Ibotenic acid-induced lesions of the medial preoptic area/anterior hypothalamus enhance the display of progesterone-facilitated lordosis in male rats.
Ibotenic acid-induced lesions of the medial preoptic area/anterior hypothalamus enhance the display of progesterone-facilitated lordosis in male rats.
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鹅膏蕈酸诱导的内侧视前区/下丘脑前部损伤增强了雄性大鼠中孕酮促进的脊柱前凸的表现。
DOI：
10.1016/0006-8993(93)90568-8
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发表时间：
1993
期刊：
影响因子：
2.9
通讯作者：
Olster,DH
中科院分区：
文献类型：
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作者：
Olster,DH
据报道，内侧视前区/下丘脑前部（MPOA/AH）的电损伤可增强去势雄性大鼠类固醇诱导的脊柱前凸的显示。本研究采用细胞体特异性神经毒素鹅膏蕈氨酸，以确定是否神经元起源于该地区（而不是轴突的通道）紧张性抑制类固醇诱导的脊柱前凸成年雄性大鼠。去势的成年Long-Evans雄性动物接受双侧电损伤或针对MPOA/AH注射鹅膏蕈氨酸或溶媒。给予苯甲酸雌二醇（EB）和孕酮后，电损伤组大鼠的脊柱前凸发生率（LQs）和脊柱前凸等级（LRs）显著升高（LQ= 62.2 ± 15.1;LR= 1.22 ± 0.34）和鹅膏蕈氨酸诱导的病变（LQ = 58.1 ± 12.2;LR= 0.99 ± 0.24）显著高于对照组（LQ= 12.8 ± 7.3;LR= 0.22 ± 0.13）。为了确定MPOA/AH损伤的雄性动物的这种接受行为的增强是否对雌二醇诱导的脊柱前凸有影响，与炔雌醇促进的脊柱前凸相比，第二个实验中的去势大鼠组接受针对MPOA/AH的鹅膏蕈氨酸或载体的双侧注射，并在单独施用EB后和注射孕酮后再次测试脊柱前凸。单独用EB治疗后，鹅膏蕈氨酸诱导的MPOA/AH病变的大鼠倾向于比对照组动物接受性略差。然而，在注射孕酮后，MPOA/AH损伤组的LQs和LRs高于对照组动物，正如第一次实验中所观察到的那样。这些数据是一致的假设，细胞体，而不是轴突的通道，起源于MPOA/AH施加紧张性抑制控制的显示，在成年雄性大鼠的甾酮促进脊柱前凸。
Electrical lesions of the medial preoptic area/anterior hypothalamus (MPOA/AH) have been reported to enhance the display of steroid-induced lordosis in castrated male rats. This study employed the cell body-specific neurotoxin, ibotenic acid, to ascertain whether neurons originating in this region (as opposed to axons of passage) tonically inhibit steroid-induced lordosis in adult male rats. Castrated, adult Long-Evans males received bilateral electrical lesions or injections of ibotenic acid or vehicle aimed at the MPOA/AH. Following administration of estradiol benzoate (EB) and progesterone, lordosis quotients (LQs) and lordosis ratings (LRs) were significantly higher in groups of rats with electrical lesions (LQ= 62.2 ± 15.1;LR= 1.22 ± 0.34) and ibotenic acid-induced lesions (LQ = 58.1 ± 12.2;LR= 0.99 ± 0.24) than in the control group (LQ= 12.8 ± 7.3;LR= 0.22 ± 0.13). To determine whether this enhancement of receptive behavior in MPOA/AH-lesioned males was an effect on estradiol-induced, as compared to progesterone-facilitated lordosis, groups of castrated rats in a second experiment received bilateral injections of ibotenic acid or vehicle aimed at the MPOA/AH and were tested for lordosis after administration of EB alone and again after injection of progesterone. Following treatment with EB alone, rats with ibotenic acid-induced MPOA/AH lesions tended to be slightly less receptive than control animals. However, following injections of progesterone, LQs and LRs were higher in the MPOA/AH-lesioned group than in the control animals, as had been observed in the first experiment. These data are consistent with the hypothesis that cell bodies, rather than axons of passage, originating in the MPOA/AH exert tonic inhibitory control over the display of progesterone-facilitated lordosis in adult male rats.