Abstract

The administration of the steroid hormone, 17 beta-estradiol (E2) to ovariectomized rats increases the levels of muscarinic cholinergic receptors by 20-40% in the hypothalamic area. Using microdissection techniques, this increase has been shown to occur in hypothalamic subregions that possess high levels of intracellular receptors for E2. Among these regions is the ventromedial nucleus (VMN), which may be the principal target site in the rat brain for the activation of feminine sexual behavior by E2. In this study, we have further characterized the increase in muscarinic binding within the VMN after E2 and show that it satisfies many of the criteria for an important regulatory mechanism by which E2 could activate sexual behavior: (1) Using quantitative receptor autoradiography, it was determined that the increase in [3H]-QNB binding in the VMN after E2 results from an increase in the number of receptors rather than a change in the affinity of the binding. (2) The increase in VMN muscarinic receptors as determined by the binding of [3H]-QNB to microdissected homogenates occurred by 18-24 h after exposure to E2, the earliest time at which sexual behavior is facilitated. (3) Increased muscarinic receptors did not occur in the VMN of male rats, which show little activation of feminine sexual behavior after E2 exposure. (4) Muscarinic receptors in the VMN of female rats are induced at 24 h by a 6 h exposure to E2, the minimum length of time that is sufficient for E2 to activate sexual behavior. A 4 h exposure to E2 is insufficient to activate both sexual behavior and induce muscarinic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

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