Gallo R V
Endocrinology. 1978 Apr;102(4):1026-35. doi: 10.1210/endo-102-4-1026.
This study examined the possible involvement of dopamine (DA) in mediating the inhibition of episodic LH release that occurs during electrical stimulation of the arcuate nucleus (ARH) in ovariectomized rats. Animals were treated before stimulation with pimozide (1.26--2.0 mg/kg) or d-butaclamol (1 mg/kg), blockers of DA receptors, or l-butaclamol. Apomorphine, which inhibits episodic LH release by activating DA receptors, was given near the end of the experiment to determine if these receptors were blocked. ARH stimulation suppressed pulsatile LH release in six rats when DA receptors were not blocked by pimozide (as well as two in which blockade was not tested). A transient increase occurred in one other animal. When DA receptors were blocked by pimozide, stimulation of the ARH inhibited episodic LH release in nine rats, suggesting that DA may have no role in mediating this inhibition. However, because increased LH release occurred in five additional animals, as well as in one with partial receptor blockade, the possibility remains that DA may perhaps have a minor role in this inhibitory response. Although ARH stimulation increased LH release after DA receptor blockade by d-butaclamol, this effect could not be ascribed to the DA antagonist property of this agent, because elevated blood LH levels also occurred during stimulation in rats treated with l-butaclamol, in which DA receptors were not blocked. d- and l-butaclamol may possess a non-stereospecific action on a non-dopaminergic event, thus reversing the response to ARH stimulation. Finally, whether DA receptors were blocked or not by pimozide, d-, or l-butaclamol, activation of the ventromedial hypothalamic and periventricular nucleus regions suppressed episodic LH release, but did not increase LH secretion. This suggests that the region through which stimulation can inhibit, but not increase, LH release may extend in the hypothalamus to these two areas.
本研究探讨了多巴胺（DA）在介导去卵巢大鼠弓状核（ARH）电刺激期间发生的促黄体生成素（LH）脉冲式释放抑制过程中可能的作用。在刺激前，给动物注射匹莫齐特（1.26 - 2.0 mg/kg）或d-布他拉莫（1 mg/kg），这两种药物是DA受体阻滞剂，或注射l-布他拉莫。在实验接近尾声时给予阿扑吗啡，它通过激活DA受体来抑制LH的脉冲式释放，以确定这些受体是否被阻断。当DA受体未被匹莫齐特阻断时（以及另外两只未测试阻断情况的大鼠），ARH刺激抑制了6只大鼠的LH脉冲式释放。在另一只动物中出现了短暂的增加。当DA受体被匹莫齐特阻断时，ARH刺激抑制了9只大鼠的LH脉冲式释放，这表明DA可能在介导这种抑制作用中不起作用。然而，由于另外5只动物以及1只部分受体被阻断的动物出现了LH释放增加的情况，所以DA在这种抑制反应中可能仍有轻微作用。尽管在d-布他拉莫阻断DA受体后，ARH刺激增加了LH释放，但这种作用不能归因于该药物的DA拮抗特性，因为在用l-布他拉莫处理的大鼠（其DA受体未被阻断）刺激期间，血液中LH水平也升高了。d-和l-布他拉莫可能对非多巴胺能事件具有非立体特异性作用，从而逆转了对ARH刺激的反应。最后，无论DA受体是否被匹莫齐特、d-或l-布他拉莫阻断，下丘脑腹内侧核和室周核区域的激活均抑制了LH的脉冲式释放，但未增加LH分泌。这表明刺激可抑制但不能增加LH释放的区域可能在下丘脑延伸至这两个区域。
