Immunocytochemical (ICC) staining for
progesterone (P) receptors (PRs) and
glutamic acid decarboxylase (GAD), the
enzyme responsible for
GABA production, reveal that there are many PRs in the ventral medial hypothalamus (VMH) and many GAD containing neurons in the ventral tegmental area (VTA). To investigate P's action on
lordosis in the VMH and VTA, anti-sense oligos specific to PRs and GAD(65&67) were intracerebrally infused into the VMH and VTA of 24 ovariectomized hamsters and 40 ovariectomized rats.
Estradiol benzoate (2 microg) primed hamsters and rats were infused to the VMH and the VTA with either PR (250 ng/1.0 microl infusion) or GAD (500 ng/1.0 microl infusion) anti-sense oligos, their scramble controls, or saline vehicle at hour 0 and again at hour 24. At hr 44, rodents were subcutaneously injected with
P (500 microg) and were tested for sexual receptivity with a male 4 h later. There were significant reductions in
lordosis of hamsters and rats following PR anti-sense infusions to the VMH compared to scrambled or vehicle control infusions. Effects of PR anti-sense to the VMH were not different from combined VMH and VTA PR anti-sense infusions; however, VMH infusions reduced
lordosis compared to VTA-only anti-sense infusions. GAD anti-sense infusions reduced
lordosis when infused into the VTA, compared to scrambled or saline vehicle infusions.
Lordosis responsiveness following VTA GAD anti-sense infusions was not different from combined VMH and VTA infusions, but VTA infusions of GAD anti-sense reduced
lordosis compared to VMH-only anti-sense infusions. These data suggest that in the VMH, PRs are important for P-facilitated
lordosis, whereas in the VTA, GABAergic neurons may be an important substrate for mediating P's actions on
lordosis of rodents.