While the neurocircuitry and mechanisms controlling the copulatory behavior in female rats has been extensively characterized, the neurocircuitry and cellular and molecular mechanisms of sexual motivation remain elusive. Sexual motivation in the female rat is mediated by activation of the neural progesterone receptors. Dopamine, which mediates natural reward signaling, phosphorylates and activates progesterone receptors. The data presented here demonstrate a novel role for dopamine and progesterone receptor interactions in the medial amygdala on enhanced female sexual motivation. Using methamphetamine, which increases extracellular catecholamines such as dopamine and norepinephrine, we have shown an increase in sexual motivation and behavior in a progesterone dependent manner. This enhanced sexual motivation correlates with increased neuronal activation and neuroplasticity of the medial amygdala. We hypothesized that progesterone receptors in the medial amygdala mediate the enhancement of female sexual motivation. Both excitotoxic lesions targeted to the posterodorsal medial amygdala and antagonist of the progesterone receptor attenuated the methamphetamine-induced increase in proceptive behavior. Methamphetamine may participate in a reciprocal feed-forward mechanism with progesterone receptor, as (1) the administration of ovarian hormones increases tyrosine hydroxylase, the rate-limiting enzyme in the production of catecholamines and (2) methamphetamine increased progesterone receptor-immunoreactivity in the medial amygdala. Both dopamine and norepinephrine have been demonstrated to enhance female sexual behavior and activate and increase the expression of progesterone receptors. To test these candidate neurotransmitters, receptor subtype specific agonists and antagonists were administered to the medial amygdala. The activation of the D1 subtype of the dopamine receptors in the medial amygdala is both necessary for the methamphetamine-induced enhancements of proceptive behavior and sufficient to enhance sexual motivation. Moreover, D1R are necessary for the methamphetamine-increased progesterone receptors. These data indicate that methamphetamine, via dopamine, converges with progesterone in the medial amygdala to activate and alter the circuitry underlying motivation for sexual behavior. While infusions of the alpha 1 adrenoceptor antagonist into the medial amygdala attenuate the methamphetamine enhanced sexual motivation, alpha 1 agonist did not enhance the motivated behaviors. Taken together our data indicate catecholamines in the medial amygdala modulate enhanced sexual motivation through a potential amplification of progesterone signaling.