RELEASE OF BETA-ENDORPHIN IMMUNOREACTIVITY INTO VENTRICULOCISTERNAL PERFUSATE BY LUMBAR INTRATHECAL CAPSAICIN IN THE RAT
RELEASE OF BETA-ENDORPHIN IMMUNOREACTIVITY INTO VENTRICULOCISTERNAL PERFUSATE BY LUMBAR INTRATHECAL CAPSAICIN IN THE RAT
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DOI：
10.1016/0006-8993(95)01003-1
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发表时间：
1995-12-01
期刊：
影响因子：
2.9
通讯作者：
YAKSH, TL
中科院分区：
文献类型：
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作者：
BACH, FW;YAKSH, TL
采用氟烷麻醉大鼠侧脑室向枕大池灌注人工脑脊液的模型，研究脑内β-内啡肽的释放。注射75微克辣椒素到腰椎鞘内空间释放β-内啡肽免疫反应到灌注液。用1.25 mg利多卡因和辣椒素受体拮抗剂辣椒平（92 μ g）鞘内预处理可阻断释放，表明释放是由辣椒素与脊髓受体结合引起的。用NMDA拮抗剂MK-801（3 μ g）和NK-1受体拮抗剂CP 96，345（200 μ g）鞘内预处理也能阻断这种释放，而AMPA受体拮抗剂NBQX（6 μ g）没有产生明显的抑制作用。令人惊讶的是，吗啡（30微克）和舒芬太尼（1.5微克）并没有阻止β-内啡肽免疫反应性的释放，尽管阻断了心血管对有害热刺激的反应。辣椒素注射后收集的灌流液的高效液相色谱表征表明，所有β-内啡肽免疫反应性与真实的β-内啡肽（1-31）共洗脱。注射辣椒素后10分钟血浆中β-内啡肽免疫反应性增加，但25分钟后没有增加。辣椒素注射消除了运动和心血管反应的尾巴浸泡在52.5摄氏度的水。在侧脑室-小脑延髓池灌流液中加入MK-801（10（-4）mol/l）可阻断辣椒素诱导的β-内啡肽释放，表明我们先前证明的NMDA受体调节弓状核β-内啡肽神经元活动具有功能意义。我们的结论是，在这种在体内，麻醉制剂，包括三个热水尾部浸泡，β-内啡肽可以释放到脑室池灌注液，通过激活的小初级传入神经元的中央轴突辣椒素。这些数据支持这样的观点，即中枢β-内啡肽可能会在长时间的强烈伤害性刺激下释放。
A model employing perfusion of artificial cerebrospinal fluid from the lateral ventricle to the cisterna magna in the halothane anesthetized rat was used to study beta-endorphin release in the brain. Injection of 75 mu g capsaicin into the lumbar intrathecal space released beta-endorphin immunoreactivity into perfusate. The release was blocked by intrathecal pretreatment with 1.25 mg lidocaine and the capsaicin receptor antagonist capsazepine (92 mu g), showing that the release is caused by binding of capsaicin to a spinal receptor. The release was also blocked by intrathecal pretreatment with the NMDA antagonist MK-801 (3 mu g) and the NK-1 receptor antagonist CP96,345 (200 mu g), whereas the AMPA receptor antagonist NBQX(6 mu g) yielded no significant inhibition. Surprisingly, morphine (30 mu g) and sufentanil(1.5 mu g) did not prevent release of beta-endorphin immunoreactivity, although blocking the cardiovascular responses to a noxious heat stimulus. High performance liquid chromatography characterization of perfusates collected after capsaicin injection showed that all beta-endorphin immunoreactivity coeluted with authentic beta-endorphin(1-31). beta-Endorphin immunoreactivity in plasma was increased 10 min, but not 25 min, after capsaicin injection. Capsaicin injection abolished the motor and cardiovascular responses to tail immersion in 52.5 degrees C water. Addition of MK-801 (10(-4) mol/l) to the lateral ventricle-cisterna magna perfusate blocked the capsaicin-induced beta-endorphin release, showing that our previous demonstration of an NMDA receptor regulating arcuate nucleus beta-endorphin neuron activity has functional significance. We conclude that in this in vivo, anesthetized preparation including three hot water tail immersions, beta-endorphin can be released into a ventriculo-cisternal perfusate, by activation of the central axons of small primary afferent neurons by capsaicin. These data support the idea that central beta-endorphin may be released in response to prolonged, intense noxious stimulation.