Miguel-Hidalgo José J, Rajkowska Grazyna
Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson 39216, USA.
J Psychiatr Res. 2003 Sep-Oct;37(5):411-20. doi: 10.1016/s0022-3956(03)00049-9.
Chronic alcohol abuse is often co-morbid with depression symptoms and in many cases it appears to induce major depressive disorder. Structural and functional neuroimaging has provided evidence supporting some degree of neuropathological convergence of alcoholism and mood disorders. In order to understand the cellular neuropathology of alcohol dependence and mood disorders, postmortem morphometric studies have tested the possibility of alterations in the number and size of cells in the prefrontal cortex and other brain regions. The present review compares the cell pathology in the prefrontal cortex between alcohol dependence and depression, and reveals both similarities and differences. One of the most striking similarities is that, although pathology affects both neuronal and glial cells, effects on glia are more dramatic than on neurons in both alcohol dependence comorbid with depression and idiopathic depression. Moreover, prefrontal cortical regions are commonly affected in both depression and alcoholism. However, the cellular changes are more prominent and spread across cortical layers in alcohol dependent subjects than in subjects with mood disorders, and changes in glial nucleus size are opposite in alcoholism and depression. It could be argued that one defining factor in the manifestation of the depressive pathology is a reduction in the glial distribution in the dlPFC that is reflected in a reduced glial density. In alcoholism reduced glial nuclear size might be related to the cytotoxic effects of prolonged alcohol exposure, while in MDD, in the absence of alcohol abuse, other processes might be responsible for the increase in average size of glial nuclei. In either case abnormal function related to glial reduction would be associated with depression due to insufficient glial support to the surrounding neurons.
长期酗酒常与抑郁症状并存，在许多情况下，它似乎会诱发重度抑郁症。结构和功能神经影像学已提供证据，支持酒精中毒和情绪障碍在一定程度上存在神经病理学趋同现象。为了了解酒精依赖和情绪障碍的细胞神经病理学，尸检形态学研究检验了前额叶皮质和其他脑区细胞数量和大小发生改变的可能性。本综述比较了酒精依赖和抑郁症患者前额叶皮质的细胞病理学，揭示了两者的异同。最显著的相似之处之一是，尽管病理学对神经元和胶质细胞均有影响，但在合并抑郁症的酒精依赖和特发性抑郁症中，对胶质细胞的影响比对神经元的影响更为显著。此外，前额叶皮质区域在抑郁症和酒精中毒中通常都会受到影响。然而，与情绪障碍患者相比，酒精依赖患者的细胞变化更显著，且遍布皮质各层，而且酒精中毒和抑郁症患者胶质细胞核大小的变化相反。可以认为，抑郁病理学表现的一个决定性因素是背外侧前额叶皮质中胶质细胞分布减少，这表现为胶质细胞密度降低。在酒精中毒中，胶质细胞核大小减小可能与长期接触酒精的细胞毒性作用有关，而在重度抑郁症中，在没有酗酒的情况下，其他过程可能导致胶质细胞核平均大小增加。无论哪种情况，与胶质细胞减少相关的异常功能都可能因胶质细胞对周围神经元支持不足而导致抑郁症。
