Wolf A, Caldarola-Pastuszka M, DeLashaw M, Uphouse L
Department of Biology, Texas Woman's University, P.O. Box 425799, Denton, TX 76204-5799, USA.
Brain Res. 1999 Apr 17;825(1-2):146-51. doi: 10.1016/s0006-8993(99)01159-2.
Adult, hormone-primed, ovariectomized rats (CDF-344) with bilateral implants within the ventromedial nucleus of the hypothalamus (VMN), were injected with 0.5 microgram estradiol benzoate followed 48 h later with 500 microgram 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-HT2A receptor antagonist, R(+)-a-(2, 3-dimethoxyphenyl)-1-[2(4-fluoro-phenylethyl)]-4-piperidine-methanol (MDL 100,907), and the 5-HT2C 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-HT2A/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-HT2C receptor antagonist, but not the 5-HT2A 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-HT2A/2C receptors within the VMN are involved in the modulation of lordosis behavior and lead to the suggestion that 5-HT2C, rather than 5-HT2A, receptors are primarily responsible for the effects of 5-HT2 receptor-active drugs on lordosis behavior.
成年、经激素预处理、双侧下丘脑腹内侧核（VMN）植入的去卵巢大鼠（CDF-344），先注射0.5微克苯甲酸雌二醇，48小时后再注射500微克孕酮。这种预处理产生了具有两种不同性接受水平的大鼠。将脊柱前凸与骑跨比值（L/M）≥0.5的大鼠用于研究5-HT2A受体拮抗剂R（+）-α-（2,3-二甲氧基苯基）-1-[2（4-氟苯基乙基）]-4-哌啶甲醇（MDL 100,907）和5-HT2C受体拮抗剂5-甲基-1-（3-吡啶甲酰基）-1,2,3,5-四氢吡咯并[2,3-f]吲哚（SB 206553）对脊柱前凸抑制作用的可能性。将性接受能力低（L/M<0.5）的大鼠双侧注入5-HT2A/2C受体激动剂（±）-1-（2,5-二甲氧基-4-碘苯基）-2-氨基丙烷盐酸盐（DOI），或DOI加MDL 100,907或SB 206553，以确定这两种药物是否会减弱DOI促进脊柱前凸的作用。5-HT2C受体拮抗剂而非5-HT2A受体拮抗剂能有效抑制脊柱前凸行为。同样，SB 206553在减少DOI诱导的脊柱前凸反应增加方面比MDL 100,907更有效。然而，两种药物都限制了DOI引发的脊柱前凸反应的持续时间。这些结果与之前的观点一致，即VMN内的5-HT2A/2C受体参与了脊柱前凸行为的调节，并表明5-HT2C受体而非5-HT2A受体是5-HT2受体活性药物对脊柱前凸行为产生影响的主要原因。
