kappa-Opioid receptor signaling and brain reward function.
kappa-Opioid receptor signaling and brain reward function.
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DOI：
10.1016/j.brainresrev.2009.09.008
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发表时间：
2009-12-11
影响因子：
--
通讯作者：
Bruijnzeel AW
中科院分区：
文献类型：
--
作者：
Bruijnzeel AW
强啡肽样肽对大脑奖赏系统的状态以及人类和动物的行为有着深远的影响。强啡肽样肽影响运动活动、食物摄入、性行为、焦虑样行为和药物摄入。强啡肽样肽的内源性受体κ-阿片样受体的刺激抑制纹状体（中脑核和尾壳核）中的多巴胺释放，并诱导人类和动物的负面情绪状态。滥用药物的施用增加纹状体中多巴胺的释放，并介导该脑区域中强啡肽样肽的伴随释放。回顾的研究表明，慢性药物摄入导致纹状体，特别是纹状体/尾壳核的背侧部分的脑强啡肽系统的上调。这可能会抑制药物诱导的多巴胺释放，并提供对高多巴胺水平的神经毒性作用的保护。在停止慢性药物摄入后，这些神经适应仍然没有受到反对，这被认为是与药物戒断和药物摄入增加相关的负面情绪状态的原因。κ-阿片样物质受体激动剂也显示出抑制钙通道。钙通道抑制剂具有抗抑郁样作用并抑制去甲肾上腺素的释放。这可能解释了在一些研究中κ-阿片受体激动剂减弱尼古丁和阿片类戒断反应。更好地理解强啡肽在调节大脑奖赏功能中的作用可能有助于开发新的治疗方法，用于治疗情绪障碍和其他源于大脑奖赏系统失调的疾病。
The dynorphin-like peptides have profound effects on the state of the brain reward system and human and animal behavior. The dynorphin-like peptides affect locomotor activity, food intake, sexual behavior, anxiety-like behavior, and drug intake. Stimulation of kappa-opioid receptors, the endogenous receptor for the dynorphin-like peptides, inhibits dopamine release in the striatum (nucleus accumbens and caudate putamen) and induces a negative mood state in humans and animals. The administration of drugs of abuse increases the release of dopamine in the striatum and mediates the concomitant release of dynorphin-like peptides in this brain region. The reviewed studies suggest that chronic drug intake leads to an upregulation of the brain dynorphin system in the striatum and in particular in the dorsal part of the striatum/caudate putamen. This might inhibit drug-induced dopamine release and provide protection against the neurotoxic effects of high dopamine levels. After the discontinuation of chronic drug intake these neuroadaptations remain unopposed which has been suggested to contribute to the negative emotional state associated with drug withdrawal and increased drug intake. Kappa-opioid receptor agonists have also been shown to inhibit calcium channels. Calcium channel inhibitors have antidepressant-like effects and inhibit the release of norepinephrine. This might explain that in some studies kappa-opioid receptor agonists attenuate nicotine and opioid withdrawal symptomatology. A better understanding of the role of dynorphins in the regulation of brain reward function might contribute to the development of novel treatments for mood disorders and other disorders that stem from a dysregulation of the brain reward system.
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5
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