The insular cortex (IC) has a crucial role in taste recognition memory, including conditioned taste aversion (CTA). CTA is a learning paradigm in which a novel taste stimulus (CS) is associated with gastric malaise (US), inducing aversion to the CS in future encounters. The role of the IC in CTA memory formation has been extensively studied. However, the functional significance of neurotransmitter release during the presentation of taste stimuli and gastric malaise-inducing agents remains unclear. Using microdialysis in free-moving animals, we evaluated simultaneous changes in glutamate, norepinephrine and dopamine release in response to the presentation of an innate appetitive or aversive gustatory novel stimulus, as well as after i.p. administration of isotonic or hypertonic gastric malaise-inducing solutions. Our results demonstrate that the presentation of novel stimuli, regardless of their innate valence, induces an elevation of norepinephrine and dopamine. Administration of a gastric malaise inducing agent (LiCl) promotes an elevation of glutamate regardless of its concentration. In comparison, norepinephrine release is related to the LiCl concentration and its equimolar NaCl control. Additionally, we evaluated their functional role on short and long-term taste aversion memory. Results indicate that the blockade of noradrenergic β1,2 receptors in the IC spares CTA acquisition and memory consolidation. In contrast, blockade of dopamine D1/D5 receptors impaired CTA consolidation, whereas the NMDA receptor blockade impedes both acquisition and consolidation of CTA. These results suggest that dopaminergic and noradrenergic release are related to the salience of conditioned taste stimuli. However, only cortical D1/D5 dopaminergic activity, but not the noradrenergic β1,2 activity, is involved in the acquisition and consolidation of taste memory formation. Additionally, glutamatergic activity signals visceral distress caused by LiCl administration and activates NMDA receptors necessary for the acquisition and consolidation of long-lasting taste aversion memory.

岛叶皮层 (IC) 在味觉识别记忆中起着至关重要的作用，包括条件性味觉厌恶 (CTA)。CTA 是一种学习范式，其中一种新的味觉刺激 (CS) 与胃不适 (US) 相关，在未来的遭遇中诱发对 CS 的厌恶。IC 在 CTA 记忆形成中的作用已被广泛研究。然而，在味觉刺激和胃不适诱导剂的呈现过程中神经递质释放的功能意义仍不清楚。在自由活动的动物中使用微透析，我们评估了谷氨酸、去甲肾上腺素和多巴胺释放的同时变化，以响应先天食欲或厌恶味觉新刺激的呈现，以及腹腔内施用等渗或高渗胃不适诱导溶液后的变化。我们的研究结果表明，无论其先天价如何，新刺激的呈现都会引起去甲肾上腺素和多巴胺的升高。胃不适诱导剂 (LiCl) 的施用促进谷氨酸的升高，无论其浓度如何。相比之下，去甲肾上腺素的释放与 LiCl 浓度及其等摩尔 NaCl 控制有关。此外，我们评估了它们在短期和长期味觉厌恶记忆中的功能作用。结果表明，IC 中去甲肾上腺素能 β1,2 受体的阻断可避免 CTA 采集和记忆巩固。相比之下，多巴胺 D1/D5 受体的阻断会损害 CTA 的巩固，而 NMDA 受体的阻断会阻碍 CTA 的获得和巩固。这些结果表明，多巴胺能和去甲肾上腺素能释放与条件味觉刺激的显着性有关。然而，只有皮质 D1/D5 多巴胺能活性，而不是去甲肾上腺素能 β1,2 活性，参与味觉记忆形成的获得和巩固。此外，谷氨酸能活性发出由 LiCl 给药引起的内脏不适的信号，并激活 NMDA 受体，这是获得和巩固长期味觉厌恶记忆所必需的。