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腹侧苍白球神经元编码动机激励:通过中脑边缘系统敏化和苯丙胺实现增强作用。

Ventral pallidal neurons code incentive motivation: amplification by mesolimbic sensitization and amphetamine.

作者信息

Tindell Amy J, Berridge Kent C, Zhang Jun, Peciña Susana, Aldridge J Wayne

机构信息

Department of Psychology, University of Michigan, Ann Arbor, MI 48109-0607, USA.

出版信息

Eur J Neurosci. 2005 Nov;22(10):2617-34. doi: 10.1111/j.1460-9568.2005.04411.x.

DOI:10.1111/j.1460-9568.2005.04411.x
PMID:16307604
Abstract

Neurons in ventral pallidum fire to reward and its predictive cues. We tested mesolimbic activation effects on neural reward coding. Rats learned that a Pavlovian conditioned stimulus (CS+1 tone) predicted a second conditioned stimulus (CS+2 feeder click) followed by an unconditioned stimulus (UCS sucrose reward). Some rats were sensitized to amphetamine after training. Electrophysiological activity of ventral pallidal neurons to stimuli was later recorded under the influence of vehicle or acute amphetamine injection. Both sensitization and acute amphetamine increased ventral pallidum firing at CS+2 (population code and rate code). There were no changes at CS+1 and minimal changes to UCS. With a new 'Profile Analysis', we show that mesolimbic activation by sensitization/amphetamine incrementally shifted neuronal firing profiles away from prediction signal coding (maximal at CS+1) and toward incentive coding (maximal at CS+2), without changing hedonic impact coding (maximal at UCS). This pattern suggests mesolimbic activation specifically amplifies a motivational transform of CS+ predictive information into incentive salience coded by ventral pallidal neurons. Our results support incentive-sensitization predictions and suggest why cues temporally proximal to drug presentation may precipitate cue-triggered relapse in human addicts.

摘要

腹侧苍白球中的神经元会对奖励及其预测线索产生反应。我们测试了中脑边缘系统激活对神经奖励编码的影响。大鼠学会了一种巴甫洛夫条件刺激(CS+1音调)预示着另一种条件刺激(CS+2喂食器咔嗒声),随后是无条件刺激(UCS蔗糖奖励)。一些大鼠在训练后对苯丙胺敏感。随后在注射赋形剂或急性苯丙胺的影响下,记录腹侧苍白球神经元对刺激的电生理活动。敏感化和急性苯丙胺都增加了腹侧苍白球在CS+2时的放电(群体编码和速率编码)。在CS+1时没有变化,对UCS的变化最小。通过一种新的“轮廓分析”,我们表明,敏感化/苯丙胺引起的中脑边缘系统激活逐渐将神经元放电轮廓从预测信号编码(在CS+1时最大)转向激励编码(在CS+2时最大),而不改变享乐影响编码(在UCS时最大)。这种模式表明,中脑边缘系统激活特异性地放大了CS+预测信息向腹侧苍白球神经元编码的激励显著性的动机转化。我们的结果支持激励敏感化预测,并解释了为什么在人类成瘾者中,与药物呈现时间上接近的线索可能会引发线索触发的复发。

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