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基底外侧杏仁核去甲肾上腺素能活动参与大鼠条件性气味厌恶的习得。

Basolateral amygdala noradrenergic activity is involved in the acquisition of conditioned odor aversion in the rat.

作者信息

Miranda Mari A Isabel, Ferry Barbara, Ferreira Guillaume

机构信息

Departamento de Neurobiologia Conductual y Cognitiva, Instituto de Neurobiologia, Universidad Nacional Autónoma de México, AP 1-1141, 76001 Querétaro, QRO, Mexico.

出版信息

Neurobiol Learn Mem. 2007 Sep;88(2):260-3. doi: 10.1016/j.nlm.2007.04.008. Epub 2007 May 30.

DOI:10.1016/j.nlm.2007.04.008
PMID:17540584
Abstract

Conditioned odor aversion (COA) is the avoidance of an odorized-tasteless solution (the conditioned stimulus, CS), the ingestion of which precedes toxicosis. Previous works have shown that the basolateral nucleus of the amygdala (BLA) is involved in the acquisition, and more precisely, the control of the CS memory trace, of COA. Since catecholamine depletion of the amygdala induced a deficit in the potentiated version of COA, this study investigated the role of the adrenergic system in the BLA during COA. Male Wistar rats bilaterally implanted with cannulae aimed at the BLA were microinjected with the beta-adrenergic antagonist propranolol (1 microg/0.2 microl) during the acquisition (5 min before the CS presentation, pre-CS, or immediately after, post-CS) or during the retrieval test (5 min before test, pre-test). Results showed that pre-CS, but neither post-CS nor pre-test, infusions of propranolol impaired COA, suggesting that beta-adrenergic system activity in the BLA is involved in the acquisition but not the expression of COA. Moreover, the fact that pre-CS, but not post-CS, treatment disrupted COA suggests that beta-adrenergic system in the BLA is involved in the initiation but not the maintenance of the CS memory trace during COA acquisition.

摘要

条件性气味厌恶(COA)是指对一种无味的加味溶液(条件刺激,CS)的回避,在摄入该溶液后会出现中毒症状。先前的研究表明,杏仁核基底外侧核(BLA)参与了COA的获得过程,更确切地说,参与了对CS记忆痕迹的控制。由于杏仁核的儿茶酚胺耗竭会导致COA强化版本出现缺陷,因此本研究调查了在COA过程中BLA内肾上腺素能系统的作用。在双侧植入针对BLA的套管的雄性Wistar大鼠中,在获得过程中(CS呈现前5分钟,即CS前,或之后立即,即CS后)或在检索测试期间(测试前5分钟,即测试前),向其微量注射β-肾上腺素能拮抗剂普萘洛尔(1微克/0.2微升)。结果显示,CS前注射普萘洛尔会损害COA,但CS后或测试前注射则不会,这表明BLA中的β-肾上腺素能系统活动参与了COA的获得,但不参与其表达。此外,CS前而非CS后治疗破坏了COA这一事实表明,BLA中的β-肾上腺素能系统在COA获得过程中参与了CS记忆痕迹的启动,但不参与其维持。

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