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Glucocorticoids enhance taste aversion memory via actions in the insular cortex and basolateral amygdala

机译:糖皮质激素通过在岛叶皮层和基底外侧杏仁核中的作用增强味觉记忆

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摘要

It is well established that glucocorticoid hormones strengthen the consolidation of hippocampus-dependent spatial and contextual memory. The present experiments investigated glucocorticoid effects on the long-term formation of conditioned taste aversion (CTA), an associative learning task that does not depend critically on hippocampal function. Corticosterone (1.0 or 3.0 mg/kg) administered subcutaneously to male Sprague–Dawley rats immediately after the pairing of saccharin consumption with the visceral malaise-inducing agent lithium chloride (LiCl) dose-dependently increased aversion to the saccharin taste on a 96-h retention test trial. In a second experiment, rats received corticosterone either immediately after saccharin consumption or after the LiCl injection, when both stimuli were separated by a 3-h time interval, to investigate whether corticosterone enhances memory of the gustatory or visceral stimulus presentation. Consistent with the finding that the LiCl injection, but not saccharin consumption, increases endogenous corticosterone levels, corticosterone selectively enhanced CTA memory when administered after the LiCl injection. Suppression of this training-induced release of corticosterone with the synthesis-inhibitor metyrapone (35 mg/kg) impaired CTA memory, and was dose-dependently reversed by post-training supplementation of corticosterone. Moreover, direct post-training infusions of corticosterone into the insular cortex or basolateral complex of the amygdala, two brain regions that are critically involved in the acquisition and consolidation of CTA, also enhanced CTA retention, whereas post-training infusions into the dorsal hippocampus were ineffective. These findings provide evidence that glucocorticoid effects on memory consolidation are not limited to hippocampus-dependent spatial/contextual information, but that these hormones also modulate memory consolidation of discrete-cue associative learning via actions in other brain regions.
机译:公认的是,糖皮质激素增强了海马依赖性空间和背景记忆的巩固。本实验研究了糖皮质激素对条件性味觉厌恶症(CTA)长期形成的影响,这是一项与学习无关的,不依赖于海马功能的相关学习任务。糖精摄入与内脏不适感药物氯化锂(LiCl)配对后,立即对雄性Sprague-Dawley大鼠皮下注射皮质酮(1.0或3.0 mg / kg),在96小时内剂量依赖性地增加了对糖精味的厌恶保留测试试验。在第二个实验中,大鼠在服用糖精后立即或在注射LiCl后立即以3小时的时间间隔分离皮质激素,以研究皮质酮是否增强味觉或内脏刺激表现的记忆。与发现LiCl注射而不是糖精消耗增加内源性皮质酮水平的发现一致,当在LiCl注射后给药时,皮质酮选择性增强CTA记忆力。用合成抑制剂甲吡酮(35 mg / kg)抑制训练诱导的皮质酮释放会损害CTA记忆力,并且在训练后补充皮质酮会剂量依赖性地逆转。此外,将训练后的皮质酮直接注入杏仁核的岛状皮层或基底外侧复合体(两个关键区域参与CTA的获取和合并)也增强了CTA的保留,而训练后向背侧海马中的输注是无效的。这些发现提供了证据,糖皮质激素对记忆巩固的作用不仅限于海马依赖的空间/语境信息,而且这些激素还通过其他大脑区域的动作来调节离散线索联想学习的记忆巩固。

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