Department of Psychology, University of Michigan, Ann Arbor, Michigan, United States of America.
PLoS One. 2010 Jun 18;5(6):e11223. doi: 10.1371/journal.pone.0011223.
GABAergic signals to the nucleus accumbens (NAc) shell arise from predominantly subcortical sources whereas glutamatergic signals arise mainly from cortical-related sources. Here we contrasted GABAergic and glutamatergic generation of hedonics versus motivation processes, as a proxy for comparing subcortical and cortical controls of emotion. Local disruptions of either signals in medial shell of NAc generate intense motivated behaviors corresponding to desire and/or dread, along a rostrocaudal gradient. GABA or glutamate disruptions in rostral shell generate appetitive motivation whereas disruptions in caudal shell elicit fearful motivation. However, GABA and glutamate signals in NAc differ in important ways, despite the similarity of their rostrocaudal motivation gradients.
METHODOLOGY/PRINCIPAL FINDINGS: Microinjections of a GABA(A) agonist (muscimol), or of a glutamate AMPA antagonist (DNQX) in medial shell of rats were assessed for generation of hedonic "liking" or "disliking" by measuring orofacial affective reactions to sucrose-quinine taste. Motivation generation was independently assessed measuring effects on eating versus natural defensive behaviors. For GABAergic microinjections, we found that the desire-dread motivation gradient was mirrored by an equivalent hedonic gradient that amplified affective taste "liking" (at rostral sites) versus "disliking" (at caudal sites). However, manipulation of glutamatergic signals completely failed to alter pleasure-displeasure reactions to sensory hedonic impact, despite producing a strong rostrocaudal gradient of motivation.
CONCLUSIONS/SIGNIFICANCE: We conclude that the nucleus accumbens contains two functional affective keyboards for amino-acid signals: a motivation-generating keyboard and a hedonic-generating keyboard. Corticolimbic glutamate signals and subcortical GABA signals equivalently engage the motivation keyboard to generate desire and-or dread. Only subcortical GABA signals additionally engage the hedonic keyboard to amplify affective "liking" and "disliking" reactions. We thus suggest that top-down cortical glutamate signals powerfully regulate motivation components, but are relatively unable to penetrate core hedonic components of emotion. That may carry implications of limits to therapeutic regulation of pathological emotions.
来自于壳核（NAc）的 GABA 能信号主要来源于皮质下来源，而谷氨酸能信号主要来源于皮质相关来源。在这里，我们对比了 GABA 能和谷氨酸能在产生愉悦感与动机过程中的作用，以此作为比较皮质下和皮质对情绪控制的代理指标。NAc 内侧核团中这两种信号的局部破坏会沿着头尾梯度产生强烈的动机行为，对应于欲望和/或恐惧。GABA 或谷氨酸在壳核头部的破坏会产生食欲动机，而在尾部的破坏会引起恐惧动机。然而，尽管它们的头尾动机梯度相似，但 NAc 中的 GABA 和谷氨酸信号在重要方面存在差异。
方法/主要发现：在大鼠 NAc 内侧核团中注射 GABA(A)激动剂（muscimol）或谷氨酸 AMPA 拮抗剂（DNQX），通过测量蔗糖-奎宁味觉的口腔情感反应来评估产生愉悦“喜欢”或“不喜欢”的情况。通过测量对进食与自然防御行为的影响，独立评估动机的产生。对于 GABA 能微注射，我们发现欲望-恐惧动机梯度与等效的愉悦梯度相匹配，该梯度放大了对味觉的情感“喜欢”（在头部部位）与“不喜欢”（在尾部部位）。然而，尽管产生了强烈的头尾动机梯度，但操纵谷氨酸能信号完全不能改变对感官愉悦影响的愉悦-不愉悦反应。
结论/意义：我们得出结论，NAc 包含两个用于氨基酸信号的功能性情感键盘：一个是产生动机的键盘，另一个是产生愉悦感的键盘。皮质边缘谷氨酸信号和皮质下 GABA 信号同样参与到动机键盘中，以产生欲望和/或恐惧。只有皮质下 GABA 信号另外参与到愉悦键盘中，以放大情感“喜欢”和“不喜欢”反应。因此，我们认为来自于皮质的谷氨酸信号可以强有力地调节动机成分，但相对而言无法穿透情感的核心愉悦成分。这可能意味着对病理性情绪的治疗调节存在限制。
