Freund G, Ballinger W E
Veterans Administration Medical Center, Gainesville, FL 32602.
Alcohol. 1988 Jul-Aug;5(4):275-82. doi: 10.1016/0741-8329(88)90065-1.
We hypothesize that chronic alcohol abuse results in a loss of neurons and their associated synaptic receptors. This encephalopathy may be a precursor of brain atrophy and end-stage dementia. Autopsies were performed on normal brains of 27 alcoholics (mean age 62.5) and 30 nonalcoholic matched controls (mean age 64.4) free of other brain and liver diseases. None had recently received benzodiazepine medications. Gross brain atrophy was slight and equal in both groups. Benzodiazepine receptor densities and affinities in homogenates of frontal cortex were determined using [3H]flunitrazepam. Bmax specific binding was reduced by 20% in alcoholics compared with nonalcoholic controls of comparable age and with similar death-autopsy time intervals. The affinity was slightly less in the alcoholics. Wet tissue brain protein concentrations and their yields of 50,000-g pellet proteins were similar. Aging, death-autopsy time intervals, pneumonia and chronic obstructive pulmonary disease (diseases usually associated with hypoxia) had no significant effect on brain proteins, receptor densities, or affinities. We conclude that chronic alcoholism is associated with a loss of benzodiazepine receptor densities. Alcohol abuse may affect the results of post-mortem neurochemical investigations of other diseases.
我们推测，长期酗酒会导致神经元及其相关突触受体的丧失。这种脑病可能是脑萎缩和终末期痴呆的先兆。对27名酗酒者（平均年龄62.5岁）和30名无其他脑部和肝脏疾病的非酗酒匹配对照者（平均年龄64.4岁）的正常大脑进行了尸检。没有人最近接受过苯二氮䓬类药物治疗。两组的脑萎缩程度均较轻且相当。使用[3H]氟硝西泮测定额叶皮质匀浆中的苯二氮䓬受体密度和亲和力。与年龄相当、死亡至尸检时间间隔相似的非酗酒对照者相比，酗酒者的Bmax特异性结合降低了20%。酗酒者的亲和力略低。脑组织湿重蛋白浓度及其50,000g沉淀蛋白产量相似。年龄、死亡至尸检时间间隔、肺炎和慢性阻塞性肺疾病（通常与缺氧相关的疾病）对脑蛋白、受体密度或亲和力没有显著影响。我们得出结论，慢性酒精中毒与苯二氮䓬受体密度降低有关。酗酒可能会影响其他疾病死后神经化学研究的结果。
