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阿片受体对大鼠伏隔核中进食诱发的多巴胺释放的调节作用。

Opioid receptor modulation of feeding-evoked dopamine release in the rat nucleus accumbens.

作者信息

Taber M T, Zernig G, Fibiger H C

机构信息

Division of Neurological Sciences, Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, V6T 1Z3, Canada.

出版信息

Brain Res. 1998 Feb 23;785(1):24-30. doi: 10.1016/s0006-8993(97)01124-4.

Abstract

Feeding is associated with increases in the activity of the mesolimbic dopamine (DA) system which originates in the ventral tegmental area (VTA) and projects heavily to the nucleus accumbens. The present study used in vivo brain microdialysis to assess the contribution of opioid receptors in feeding-evoked DA release in the nucleus accumbens. Feeding in 18 h food-deprived rats increased DA release by about 50% above baseline. Systemic injection of the opioid receptor antagonist naltrexone (1 mg/kg, s.c.) blocked the effect of feeding on DA release and reduced the amount of food consumed. Unilateral application of naltrexone (100 microM) in the VTA via a microdialysis probe failed to affect the DA response to feeding, the amount of food consumed, or the latency to eat. In contrast, intra-VTA naltrexone significantly reduced the effect of systemic heroin (0.5 mg/kg, s.c.) on accumbal DA release. These results indicate that: (1) opioid receptor activation is a component of the neural substrates of deprivation-induced feeding: (2) opioid receptors in the VTA do not contribute significantly to feeding-associated increases in DA release in the nucleus accumbens; and (3) heroin-induced increases in accumbal DA release are mediated, at least in part, by opioid receptors in the VTA.

摘要

进食与中脑边缘多巴胺(DA)系统活动的增加有关,该系统起源于腹侧被盖区(VTA),并大量投射到伏隔核。本研究采用体内脑微透析技术,评估阿片受体在进食诱发的伏隔核DA释放中的作用。对禁食18小时的大鼠进行喂食,可使DA释放量比基线水平增加约50%。全身注射阿片受体拮抗剂纳曲酮(1毫克/千克,皮下注射)可阻断进食对DA释放的影响,并减少食物摄入量。通过微透析探针在VTA单侧应用纳曲酮(100微摩尔),未能影响DA对进食的反应、食物摄入量或进食潜伏期。相比之下,VTA内注射纳曲酮可显著降低全身注射海洛因(0.5毫克/千克,皮下注射)对伏隔核DA释放的影响。这些结果表明:(1)阿片受体激活是剥夺诱导进食的神经基质的一个组成部分;(2)VTA中的阿片受体对进食相关的伏隔核DA释放增加没有显著贡献;(3)海洛因诱导的伏隔核DA释放增加至少部分是由VTA中的阿片受体介导的。

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