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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Cocaine self-administration selectively decreases noradrenergic regulation of metabotropic glutamate receptor-mediated inhibition in dopamine neurons.
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Cocaine self-administration selectively decreases noradrenergic regulation of metabotropic glutamate receptor-mediated inhibition in dopamine neurons.

机译：可卡因自我给药选择性地降低了多巴胺神经元中代谢型谷氨酸受体介导的抑制的去甲肾上腺素能调节。

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摘要

Stimulant drugs of abuse have several effects on neural activity, including altering the excitability of dopamine neurons via the noradrenergic and glutamatergic systems. Thus, an interaction between noradrenergic and glutamatergic systems may play a role in drug-seeking behavior. Although many of the direct pharmacological effects of psychostimulants on dopamine neuron physiology are well established, the neurophysiological bases of drug-seeking behavior have yet to be fully elucidated. The present study measured short-term (3 d) and long-term (14 d) access to cocaine, by self-administration or passive exposure, and the regulation of metabotropic glutamate receptor (mGluR)-mediated inhibition of dopamine cells in rat midbrain slices. The results indicated that alpha-adrenoreceptor modulation of the mGluR-mediated inhibition is selectively reduced in animals that self-administered cocaine for 3 d. This effect was not observed in slices from either yoked cocaine animals, which were given cocaine in an amount and pattern equal to that used for the self-administering animals, or saline control animals. However, after 14 d of cocaine, alpha-adrenoreceptor regulation of the mGluR-mediated inhibition was equally reduced in both self-administering and yoked cocaine animals relative to saline controls. The results suggest that alpha-adrenoreceptor regulation of the mGluR-mediated inhibition is an adaptive cellular mechanism involved in early cocaine self-administration that is distinct from a direct pharmacological effect of cocaine on dopamine neurons. The noradrenergic system could therefore serve to alter the reward value of stimuli that have significant effects on dopamine neuron firing pattern through mGluRs.
机译：滥用刺激性药物对神经活动有多种影响，包括通过去甲肾上腺素能和谷氨酸能系统改变多巴胺神经元的兴奋性。因此，去甲肾上腺素能系统和谷氨酸能系统之间的相互作用可能在寻求药物的行为中起作用。尽管精神兴奋剂对多巴胺神经元生理学的许多直接药理作用已得到充分证实，但尚未充分阐明药物寻求行为的神经生理学基础。本研究通过自我给药或被动暴露以及对代谢型谷氨酸受体（mGluR）介导的对大鼠中脑多巴胺细胞的抑制作用，测量了可卡因的短期（3 d）和长期（14 d）访问。片。结果表明，在自行服用可卡因3天的动物中，mGluR介导的抑制作用的α-肾上腺素能受体选择性降低。在带轭可卡因动物的切片中未观察到这种效果，该可卡因动物的可卡因的剂量和样式与自给动物或盐水对照动物的可卡因相同。但是，在可卡因14天后，与盐水对照组相比，可卡因可自食和受轭动物中mGluR介导的抑制作用的α-肾上腺素受体调节均被降低。结果表明，mGluR介导的抑制作用的α-肾上腺素受体调节是参与可卡因早期自我给药的一种适应性细胞机制，与可卡因对多巴胺神经元的直接药理作用不同。因此，去甲肾上腺素能系统可以通过mGluR改变对多巴胺神经元放电模式有重大影响的刺激的奖励价值。

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