Drouva S V, Gallo R V
Endocrinology. 1976 Sep;99(3):651-8. doi: 10.1210/endo-99-3-651.
This study was intended to examine the role of hypothalamic norepinephrine (HNE) and dopamine (HDA) in episodic luteinizing hormone (LH) release in adult ovariectomized rats. Unrestrained, unanesthetized rats with indwelling right atrial cannulae were bled continuously (30, 50, or 100 mul of whole blood/4-6 min for 3-4 hours), and the blood samples were analyzed for LH by radio-immunoassay. In other individual rats, changes in the hypothalamic levels of norepinephrine and dopamine after drug administration were determined by a radioisotopic-enzymatic catechol-O-methyl transferase assay. alpha-Methyl-p-tyrosine significantly decreased HNE and HDA concentrations but failed to alter episodic LH release. Two dopamine-beta-hydroxylase inhibitors (U-14,624 and FLA-63) caused marked reductions in HNE, small but not statistically significant increases in HDA, and an inhibition of episodic LH secretion. Apomorphine, a dopamine receptor stimulator, caused a transient (50-60 min) but marked inhibition of episodic LH release. Saline injection had no effect. Pimozide, a blocker of dopamine receptors, prevented the inhibitory effects seen following apomorphine. Although not studied in detail, pimozide alone did not appear to alter episodic LH secretion. These data suggest that in adult ovariectomized rats norepinephrine may be an excitatory neurotransmitter in the modulation of episodic LH release. The activation of dopamine receptors may be capable of inhibiting this release process. However, the apparent inability of pimozide alone to alter episodic LH discharge suggests that under physiological conditions dopamine may not play a role in the modulation of episodic LH secretion.
本研究旨在探讨下丘脑去甲肾上腺素（HNE）和多巴胺（HDA）在成年去卵巢大鼠促黄体生成素（LH）脉冲式释放中的作用。对留置右心房插管的未束缚、未麻醉大鼠进行连续采血（30、50或100微升全血/4 - 6分钟，持续3 - 4小时），并通过放射免疫分析法对血样中的LH进行分析。在其他单独的大鼠中，通过放射性同位素 - 酶促儿茶酚 - O - 甲基转移酶测定法测定给药后下丘脑去甲肾上腺素和多巴胺水平的变化。α - 甲基 - p - 酪氨酸显著降低了HNE和HDA的浓度，但未能改变LH的脉冲式释放。两种多巴胺 - β - 羟化酶抑制剂（U - 14,624和FLA - 63）导致HNE显著降低，HDA有小幅但无统计学意义的升高，并抑制了LH的脉冲式分泌。多巴胺受体激动剂阿扑吗啡引起了短暂（50 - 60分钟）但显著的LH脉冲式释放抑制。注射生理盐水无作用。多巴胺受体阻滞剂匹莫齐特可防止阿扑吗啡后的抑制作用。虽然未进行详细研究，但单独使用匹莫齐特似乎并未改变LH的脉冲式分泌。这些数据表明，在成年去卵巢大鼠中，去甲肾上腺素可能是调节LH脉冲式释放的兴奋性神经递质。多巴胺受体的激活可能能够抑制这一释放过程。然而，单独使用匹莫齐特明显无法改变LH的脉冲式释放，这表明在生理条件下多巴胺可能在调节LH脉冲式分泌中不起作用。
