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首页> 外文期刊>The European Journal of Neuroscience >Neural circuit competition in cocaine-seeking: roles of the infralimbic cortex and nucleus accumbens shell.
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Neural circuit competition in cocaine-seeking: roles of the infralimbic cortex and nucleus accumbens shell.

机译：可卡因寻找过程中的神经回路竞争：下肢皮质和伏隔核壳的作用。

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Following cocaine self-administration and extinction training, activity in the infralimbic cortex (IL) suppresses cocaine-seeking behavior. IL inactivation induces cocaine-seeking whereas activation suppresses cocaine-reinstated drug-seeking. We asked how the suppression of cocaine-seeking induced by IL activation integrates with the circuitry promoting reinstated cocaine-seeking. Following cocaine self-administration and extinction training, rats underwent cue-induced reinstatement. In order to activate IL projections, microinjections of PEPA, a positive allosteric modulator of AMPA receptors, were made into the IL in combination with microinjections into a variety of nuclei known to regulate cocaine-seeking. Intra-IL PEPA administration suppressed cue-induced reinstatement without affecting locomotor activity. The suppression of cocaine-seeking was reversed by activating dopamine neurons in the ventral tegmental area with microinjections of the μ-opioid receptor agonist DAMGO, and was partially reversed by dopamine microinjections into the prelimbic cortex or basolateral amygdala. Previous evidence suggests that the nucleus accumbens shell both promotes and suppresses cocaine-seeking. The suppression of cue-induced cocaine seeking by PEPA in the IL was reversed by intra-shell microinjections of either dopamine or the AMPA receptor antagonist CNQX, suggesting that the accumbens shell bidirectionally regulates cocaine-seeking depending on whether dopamine input is mimicked or glutamate input is inhibited. Together, these findings indicate that the IL acts 'upstream' from structures promoting cocaine-seeking, including from the mesolimbic dopamine projections to the prelimbic cortex and basolateral amygdala, and that the accumbens shell may be a crucial point of integration between the circuits that promote (ventral tegmental area) and inhibit (IL) reinstated cocaine-seeking.
机译：经过可卡因自我管理和灭绝训练后，下肢皮质（IL）中的活动抑制了可卡因的寻觅行为。 IL失活诱导可卡因寻求，而激活抑制可卡因恢复的药物寻求。我们问到由IL激活诱导的可卡因寻求抑制与促进恢复可卡因寻求的电路如何整合。经过可卡因自我给药和灭绝训练后，大鼠进行了提示诱导的恢复。为了激活IL投射，将微注射的PEPA（AMPA受体的正向变构调节剂）与微注射结合到已知调节可卡因寻找的各种细胞核中，制成IL。 IL-PEPA内给药抑制提示诱导的恢复，而不会影响运动活性。通过微量注射μ阿片受体激动剂DAMGO激活腹侧被盖区的多巴胺神经元，可以逆转可卡因的抑制作用，而通过多巴胺显微注射至前缘皮层或基底外侧杏仁核则可以部分逆转可卡因的抑制作用。先前的证据表明伏隔核壳既促进又抑制可卡因的寻找。通过多巴胺或AMPA受体拮抗剂CNQX的壳内显微注射逆转了IL中PEPA对线索诱导的可卡因的抑制作用，这表明伏伏核壳根据模拟的多巴胺输入或谷氨酸输入双向调节可卡因的寻找被禁止。总之，这些发现表明，IL在促进可卡因寻找的结构中“上游”起作用，包括从中边缘多巴胺投射到前边缘皮层和基底外侧杏仁核，伏隔壳可能是促进这些途径之间整合的关键点。 （腹侧被盖区）和抑制（IL）恢复可卡因搜寻。

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