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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Coincident activation of NMDA and dopamine D1 receptors within the nucleus accumbens core is required for appetitive instrumental learning.
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Coincident activation of NMDA and dopamine D1 receptors within the nucleus accumbens core is required for appetitive instrumental learning.

机译：竞争性仪器学习需要伏伏核核心内NMDA和多巴胺D1受体的同时激活。

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摘要

The nucleus accumbens, a brain structure ideally situated to act as an interface between corticolimbic information-processing regions and motor output systems, is well known to subserve behaviors governed by natural reinforcers. In the accumbens core, glutamatergic input from its corticolimbic afferents and dopaminergic input from the ventral tegmental area converge onto common dendrites of the medium spiny neurons that populate the accumbens. We have previously found that blockade of NMDA receptors in the core with the antagonist 2-amino-5-phosphonopentanoic acid (AP-5; 5 nmol) abolishes acquisition but not performance of an appetitive instrumental learning task (Kelley et al., 1997). Because it is currently hypothesized that concurrent dopamine D(1) and glutamate receptor activation is required for long-term changes associated with plasticity, we wished to examine whether the dopamine system in the accumbens core modulates learning via NMDA receptors. Co-infusion of low doses of the D(1) receptor antagonist SCH-23390 (0.3 nmol) and AP-5 (0.5 nmol) into the accumbens core strongly impaired acquisition of instrumental learning (lever pressing for food), whereas when infused separately, these low doses had no effect. Infusion of the combined low doses had no effect on indices of feeding and motor activity, suggesting a specific effect on learning. We hypothesize that co-activation of NMDA and D(1) receptors in the nucleus accumbens core is a key process for acquisition of appetitive instrumental learning. Such an interaction is likely to promote intracellular events and gene regulation necessary for synaptic plasticity and is supported by a number of cellular models.
机译：伏伏核是一种理想的大脑结构，可以充当皮质小腿信息处理区域和运动输出系统之间的接口，众所周知，它可以顺应自然增强者的行为。在伏伏核的核心，来自皮质皮质突入的谷氨酸能输入和腹侧被盖区的多巴胺能输入汇聚到填充伏伏核的中型棘突神经元的常见树突上。我们以前已经发现，用拮抗剂2-氨基-5-膦基戊酸（AP-5; 5 nmol）阻断核心中的NMDA受体可消除习得性工具学习任务的获取，但不能消除其行为（Kelley et al。，1997）。 。因为目前假设与可塑性相关的长期变化需要同时发生多巴胺D（1）和谷氨酸受体激活，所以我们希望研究伏安核中的多巴胺系统是否通过NMDA受体调节学习。将小剂量的D（1）受体拮抗剂SCH-23390（0.3 nmol）和AP-5（0.5 nmol）共同注入伏伏隔核中会严重损害工具学习的获得（杠杆压食物），而分别注入时，这些低剂量没有作用。组合低剂量的输注对进食和运动活动指数没有影响，表明对学习有特定影响。我们假设NM伏安和伏隔核核心中的D（1）受体的共同激活是获取竞争性工具学习的关键过程。这种相互作用很可能促进突触可塑性所必需的细胞内事件和基因调控，并受到许多细胞模型的支持。

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