Abstract

Ovariectomized rats were hormonally primed with 0.5 μg estradiol benzoate and 500 μg progesterone to produce two groups of rats differing in their lordosis behavior. Females with a lordosis to mount (L/M) ratio <0.5 were used to test the hypothesis that 5-HT 2A/2C receptor agonists could facilitate lordosis behavior. Females with L/M ratios ≥0.5 were used to evaluate the potential suppressive effect of 5-HT 2A/2C receptor compounds. Lordosis behavior was examined following bilateral infusion of drugs into the ventromedial nucleus of the hypothalamus (VMN). Drugs examined were the 5-HT 2A/2C receptor agonist, (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI), the 5-HT 2A/2C receptor antagonist, 3-[2-[4-(4-fluorobenzoyl)-1-piperdinyl]ethyl]-2,4(1 H,3 H)-quinazolinedione tartrate (ketanserin tartrate), and the non-selective 5-HT receptor agents, 2-(1-piperazinyl)quinoline dimaleate (quipazine) and N-(3-trifluoromethylphenyl)piperazine HCl (TFMPP). Drugs with agonist action at 5-HT 2A/2C receptors increased lordosis behavior in rats with low sexual receptivity. The 5-HT 2A/2C receptor antagonist, ketanserin, inhibited lordosis behavior in sexually receptive rats. DOI attenuated the lordosis-inhibiting effect of ketanserin, but ketanserin was less effective in preventing DOI from increasing lordosis behavior. These results strengthen prior inferences that activation of 5-HT 2A/2C receptors can facilitate lordosis behavior and that the VMN is one site at which such facilitation can occur.

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