Chan J Y, Tsai H F, Kuo T B, Chan S H
Institute of Physiology, National Yang-Ming Medical College, Taipei, Taiwan, ROC.
Regul Pept. 1994 Mar 17;50(3):247-57. doi: 10.1016/0167-0115(94)90005-1.
We evaluated possible modulation by angiotensin III (AIII) of the interactive effect of noxious stimuli and elevation in systemic arterial pressure on the responsiveness of neurons in the nucleus reticularis gigantocellularis (NRGC) of the medulla oblongata. Combined extracellular single-neuron recording and microiontophoresis were carried out on male, adult Sprague-Dawley rats anesthetized with pentobarbital sodium. The responsiveness of NRGC neurons to nociception (tail clamp) and/or transient hypertension elicited by phenylephrine (5 micrograms/kg, i.v.), in the absence or presence of AIII, was used as the experimental index. Microiontophoretic application of the heptapeptide suppressed the responses of spontaneously active NRGC neurons to individually delivered nociception or hypertension. Interestingly, the preferential reduction in responsiveness to tail clamp upon simultaneous elevation in arterial pressure was reversed to one that favored nociception in the presence of AIII. These actions of the heptapeptide appeared to be receptor-specific, since they were discernibly blocked by its selective antagonist, Ile7-angiotensin III. Our results reveal that neuropeptides such as AIII may differentially modulate neuronal responsiveness according to the prevailing physiologic input(s) to the central nervous system of the animal.
我们评估了血管紧张素III（AIII）对伤害性刺激与全身动脉压升高之间相互作用的可能调节作用，这种相互作用会影响延髓巨细胞网状核（NRGC）中神经元的反应性。在戊巴比妥钠麻醉的成年雄性Sprague-Dawley大鼠上进行了细胞外单神经元记录和微离子透入法相结合的实验。以NRGC神经元对伤害感受（夹尾）和/或去氧肾上腺素（5微克/千克，静脉注射）引起的短暂高血压的反应性作为实验指标，观察有无AIII时的情况。七肽的微离子透入应用抑制了自发活动的NRGC神经元对单独施加的伤害感受或高血压的反应。有趣的是，在动脉压同时升高时，对夹尾反应性的优先降低在有AIII存在时逆转，变为有利于伤害感受的情况。七肽的这些作用似乎具有受体特异性，因为它们可被其选择性拮抗剂Ile7-血管紧张素III明显阻断。我们的结果表明，诸如AIII之类的神经肽可能根据动物中枢神经系统中占主导的生理输入，对神经元反应性进行不同的调节。
