Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.
Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.
复制标题
体细胞刺激从猫脊髓释放单胺：内在调节系统。
DOI：
10.1113/jphysiol.1981.sp013722
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Yaksh,TL
中科院分区：
文献类型：
--
作者：
Tyce,GM;Yaksh,TL
1. 通过高压液相色谱和电化学检测，对取自氯醛糖和尿烷麻醉的猫脊髓中的上清液中的内源性血清素和去甲肾上腺素进行测定。 2.刺激脊髓横断面尾部的背外侧索，以频率依赖的方式增强脊髓过流液中单胺的水平。 3.添加到过流液中的酪胺增强了去甲肾上腺素和血清素的释放。 4. 在神经轴完整的猫中，高强度而不是低强度刺激坐骨神经会使脊髓过流液中的单胺水平增加 2 至 3 倍。这种引起的单胺流出因颈脊髓的冷阻滞而减弱。 5. 刺激三叉神经的眶下分支会引起神经轴完整的动物腰索释放去甲肾上腺素和血清素。颈髓的冷阻滞阻止了三叉神经诱发的腰椎血清素和去甲肾上腺素的释放。 6. vasoxyl（一种产生高血压的α激动剂）未能引起脊髓单胺水平的任何变化，表明单胺流出不是由于血压升高。 7. 单胺释放不依赖于阿片敏感环节或交感神经节的激活，因为纳洛酮（阿片拮抗剂）和氯茚明（神经节阻断剂）的全身给药未能拮抗胺的诱发释放。 8. 这些结果表明存在由外周刺激激活的刺瓣单胺系统。与脊髓中单胺张力增加相关的调节影响清楚地表明，体刺激可能激活下行单胺通路，该通路用于调节上行感觉信息的强度。
1. Superfusates taken from spinal cords of cats anaesthetized with chloralose and urethane were assayed for endogenous serotonin and noradrenaline by high‐pressure liquid chromatography with electrochemical detection. 2. Stimulating the dorsolateral funiculus, caudal to a spinal transection, enhanced in a frequency‐dependent manner the levels of monoamines in the spinal superfusate. 3. Tyramine added to the superfusate enhanced the release of noradrenaline and serotonin. 4. In cats with intact neuraxes, stimulation of the sciatic nerve at high, but not low intensities produced a 2‐ to 3‐fold increase in the levels of monoamines in the spinal superfusate. This evoked monoamine efflux was attenuated by cold block of the cervical spinal cord. 5. Stimulation of the infraorbital branch of the trigeminal nerve evoked the release of noradrenaline and serotonin from the lumbar cord in animals with intact neuraxes. Cold block of the cervical cord blocked trigeminal‐evoked release of lumbar serotonin and noradrenaline. 6. That the monoamine efflux was not due to elevations in blood pressure was indicated by the failure of vasoxyl, an alpha‐agonist producing hypertension, to evoke any changes in spinal monoamine levels. 7. The monoamine release was not dependent upon either an opiate‐sensitive link or upon the activation of the sympathetic ganglia, because systemic administration of naloxone (an opiate antagonist) and chlorisondamine (a ganglionic blocking agent) failed to antagonize the evoked release of amines. 8. These results suggest the existence of a spinopetal monoamine system which is activated by peripheral stimuli. The modulatory influence associated with increasing monoamine tone in the spinal cord clearly indicated that somatic stimuli may activate a descending monoamine pathway which serves to modulate the magnitude of the ascending sensory message.