PR and D1 signaling likely converge at Src to deactivate medial preoptic ì-opioid receptor (MOP) and facilitate lordosis.
|Commitee:||Tsai, Houng-Wei, Young, Kelly|
|School:||California State University, Long Beach|
|School Location:||United States -- California|
|Source:||MAI 54/03M(E), Masters Abstracts International|
|Keywords:||Dopamine d1 receptor, Lordosis, Progesterone receptor, Rat sexual behavior, Src kinase|
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