RELEASE INTO VENTRICULOCISTERNAL PERFUSATE OF BETA-ENDORPHIN-IMMUNOREACTIVITY AND MET-ENKEPHALIN-IMMUNOREACTIVITY - EFFECTS OF ELECTRICAL-STIMULATION IN THE ARCUATE NUCLEUS AND PERIAQUEDUCTAL GRAY OF THE RAT
RELEASE INTO VENTRICULOCISTERNAL PERFUSATE OF BETA-ENDORPHIN-IMMUNOREACTIVITY AND MET-ENKEPHALIN-IMMUNOREACTIVITY - EFFECTS OF ELECTRICAL-STIMULATION IN THE ARCUATE NUCLEUS AND PERIAQUEDUCTAL GRAY OF THE RAT
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DOI：
10.1016/0006-8993(95)00600-u
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发表时间：
1995-09-04
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
为了研究内源性阿片肽β-内啡肽和甲硫氨酸脑啡肽从脑中的静息和诱发释放，我们检测了氟烷麻醉大鼠侧脑室-枕大池灌注液中相应免疫反应性的水平。10 Hz而不是100 Hz刺激下丘脑弓状核（ARC）释放β-内啡肽免疫反应（β-EPir）的灌注液，而100 Hz而不是10 Hz刺激中脑导水管周围灰质（FAG）释放甲硫氨酸脑啡肽免疫反应（MEir）。在ARC中刺激不释放MEir，在FAG中刺激不释放β-EPir。通过高效液相色谱法对释放的β-EPir和MEir的表征表明，真实的β-内啡肽和甲硫氨酸脑啡肽分别是β-EPir和MEir的主要成分。多巴胺能拮抗剂氟哌啶醇的全身给药增加血浆，但不灌流液中β-EPir的水平。阿片受体拮抗剂纳洛酮和NMDA受体拮抗剂MK-801均不能影响β-EPir或MEir的释放。ARC和FAG刺激抑制伤害性反射（尾部浸入52.5 ℃水中），纳洛酮不能可靠地逆转这种抑制。这些数据支持先前提出的阿片类药物介导刺激诱导镇痛的可能性，尽管我们在本研究中无法通过纳洛酮可逆性证实该理论。此外，数据支持的假设，在脑脊液中的阿片肽的测量是一个相关的研究方法，旨在阐明内源性阿片肽的生理和病理生理作用。
To examine the resting and evoked release of the endogenous opioid peptides beta-endorphin and Met-enkephalin from brain, we examined the levels of the respective immunoreactivities in the lateral ventricle-cisterna magna perfusate of the halothane-anesthetized rat. Ten Hz but not 100 Hz stimulation in the arcuate nucleus (ARC) of the hypothalamus released beta-endorphin immunoreactivity (beta-EPir) to the perfusate, whereas 100 Hz but not 10 Hz stimulation in the periaqueductal gray (FAG) of the mid brain released Met-enkephalin immunoreactivity (MEir). MEir was not released by stimulation in ARC and beta-EPir was not released by stimulation in FAG. Characterization of the released beta-EPir and MEir by high performance liquid chromatography showed that authentic beta-endorphin and Met-enkephalin were the major constituents of beta-EPir and MEir, respectively. Systemic administration of the dopaminergic antagonist haloperidol increased plasma, but not perfusate levels of beta-EPir. Both the opioid antagonist naloxone and the NMDA antagonist MK-801 failed to affect beta-EPir or MEir release. ARC and FAG stimulation inhibited a nociceptive reflex (tail-dip in 52.5 degrees C water), and naloxone did not reliably reverse this inhibition. These data support the previously suggested possibility of opioid mediation of stimulation induced analgesia, although we were unable to confirm the theory by naloxone reversibility in this study. Furthermore, the data support the assumption that measurement of opioid peptides in cerebrospinal fluid is a relevant approach in research aimed at elucidating the physiological and pathophysiological roles of endogenous opioid peptides.