Interactions of delta 9-tetrahydrocannabinol (THC) with hypothalamic neurotransmitters controlling luteinizing hormone and prolactin release.

Interactions of delta 9-tetrahydrocannabinol (THC) with hypothalamic neurotransmitters controlling luteinizing hormone and prolactin release.
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δ9-四氢大麻酚 (THC) 与控制黄体生成素和催乳素释放的下丘脑神经递质的相互作用。

DOI:
10.1159/000123576
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发表时间:
1983
期刊:
影响因子:
4.1
通讯作者:
Silverman,AY
Silverman,AY
中科院分区:
医学2区
文献类型:
--
作者:
Steger,RW;DePaolo,L;Asch,RH;Silverman,AY

文献摘要

被引文献

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在去卵巢雌激素预处理大鼠模型上,研究了Δ9-四氢大麻酚(THC)对孕酮(P)诱导的LH和PRL峰前和峰时下丘脑去甲肾上腺素(NE)和多巴胺(DA)转换以及下丘脑5-羟色胺(5-HT)、5-羟吲哚乙酸(5-HIAA)和LHRH含量的影响。THC对基础LH水平无影响,但可抑制基础PRL水平,阻断LH和PRL的激增。用α-甲基酪氨酸(250 mg/kg)抑制酪氨酸羟化酶后,通过测定NE消耗量来估计下丘脑前部(AH)和内侧基底部(MBH)中NE的周转率,THC均显著抑制。THC对AH或MBH DA或5-HT含量及MBH-DA周转率无显著影响。下丘脑LHRH水平显着升高4小时后,THC管理相比,溶剂注射的控制,但垂体对外源性LHRH的反应不受影响。这些数据表明,THC通过减少NE代谢和下丘脑LHRH的释放来抑制类固醇诱导的LH正反馈释放。虽然THC抑制PRL释放的机制尚不清楚,从这些实验中,它似乎并没有改变DA营业额是一个促成因素。
The effects of Δ9-tetrahydrocannabinol (THC) on hypothalamic norepinephrine (NE) and dopamine (DA) turnover and hypothalamic serotonin (5-HT), 5-hydroxyindole acetic acid (5-HIAA) and LHRH content preceding and during a progesterone- (P) induced LH and prolactin (PRL) surge were investigated in ovariectomized estrogen-primed rats. THC had no effect on basal LH levels, but it inhibited basal PRL levels and blocked the surges of both LH and PRL. The turnover of NE, as estimated by measuring NE depletion after inhibition of tyrosine hydroxylase with α-methyl tyro-sine (250 mg/kg), in both the anterior (AH) and medial basal hypothalamus (MBH) was significantly inhibited by THC. THC did not significantly affect AH or MBH DA or 5-HT content nor MBH-DA-turnover. Hypothalamic LHRH levels were significantly elevated 4 h after THC administration as compared to the vehicle-injected controls, but pituitary response to exogenous LHRH was not affected. These data suggest that THC inhibits the steroid-induced positive feedback release of LH by reducing NE metabolism and the release of hypothalamic LHRH. Although the mechanism for the inhibition of PRL release by THC is not clear from these experiments, it does not appear that alterations in DA turnover are a contributing factor.