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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Redundant basal forebrain modulation in taste aversion memory formation.
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Redundant basal forebrain modulation in taste aversion memory formation.

机译：味觉厌恶记忆形成中的基础基础前脑调节。

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Mnemonic deficits resulting from excitotoxic lesion of the basal forebrain have been classically attributed to the resulting depletion of cortical acetylcholine activity. It has been demonstrated that in spite of the strong cholinergic depletion after injections into the basal forebrain of the immunotoxin 192IgG-saporin, no detectable deficit can be found in the acquisition of several learning tasks, including conditioned taste aversion. Conversely, NMDA-induced lesions of the basal forebrain strongly impair taste aversion learning. In this study we show that 192IgG-saporin produces an efficient and selective cholinergic deafferentation of the rat neocortex but not the amygdala. Furthermore, a stronger relationship between severity of memory impairment after NMDA lesions and basoamygdaloid cholinergic deafferentation was found. Therefore, in a second experiment, we show that combining NMDA-induced lesions into the basolateral amygdala with 192IgG-saporin injections into the basal forebrain results in a strong disruption of taste aversion learning, whereas none of these treatments were by themselves capable of producing any detectable impairment in this learning task. The double lesion effect was only paralleled by simple NMDA lesions into the basal forebrain, suggesting that the learning deficits associated to excitotoxic lesions of the basal forebrain are the result of the simultaneous destruction of the corticopetal and basoamygdaloid interaction. A model is proposed, according to which the modulation of learning processes exerted by the basal forebrain can be redundantly performed by both the basocortical and basoamygdaloid pathway.
机译：由基底前脑的兴奋性毒性损害引起的记忆缺陷通常归因于皮质乙酰胆碱活性的降低。已经证明，尽管在免疫毒素192IgG-saporin的基础前脑中注射后胆碱能很强地消耗，但是在完成一些学习任务，包括条件性厌恶中，没有发现可检测到的缺陷。相反，NMDA诱导的基底前脑病变严重损害了味觉厌恶的学习。在这项研究中，我们显示192IgG-saporin对大鼠新皮层产生了有效而选择性的胆碱能脱除咖啡因，但对杏仁核却没有。此外，发现NMDA损伤后记忆障碍的严重程度与基底淀粉样胆碱能脱除咖啡因之间的关系更强。因此，在第二个实验中，我们显示了将NMDA诱导的病变与基底外侧杏仁核相结合并向基础前脑注射192IgG-saporin会强烈破坏味觉厌恶学习，而这些疗法本身均不能产生任何在此学习任务中可检测到的障碍。双重损伤作用仅与简单的NMDA损伤并入基底前脑，这表明与基底前脑兴奋毒性损伤相关的学习缺陷是皮质足和基底淀粉样蛋白相互作用同时破坏的结果。提出了一种模型，根据该模型，基底皮质和基底淀粉样蛋白途径均可冗余地执行对基底前脑施加的学习过程的调节。

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