纳洛酮阻断9-四氢大麻酚对大鼠血清促黄体生成素和催乳素的影响。

Substance and alcohol actions/misuse Pub Date : 1983-01-01
M S Kumar, J W Simpkins
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引用次数: 0

摘要

本研究旨在确定9-四氢大麻酚对大鼠促性腺激素分泌的影响是否通过内源性阿片神经元介导。去卵巢大鼠第0天给予雌二醇-苯甲酸酯(EB),第2天11:00给予孕酮(P)。在13:00 h(第2天),这些雌二醇启动和孕激素处理(EBP)的动物接受了δ 9-四氢大麻酚(3mg/kg,油中,im);纳洛酮(Nal) 3mg /kg生理盐水,s.c)或δ 9-THC + Nal。于16:00 h处死所有动物,检测躯干血清促黄体生成素(LH)和催乳素(Prl)水平,同时检测内侧基底下丘脑(MBH)促黄体生成素释放激素(LHRH)水平。纳洛酮可使ebp诱导的LH高分泌增强2倍,而δ 9-THC可完全阻断ebp诱导的LH分泌。δ 9-THC轻微减弱Nal对黄体生成素分泌的刺激作用,使血清Prl浓度升高2倍,而Nal对EBP大鼠血清Prl水平没有影响。然而,Nal确实阻断了δ 9-THC对Prl分泌的刺激作用。δ 9-THC显著增加了LHRH的MBH含量,而Nal阻止了这一作用。这些结果表明,δ 9-THC对血清LH的抑制作用和大麻素对Prl的刺激作用是通过阿片机制介导的。
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Naloxone blocks the effects of delta 9-tetrahydrocannabinol on serum luteinizing hormone and prolactin in rats.

The present study was undertaken to determine if the effects of delta 9-tetrahydrocannabinol on gonadotropin secretion are mediated through endogenous opioid neurons in the rat. Ovariectomized rats were treated with estradiol-benzoate (EB, day O) and with progesterone (P) at 11:00 h on day 2. At 13:00 h (day 2), these estradiol primed and progesterone-treated (EBP) animals received either delta 9-THC (3mg/kg in oil, i.m.); naloxone (Nal) 3 mg/kg in saline, s.c.) or delta 9-THC + Nal. All animals were decapitated at 16:00 h and trunk sera were assayed for luteinizing hormone (LH) and prolactin (Prl), while medial basal hypothalami (MBH) were assayed for luteinizing hormone-releasing hormone (LHRH). Naloxone enhanced the EBP-induced hypersecretion of LH by 2-fold while delta 9-THC completely blocked the EBP-induced secretion of LH. delta 9-THC slightly diminished the stimulatory effect of Nal on LH secretion and caused a 2-fold increase in serum Prl concentrations, while Nal did not influence the serum PRL levels in these EBP rats. However, Nal did block the stimulatory effects of delta 9-THC on Prl secretion. delta 9-THC caused a significant increase in MBH content of LHRH, an effect which was prevented by Nal. These results suggest that the inhibitory effects of delta 9-THC on serum LH and the stimulatory effect of the cannabinoid on Prl are mediated by an opioid mechanism.

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