Cell Reactions in the Limbic Cerebral Cortex After Ethanol Poisoning, Alcohol Abstinence and Chronic Alcohol Intoxication in Humans
The aim of the study was to identify characteristics of the neuron reactions and macroglial cells in the limbic cerebral cortex after ethanol poisoning, alcohol withdrawal and chronic alcohol intoxication in humans. Material and methods. The study included Nissl stained histological sections in the area 24 b in healthy people (n=5), in people died from ethanol poisoning (in the period of ethanol resorption, n=5) and in people during alcohol withdrawal (at the end of ethanol elimination, n=5) having early signs of an alcohol disease. The number and proportion of neurons in identification groups (unmodified/low-modified, hypochromic, shriveled hyperchromic, “shadow cells”), the number of satellite cells and the ratio of satellite cells to the number of unchanged neurons (glio-neuronal index), the average area of the neuron bodies was calculated on horizontal sections of the anterior limbic cortex 1 mm<sup>2</sup> in area. Results. The study proposed to distinguish between acute (or transient), delayed and chronic response of neuronal cells. The acute reaction that develops during ethanol poisoning is expressed by acute swelling of neurons and results from a combination of altering factors: the toxic effects of ethanol and the overproduction of catecholamines. The acute reaction is more pronounced in the dopaminergic layer III of the anterior limbic cortex than in layer V. It is transient, since in the period of alcohol withdrawal (ethanol elimination) it regresses and becomes delayed. The latter is to increase and dominate the proportion of atrophic reduced in the size of low-modified and atrophic wrinkled neurons, increased phagocytic activity of dead neurons, as well as the development of compensatory-adaptive reaction of the satellite form of glia, the most pronounced in layer III. Delayed reaction of neurons is due to the weakening and cessation of acute effects of toxicants; as a result, the signs of previous long-term intoxication effects of ethanol, its toxic metabolites and increased concentrations of catecholamines, which caused cell atrophy, come to the fore. Chronic cell response is expressed by a significant increase in the proportion of neurons-"shadows", the number of macroglial cells and atrophic wrinkling of neurons. In people with early manifestations of an alcohol disease, signs of acute neuronal damage are combined with signs of atrophic ones.