成瘾性突触：伏隔核中突触和结构可塑性的机制。
The addicted synapse: mechanisms of synaptic and structural plasticity in nucleus accumbens.
机构信息
Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.
出版信息
Trends Neurosci. 2010 Jun;33(6):267-76. doi: 10.1016/j.tins.2010.02.002. Epub 2010 Mar 5.
Abstract
Addictive drugs cause persistent restructuring of several neuronal cell types in the limbic regions of brain thought to be responsible for long-term behavioral plasticity driving addiction. Although these structural changes are well documented in nucleus accumbens medium spiny neurons, little is known regarding the underlying molecular mechanisms. Additionally, it remains unclear whether structural plasticity and its synaptic concomitants drive addictive behaviors or whether they reflect homeostatic compensations to the drug not related to addiction per se. Here, we discuss recent paradoxical data, which either support or oppose the hypothesis that drug-induced changes in dendritic spines drive addictive behavior. We define areas where future investigation can provide a more detailed picture of drug-induced synaptic reorganization, including ultrastructural, electrophysiological and behavioral studies.
摘要
成瘾药物会导致大脑边缘区域中几种神经元细胞类型的持续重构，这些区域被认为是导致成瘾的长期行为可塑性的原因。尽管在伏隔核中间神经元中已经很好地记录了这些结构变化，但对于潜在的分子机制知之甚少。此外，尚不清楚结构可塑性及其突触伴随物是否驱动成瘾行为，或者它们是否反映了与成瘾本身无关的药物的稳态补偿。在这里，我们讨论了最近一些矛盾的数据，这些数据要么支持，要么反对药物引起的树突棘变化驱动成瘾行为的假说。我们定义了未来研究可以提供更详细的药物引起的突触重组图景的领域，包括超微结构、电生理和行为研究。
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