Koibuchi N, Kato M, Kakegawa T, Suzuki M
Brain Res. 1986 Sep 10;382(1):104-8. doi: 10.1016/0006-8993(86)90116-2.
The aim of this study was to clarify the neural pathway leading to the growth hormone (GH) release when the basolateral amygdala (ABL) was electrically stimulated. Concentric bipolar stimulating electrode was implanted in the unilateral ABL. Blood samples were taken from a cannula implanted into the right atrium via the right external jugular vein. Electrical stimulation of the ABL for 10 min caused a significant increase in plasma GH level from resting value 27.5 +/- 5.7 ng/ml (mean +/- S.E.M.) to 62.2 +/- 7.5 ng/ml at the termination of stimulation. This increase in GH level was markedly augmented to 152.0 +/- 23.0 ng/ml after lesion of the periventricular hypothalamic nucleus (Pe), where somatostatinergic neurons send their axons to the median eminence. Lesion of the stria terminalis (st) fully or partly abolished GH release induced by ABL stimulation. These results suggest that stimulation of the ABL accelerates GH secretion. The st is an essential pathway for this release, whereas the activity of Pe-neurons is rather inhibitory to this release.
本研究的目的是阐明电刺激基底外侧杏仁核（ABL）时导致生长激素（GH）释放的神经通路。将同心双极刺激电极植入单侧ABL。通过右颈外静脉将插管插入右心房采集血样。ABL电刺激10分钟导致血浆GH水平从静息值27.5±5.7 ng/ml（平均值±标准误）显著增加至刺激结束时的62.2±7.5 ng/ml。在室旁下丘脑核（Pe）受损后，GH水平的这种增加显著增强至152.0±23.0 ng/ml，生长抑素能神经元在此处将其轴突发送至正中隆起。终纹床核（st）损伤完全或部分消除了ABL刺激诱导的GH释放。这些结果表明，ABL刺激可加速GH分泌。st是这种释放的必要通路，而Pe神经元的活动对这种释放具有抑制作用。
