Abstract
Adult, hormone-primed, ovariectomized rats (CDF-344) with bilateral implants within the ventromedial nucleus of the hypothalamus (VMN), were injected with 0.5 μg estradiol benzoate followed 48 h later with 500 μg progesterone. This priming produced rats with 2 different levels of sexual receptivity. Rats with a lordosis to mount ratio (L/M)≥0.5 were used to examine the potential lordosis-inhibiting effects of the 5-HT 2A receptor antagonist, R(+)-a-(2,3-dimethoxyphenyl)-1-[2(4-fluoro-phenylethyl)]-4-piperidine-methanol (MDL 100,907), and the 5-HT 2C receptor antagonist, 5-methyl-1-(3-pyridylcarbamoyl)-1,2,3,5-tetrahydropyrrolo[2,3- f]indole (SB 206553). Rats with low sexual receptivity (L/M<0.5) were bilaterally infused with the 5-HT 2A/2C receptor agonist, (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI), or DOI plus either MDL 100,907 or SB 206553 to determine if either drug would attenuate the lordosis-facilitating effects of DOI. The 5-HT 2C receptor antagonist, but not the 5-HT 2A receptor antagonist, effectively inhibited lordosis behavior. Similarly, SB 206553 was more effective than MDL 100,907 in reducing the DOI-induced increase in lordosis responding. However, both drugs limited the duration of lordosis responding initiated by DOI. These results are consistent with prior suggestions that 5-HT 2A/2C receptors within the VMN are involved in the modulation of lordosis behavior and lead to the suggestion that 5-HT 2C, rather than 5-HT 2A, receptors are primarily responsible for the effects of 5-HT 2 receptor-active drugs on lordosis behavior.
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