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阿片类物质对雌性大鼠视前区神经元对腹侧去甲肾上腺素能束刺激反应的调节作用。

Opioid modulation of the response of preoptic neurones to stimulation of the ventral noradrenergic tract in female rats.

作者信息

Dyer R G, Grossman R

机构信息

AFRC Institute of Animal Physiology and Genetics Research, Babraham, Cambridge.

出版信息

J Physiol. 1988 Jun;400:631-44. doi: 10.1113/jphysiol.1988.sp017140.

Abstract
  1. Experiments were undertaken on twenty-nine ovariectomized female rats, pretreated with oestrogen and anaesthetized with urethane, to test the hypothesis that opioid peptides regulate noradrenergic transmission in the medial preoptic area and thereby influence the neural circuitry controlling the secretion of luteinizing hormone. 2. Extracellular recordings were obtained with glass micropipettes from ninety-four neurones in the medial preoptic area. These recordings were continued whilst both the ventral noradrenergic tract, the noradrenergic projection to the medial preoptic area, and orthodromic pathways originating in the arcuate nucleus, the main source for endogenous opioid peptides in the hypothalamus, were stimulated electrically. Forty of the ninety-four neurones responded to stimulation at one or both of the test sites. 3. Electrical stimulation of the ventral noradrenergic tract excited fifteen neurones (greater than 30% change in number of action potentials recorded during the 'response time period') and inhibited a further ten cells. When the nucleus arcuatus was stimulated electrically thirteen cells were inhibited and twelve neurones showed an excitatory response. 4. The opioid antagonist naloxone (80 mM) and/or morphine (50 mM) were ejected into the immediate vicinity of eighty-six of the recorded cells by passage of balanced currents (range 15-80 nA) through a multi-barrelled electrode glued to the recording electrode. The tip of the drug-containing electrode was about 15-25 microns behind the tip of the recording electrode. 5. The ionophoretic application of naloxone, during electrical stimulation of the ventral noradrenergic tract, diminished the inhibitory response in four of ten cells and enhanced the excitatory response in nine out of fifteen neurones. By contrast, morphine diminished the excitatory response in seven of these fifteen cells tested, an effect that was prevented by the simultaneous application of naloxone. 6. Similarly, the application of naloxone during stimulation of the nucleus arcuatus reduced the inhibitory effect in eight out of thirteen cells. When four of these eight responsive neurones were exposed to morphine either the effect of naloxone was reversed or, when given alone, the inhibition was enhanced. 7. Finally, for seventeen cells categorized as non-responsive to stimulation at either site, the application of naloxone during hind brain stimulation revealed an excitatory input from the ventral noradrenergic tract in seven cases. 8 The experiments demonstrate that opioid peptides modulate the neural inputs to the medial preoptic area arising from the nucleus arcuatus and the ventral noradrenergic tract.(ABSTRACT TRUNCATED AT 400 WORDS)
摘要
  1. 对29只经雌激素预处理并用乌拉坦麻醉的去卵巢雌性大鼠进行了实验,以检验阿片肽调节视前内侧区去甲肾上腺素能传递从而影响控制黄体生成素分泌的神经回路这一假说。2. 用玻璃微电极从视前内侧区的94个神经元记录细胞外电活动。在分别电刺激腹侧去甲肾上腺素能束(投射到视前内侧区的去甲肾上腺素能投射)以及起源于弓状核(下丘脑内源性阿片肽的主要来源)的顺行通路时,持续进行这些记录。94个神经元中有40个在一个或两个测试部位对刺激有反应。3. 电刺激腹侧去甲肾上腺素能束使15个神经元兴奋(在“反应时间段”记录的动作电位数量变化大于30%),并使另外10个细胞受到抑制。电刺激弓状核时,13个细胞受到抑制,12个神经元表现出兴奋反应。4. 通过将平衡电流(范围为15 - 80 nA)通过粘贴在记录电极上的多管电极,将阿片拮抗剂纳洛酮(80 mM)和/或吗啡(50 mM)注入86个记录细胞的紧邻区域。含药电极的尖端位于记录电极尖端后方约15 - 25微米处。5. 在电刺激腹侧去甲肾上腺素能束期间,离子电泳施加纳洛酮,使10个细胞中的4个细胞的抑制反应减弱,15个神经元中的9个神经元的兴奋反应增强。相比之下,吗啡使这15个受试细胞中的7个细胞的兴奋反应减弱,同时施加纳洛酮可防止这种效应。6. 同样,在刺激弓状核期间施加纳洛酮,使13个细胞中的8个细胞的抑制效应减弱。当这8个有反应的神经元中的4个暴露于吗啡时,要么纳洛酮的效应被逆转,要么单独给予吗啡时抑制作用增强。7. 最后,对于在两个部位对刺激均无反应的17个细胞,在后脑刺激期间施加纳洛酮,在7个案例中揭示了来自腹侧去甲肾上腺素能束的兴奋性输入。8. 这些实验表明,阿片肽调节来自弓状核和腹侧去甲肾上腺素能束至视前内侧区的神经输入。(摘要截短为400字)

相似文献

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A1 noradrenergic input to medial preoptic-medial septal area: an electrophysiological study.
Neuroendocrinology. 1987 Jan;45(1):77-85. doi: 10.1159/000124706.

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3
Augmentation by naloxone of efflux of LRF from superfused medial basal hypothalamus.
Life Sci. 1981 May 21;28(21):2355-9. doi: 10.1016/0024-3205(81)90500-2.

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