Intrahypothalamic implants of noradrenergic antagonists disrupt lordosis behavior in female rats

Abstract

There is considerable experimental evidence that hormonal activation of lordosis in female rats involves norepinephrine (NE) neurotransmission. However, no clear picture has emerged regarding either: 1) the neural sites at which NE influences lordosis, or 2) the NE receptor subtype(s) mediating NE effects on lordosis. To address these two issues, the behavioral effects of antagonists with relative specificity for α 1, α 2, or β adrenergic receptors were axamined. Drugs were administered via bilateral crystalline implants directly into the ventromedial nucleus of the hypothalamus (VMN) or medial preoptic area (MPOA) of ovariectomized female rats primed for 48 hr with 3 μg of estradiol benzoate (EB) and given 200 μg of progesterone (P) 3.5–4 hr before testing. When applied to the VMN 1 hr before the P injection, the α 1 receptor antagonist prazosin reduced lordosis behavior in 86% of animals but in only 10% of rats when applied to the MPOA. However, prazosin did not inhibit lordosis when implanted into the VMN just prior to EB administration. Yohimbine, an α 2 receptor antagonist with low affinity for α 1 receptors, also suppressed lordosis in 41% of animals with VMN implants and in 37% of rats with MPOA implants. By contrast, the α 2 antagonist idazoxan, which has little activity at α 1 receptors, did not significantly affect estrous responding when implanted into either the VMN or MPOA. VMN implants of the β receptor antagonists propranolol and pindolol reduced lordosis behavior in 50% and 86% of rats, respectively. However, metoprolol, a β receptor antagonist which has neither the membrane stabilizing properties of propranolol nor the β agonist properties of pindolol, reduced lordosis in only 11% of rats when implanted into the VMN. Pindolol and metoprolol implants into the MPOA suppressed lordosis in 42% and 55% of rats, respectively. Taken together, the results suggest that α 1 receptors in the VMN play a central role in hormonal facilitation of lordosis behavior in female rats.