Glutamatergic activation of anterior cingulate cortex produces an aversive teaching signal
Glutamatergic activation of anterior cingulate cortex produces an aversive teaching signal
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DOI：
10.1038/nn1207
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发表时间：
2004-04-01
影响因子：
25
通讯作者：
Fields, HL
中科院分区：
文献类型：
--
作者：
Johansen, JP;Fields, HL
伤害刺激具有激励力量，可以支持联想学习，但调节这种回避学习的神经回路知之甚少。前扣带皮层（ACC）参与伤害性刺激的情感反应和预测伤害性刺激的条件刺激的动机特性。使用大鼠条件性位置厌恶（CPA），我们发现，在条件反射过程中，在ACC中微量注射兴奋性氨基酸产生回避学习在没有外周伤害性刺激。此外，在条件反射过程中向ACC中微量注射兴奋性氨基酸拮抗剂可阻断伤害性刺激引起的学习。ACC病变后，空调没有损害CPA的表达。因此，ACC神经元的活动是必要的和足够的伤害性刺激，以产生一个令人厌恶的教学信号。我们的研究结果支持这样的想法，即一个共享的ACC通路介导疼痛引起的负面影响和伤害感受器驱动的厌恶教学信号。
Noxious stimuli have motivational power and can support associative learning, but the neural circuitry mediating such avoidance learning is poorly understood. The anterior cingulate cortex (ACC) is implicated in the affective response to noxious stimuli and the motivational properties of conditioned stimuli that predict noxious stimulation. Using conditioned place aversion (CPA) in rats, we found that excitatory amino acid microinjection into the ACC during conditioning produces avoidance learning in the absence of a peripheral noxious stimulus. Furthermore, microinjection of an excitatory amino acid antagonist into the ACC during conditioning blocked learning elicited by a noxious stimulus. ACC lesions made after conditioning did not impair expression of CPA. Thus, ACC neuronal activity is necessary and sufficient for noxious stimuli to produce an aversive teaching signal. Our results support the idea that a shared ACC pathway mediates both pain-induced negative affect and a nociceptor-driven aversive teaching signal.