In the ventral tegmental area,
progestogens facilitate sexual receptivity of rodents via actions at
dopamine type 1-like and/or
gamma-aminobutyric acid type A receptors and activation of downstream signal transduction molecules. In the present study, we investigated whether effects of
progesterone's metabolite, 3alpha,5alpha-THP, to enhance
lordosis via actions at these receptors in the ventral tegmental area requires
phospholipase C-dependent
protein kinase C. The objective of this study was to test the hypothesis that: if
progestogens' actions through
dopamine type 1-like and/or
gamma-aminobutyric acid type A receptors in the ventral tegmental area for
lordosis require
protein kinase C, then inhibiting
protein kinase C in the ventral tegmental area should reduce 3alpha,5alpha-THP-facilitated
lordosis and its enhancement by
dopamine type 1-like or
gamma-aminobutyric acid type A receptor agonists. Ovariectomized,
estradiol (E(2); 10 microg s.c. at h 0)-primed rats were tested for their baseline
lordosis responses and then received a series of three infusions to the ventral tegmental area: first,
bisindolylmaleimide (75 nM/side) or vehicle; second,
SKF38393 (100 ng/side),
muscimol (100 ng/side), or vehicle; third, 3alpha,5alpha-THP (100, 200 ng/side) or vehicle. Rats were pre-tested for
lordosis and motor behavior and then tested for
lordosis after each infusion and 10 and 60 min after the last infusion. Rats were tested for motor behavior following their last
lordosis test. As has been previously demonstrated, 3alpha,5alpha-THP infusions to the ventral tegmental area increased
lordosis and effects were further enhanced by infusions of
SKF38393 and
muscimol. Infusions of
bisindolylmaleimide to the ventral tegmental area attenuated 3alpha,5alpha-THP-, SKF38393-, and/or
muscimol-facilitated
lordosis. Effects on
lordosis were not solely due to changes in general motor behavior. Thus, 3alpha,5alpha-THP's actions in the ventral tegmental area through membrane receptors may require activity of
protein kinase C.