I just remember that the walls are with wallpaper…
Everyone knows people who, even after a fair libation, can continue to have fun and communicate, while looking quite sane. However, the next morning it turns out that they don't remember most of the party. Such periods of amnesia or "memory lapses" can last from several minutes to several hours.
Neuroscientists at the University of Washington, working under the guidance of Professor Charles F. Zorumski, identified brain cells and molecular mechanisms to blame for the lack of memories. It turned out that, contrary to popular belief, large doses of alcohol do not kill nerve cells. Instead, ethanol first suppresses and then stimulates the activity of NMDA receptors in nerve cells that selectively bind N-methyl-D-aspartate (NMDA), which is necessary for the transmission of nerve impulses between neurons. This triggers the synthesis of steroid hormones, which, in turn, suppress the process of long–term potentiation - the strengthening of contacts between neurons (synapses) necessary for learning and the formation of memories.
The synaptic plasticity underlying memory formation – the possibility of changing the strength of interaction between neurons – is due to the regulation of the activity level of various synaptic receptors. The cells exposed to alcohol are located in the hippocampus and other brain structures responsible for the cognitive function of the brain and the formation of long-term memory.
Experiments on slices of rat hippocampal tissue have shown that exposure to moderate doses of alcohol does not affect the activity of NMDA receptors in any way. As it turned out, high doses also not only do not kill cells "on the spot", but also do not disrupt their ability to interact with each other. However, at the same time, NMDA receptors begin to behave, at first glance, contradictory. The activity of some of the receptors is blocked, after which other NMDA receptors are activated. The result of this paradoxical reaction is the launch of the production of steroid hormones that disrupt the formation of memory.
Under the influence of high doses of alcohol, hippocampal neurons produce steroid hormones
(on the left, bright green), suppressing memory formation.
The neurons of the same brain region are shown on the right,
not exposed to alcohol.
Thus, alcohol does not damage nerve cells and does not deprive them of the ability to process information, they simply stop assimilating it. Stressful effects and the use of other narcotic substances can also block the formation of memory, so the combination of alcohol with other "recreational drugs" can increase the likelihood of subsequent amnesia.
The researchers also found that blocking the synthesis of steroids by neurons using alpha-reductase enzyme inhibitors currently prescribed to men with prostatic hyperplasia (finasteride and dutasteride) preserves the activity of mechanisms that ensure long-term potentiation of synapses in the hippocampus. Therefore, it can be assumed that taking drugs of this group can change a person's reaction to alcohol consumption for the better.
In the near future, scientists plan to study the ability of alpha-reductase enzyme inhibitors to penetrate the blood-brain barrier into brain tissue and the possibility of using such drugs to improve memory.
Article by Kazuhiro Tokuda et al. Ethanol Enhances Neurosteroidogenesis in Hippocampal Pyramidal Neurons by Paradoxical NMDA Receptor Activation published July 6 in The Journal of Neuroscience.
Evgeniya Ryabtseva
Portal "Eternal youth" www.vechnayamolodost.ru based on the materials of Washington University School of Medicine – The biology behind alcohol-induced blackouts.
11.07.2011