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首页> 外文期刊>The European Journal of Neuroscience >Excessive disgust caused by brain lesions or temporary inactivations: mapping hotspots of the nucleus accumbens and ventral pallidum
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Excessive disgust caused by brain lesions or temporary inactivations: mapping hotspots of the nucleus accumbens and ventral pallidum

机译：由脑部病变或暂时性失活引起的过度厌恶：绘制伏隔核和腹侧苍白球的热点

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摘要

Disgust is a prototypical type of negative affect. In animal models of excessive disgust, only a few brain sites are known in which localized dysfunction (lesions or neural inactivations) can induce intense disgust reactions' (e.g. gapes) to a normally pleasant sensation such as sweetness. Here, we aimed to map forebrain candidates more precisely, to identify where either local neuronal damage (excitotoxin lesions) or local pharmacological inactivation (muscimol/baclofen microinjections) caused rats to show excessive sensory disgust reactions to sucrose. Our study compared subregions of the nucleus accumbens shell, ventral pallidum, lateral hypothalamus, and adjacent extended amygdala. The results indicated that the posterior half of the ventral pallidum was the only forebrain site where intense sensory disgust gapes in response to sucrose were induced by both lesions and temporary inactivations (this site was previously identified as a hedonic hotspot for enhancements of sweetness liking'). By comparison, for the nucleus accumbens, temporary GABA inactivations in the caudal half of the medial shell also generated sensory disgust, but lesions never did at any site. Furthermore, even inactivations failed to induce disgust in the rostral half of the accumbens shell (which also contains a hedonic hotspot). In other structures, neither lesions nor inactivations induced disgust as long as the posterior ventral pallidum remained spared. We conclude that the posterior ventral pallidum is an especially crucial hotspot for producing excessive sensory disgust by local pharmacological/lesion dysfunction. By comparison, the nucleus accumbens appears to segregate sites for pharmacological disgust induction and hedonic enhancement into separate posterior and rostral halves of the medial shell.
机译：厌恶是负面影响的典型代表。在过度厌恶的动物模型中，只有少数几个大脑部位的局部功能障碍（病变或神经失活）会引起强烈的厌恶反应（例如，气孔），使人感到正常的愉悦感（如甜味）。在这里，我们旨在更精确地绘制前脑候选者的图谱，以确定局部神经元损伤（兴奋毒素损伤）或局部药理失活（muscimol / baclofen显微注射）导致大鼠对蔗糖表现出过度的感觉厌恶反应的地方。我们的研究比较了伏隔核壳，腹侧苍白球，下丘脑外侧和邻近的延伸杏仁核等亚区域。结果表明，腹侧后半部是唯一的前脑部位，在该部位前部病变和暂时性失活均引起强烈的对蔗糖的厌恶感（该部位以前被认为是享乐性增强的喜乐热点'）。 。相比之下，对于伏伏核，内侧壳尾半部的暂时性GABA失活也会产生感觉上的厌恶，但病变从未在任何部位发生。此外，即使灭活也不能引起伏伏贝壳的前半部（也包含享乐性热点）的厌恶感。在其他结构中，只要保留后腹侧苍白球，病变和灭活都不会引起厌恶感。我们得出结论，后腹侧苍白球是通过局部药理/病变功能障碍产生过度感觉厌恶的特别关键的热点。相比之下，伏隔核似乎将药理恶心诱导和享乐性增强的位点分离成内侧壳的后半部和延髓部。

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