Millan M J, Członkowski A, Millan M H, Herz A
Brain Res. 1987 Mar 24;407(1):199-203. doi: 10.1016/0006-8993(87)91239-x.
Electrical stimulation of the ventral midbrain periaqueductal grey (PAG) elicited an antinociception (analgesia) in freely moving rats. Stimulated animals displayed a pronounced decrease in levels of immunoreactive (ir)-beta-endorphin (beta-EP) in the midbrain PAG. This depletion was selective in that: animals placed in the chamber and not stimulated revealed neither an analgesia nor an alteration in levels of ir-beta-EP. No change in levels of ir-beta-EP was detectable in other brain regions. Both stimulated rats and rats placed in the chamber and not stimulated revealed a rise in circulating ir-beta-EP: the magnitude of this rise did not, however, differ between these groups. Levels of ir-Met-enkephalin, ir-Leu-enkephalin and ir-dynorphin A were modified neither in the PAG nor in other CNS tissues. The data demonstrate that electrical stimulation of the midbrain PAG selectively influences (presumably activates) pools of beta-EP therein. Together with our finding that destruction of PAG-localized beta-EP neurones to block stimulation-analgesia, the data suggest that an activation of intrinsic pools of beta-EP underlies stimulation-produced analgesia elicited from the PAG in the rat.
对自由活动大鼠的腹侧中脑导水管周围灰质（PAG）进行电刺激可引发抗伤害感受（镇痛）。受刺激的动物中脑PAG内免疫反应性（ir）-β-内啡肽（β-EP）水平显著降低。这种减少具有选择性，即：置于实验箱中但未受刺激的动物既未出现镇痛，ir-β-EP水平也未改变。在其他脑区未检测到ir-β-EP水平的变化。受刺激的大鼠以及置于实验箱中未受刺激的大鼠循环ir-β-EP均升高：然而，两组间这种升高的幅度并无差异。PAG以及其他中枢神经系统组织中ir-甲硫氨酸脑啡肽、ir-亮氨酸脑啡肽和ir-强啡肽A的水平均未改变。这些数据表明，对中脑PAG进行电刺激可选择性地影响（可能激活）其中的β-EP库。连同我们发现破坏PAG定位的β-EP神经元可阻断刺激镇痛这一结果，这些数据表明，内源性β-EP的激活是大鼠PAG引发的刺激镇痛的基础。
