We have previously shown that an NPY antagonist decreases
lordosis behavior and that this decrease can be reversed with NPY administration. The present experiments examined whether intracerebroventricular (icv) administration of NPY would facilitate
lordosis behavior and whether it would increase feeding behavior in the female guinea pig. Additionally, we examined whether icv administration of a more specific NPY Y1 and/or Y2 receptor agonist would facilitate
lordosis behavior. Although NPY (1 μg) increased feeding behavior when it was administered to the lateral ventricle of ovariectomized (ovx)
estrogen (i.e.,
estradiol benzoate; EB) and
progesterone- (P) treated guinea pigs, it had no facilitatory effect on
lordosis behavior at any of the doses tested (0.5, 1, 5, or 10μg). In fact, the lower doses had a small, delayed inhibitory effect. NPY also had no effect on
lordosis in females treated with EB alone. In contrast, the NPY Y1 agonist (
Leu(31)Pro(34)) NPY significantly facilitated
lordosis in ovx EB- and P-treated females. It had no effect in ovx females treated with EB alone. The NPY Y2 agonist
NPY (13-36) had a slight, delayed inhibitory effect in ovx EB- and P-treated females. These data are consistent with the hypothesis that NPY can act at a number of receptor subtypes to affect
lordosis behavior, and that NPY can facilitate
lordosis behavior by acting at Y1 receptors. Furthermore, it appears that this facilitatory effect of Y1 receptors is an effect on some
progesterone-mediated component of
lordosis, as the Y1 agonist facilitated EB- and P-induced
lordosis, but not that induced with EB alone.