Basolateral amygdala glutamatergic activation enhances taste aversion through NMDA receptor activation in the insular cortex
Basolateral amygdala glutamatergic activation enhances taste aversion through NMDA receptor activation in the insular cortex
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DOI：
10.1111/j.1460-9568.2005.04440.x
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发表时间：
2005-11-01
影响因子：
3.4
通讯作者：
Bermúdez-Rattoni, F
中科院分区：
文献类型：
--
作者：
Ferreira, G;Miranda, MI;Bermúdez-Rattoni, F
在条件性味觉厌恶（CTA）中，受试者学会将新的味道与内脏不适联系起来。脑干、边缘系统和新皮质结构与CTA记忆形成有关。然而，在这些过程中前脑结构之间的相互作用的作用仍然是未知的。本实验旨在研究CTA记忆形成过程中杏仁基底外侧核（BLA）和岛叶皮质（IC）之间的相互作用。注射低剂量氯化锂（30 mg/kg，i. p.）新口味消费后30分钟（糖精0.1%）诱导弱CTA。就在低锂诱导更强的CTA之前，单侧BLA注射谷氨酸盐（0.5 μ L中2 μ g）。在IC中单侧注射N-甲基-D-天冬氨酸（NMDA）受体拮抗剂（AP 5，5 μ g/0.5 μ L）没有影响。然而，在同侧BLA注射的同一时间或1小时后，IC中的AP 5处理逆转了谷氨酸诱导的CTA增强。在BLA注射后3小时在IC中注射AP 5不干扰谷氨酸作用。同时向对侧脑内注射AP 5也可阻断谷氨酸的CTA增强作用。这些结果提供了强有力的证据，即IC中的NMDA受体活化对于在延长至1小时但不延长至3小时的有限时间段内通过BLA中的谷氨酸输注诱导CTA增强是必不可少的。这些发现表明BLA-IC相互作用调节CTA的强度。这些杏仁皮质相互作用的双边性质进行了讨论。
In conditioned taste aversion (CTA), a subject learns to associate a novel taste with visceral malaise. Brainstem, limbic and neocortical structures have been implicated in CTA memory formation. Nevertheless, the role of interactions between forebrain structures during these processes is still unknown. The present experiment was aimed at investigating the possible interaction between the basolateral nucleus of the amygdala (BLA) and the insular cortex (IC) during CTA memory formation. Injection of a low dose of lithium chloride (30 mg/kg, i.p.) 30 min after novel taste consumption (saccharin 0.1%) induces a weak CTA. Unilateral BLA injection of glutamate (2 mu g in 0.5 mu L) just before low lithium induces a stronger CTA. Unilateral injection of an N-methyl-D-aspartate (NMDA) receptor antagonist (AP5, 5 mu g in 0.5 mu L) in IC has no effect. However, AP5 treatment in IC at the same time or 1 h after the ipsilateral BLA injection reverses the glutamate-induced CTA enhancement. Injection of AP5 in IC 3 h after BLA injection does not interfere with the glutamate effect. Moreover, the CTA-enhancing effect of glutamate was also blocked by contralateral IC injection of AP5 at the same time. These results provide strong evidence that NMDA receptor activation in the IC is essential to enable CTA enhancement induced by glutamate infusion in the BLA during a limited time period that extends to 1 but not to 3 hours. These findings indicate that BLA-IC interactions regulate the strength of CTA. The bilateral nature of these amygdalo-cortical interactions is discussed.