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Gustatory Insular Cortex Lesions Disrupt Drug-Induced, but Not Lithium Chloride-Induced, Suppression of Conditioned Stimulus Intake

机译:味觉岛状皮层病变破坏药物诱导的但不刺激氯化锂诱导的条件刺激摄入的抑制

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摘要

Rats suppress intake of a normally preferred 0.15% saccharin conditioned stimulus (CS) when it is paired with an aversive agent like lithium chloride (LiCl) or a preferred substances such as sucrose or a drug of abuse. The reward comparison hypothesis suggests that rats avoid intake of a saccharin cue following pairings with a drug of abuse because the rats are anticipating the availability of the rewarding properties of the drug. The present study used bilateral ibotenic acid lesions to examine the role of the gustatory cortex in the suppression of CS intake induced by cocaine, morphine, and LiCl. The results show that bilateral lesions of the insular gustatory cortex (1) fully prevent the suppressive effects of both a 15 and a 30 mg/kg dose of morphine, (2) attenuate the suppressive effect of a 10 mg/kg dose of cocaine, but (3) are overridden by a 20 mg/kg dose of the drug. Finally, these same cortical lesions had no impact on LiCl-induced conditioned taste aversion. The current data show that the insular taste cortex plays an integral role in drug-induced avoidance of a gustatory CS.
机译:当与厌食剂(如氯化锂(LiCl))或首选物质(如蔗糖或滥用药物)配对使用时,大鼠会抑制通常优选的0.15%糖精条件刺激物(CS)的摄入。奖励比较假说表明,大鼠避免与滥用药物配对后摄入糖精提示,因为大鼠预期该药物的奖励特性将可用。本研究使用双侧ibotenic acid病变来检查味觉皮质在抑制可卡因,吗啡和LiCl诱导的CS摄入中的作用。结果表明,岛上味觉皮质的双侧病变(1)完全阻止了15和30 mg / kg剂量的吗啡的抑制作用;(2)减弱了10 mg / kg剂量的可卡因的抑制作用;但(3)被20 mg / kg剂量的药物取代。最后,这些相同的皮质病变对LiCl诱导的条件性味觉厌恶没有影响。目前的数据表明,在药物诱导的味觉性CS回避中,岛s味皮层起着不可或缺的作用。

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