Abstract
The role of hypothalamic α- and β-adrenergic receptors in the control of lordotic behavior was studied by infusing α and β receptor stimulants and blockers into either the medial preoptic area (MPOA), arcuate-ventromedial area (ARC-VM) or lateral hypothalamic area (LHA) in ovariectomized (OVX), estrone primed rats. In the first experiment, OVX rats were primed with low doses of estrone (100–250 μg) in order to maintain low preinfusion receptivity (mean preinfusion L/M=0.169). The infusion of α receptor blockers, phentolamine and phenoxybenzamine; β receptor stimulants, isoroterenol; dopamine, norepinephrine; or epinephrine into either the MPOA or ARC-VM produced increases in lordotic behavior in OVX rats primed with low doses of estrone. Using the same protocol, MPOA or ARC-VM infusions of methoxamine, an α receptor stimulant, or propranolol, a β receptor blocker, produced decreases in the lordotic behavior. Infusions of any of these agents into the LHA had no effect upon sexual receptivity. In order to corroborate the pharmacological effects observed with low preinfusion receptivity, a second experiment was conducted in which high preinfusion receptivity (mean preinfusion L/M=0.898) was maintained by priming the OVX rats with higher doses of estrone. Using this second protocol, methoxamine and propranolol infusions into the MPOA or ARC-VM depressed lordotic response. However, further enhancement by α receptor blockade or β receptor stimulation from the initially near maximal lordotic response could not be obtained. A third experiment was designed to evaluate the effects of adrenergic receptor activity on the stimulatory effects of luteinizing hormone-releasing hormone (LRH) upon lordotic behavior. This protocol allowed comparisons among lordotic responses to MPOA and ARC-VM infusions of vehicle, LRH, LRH with methoxamine and LRH with propranolol. Infusions of LRH into the MPOA or ARC-VM significantly enhanced lordotic behavior, whereas the addition of either methoxamine or propranolol to LRH infusates abolished this response. Alternative mechanisms were proposed for the possible roles of α- and β-adrenergic receptors in the hypothalamic control of estrogen-induced and LRH-facilitated lordotic behavior.
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