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Alcohol-related brain damage [1] [2] alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe , [ 3 ] limbic system , and cerebellum , [ 4 ] with widespread ...
Alcohol acts as a general central nervous system depressant, but it also affects some specific areas of the brain to a greater extent than others. Memory impairment caused by alcohol has been linked to the disruption of hippocampal function—particularly affecting gamma-Aminobutyric acid (GABA) and N-methyl-D-aspartate (NMDA) neurotransmission which negatively impacts long-term potentiation ...
In the past, alcohol was believed to be a non-specific pharmacological agent affecting many neurotransmitter systems in the brain, [25] but progress has been made over the last few decades. [ 26 ] [ 21 ] It appears that it affects ion channels, in particular ligand-gated ion channels , to mediate its effects in the CNS.
The long-term impact of alcohol on the brain has become a growing area of research focus. While researchers have found that moderate alcohol consumption in older adults is associated with better cognition and well-being than abstinence, [1] excessive alcohol consumption is associated with widespread and significant brain lesions.
Alcohol has a powerful effect on glutamate as well. Alcohol decreases glutamate's ability to bind with NMDA and acts as an antagonist of the NMDA receptor, which plays a critical role in LTP by allowing Ca2+ to enter the cell. These inhibitory effects are thought to be responsible for the "memory blanks" that can occur at levels as low as 0.03% ...
Alcohol (from Arabic al-kuḥl 'the kohl'), [11] sometimes referred to by the chemical name ethanol, is the second most consumed psychoactive drug globally behind caffeine. [12] Alcohol is a central nervous system (CNS) depressant, decreasing electrical activity of neurons in the brain. [13]
Alcohol can change the phosphorylation patterns to characterize alcohol-tolerant BK channels. [93] In addition, in rat magnocellular neurons it was shown that miRNA contributes to rapid and chronic ethanol tolerance by altering the expression of many proteins. [91] Rapid tolerance is defined as tolerance produced following a single ethanol ...
[74] [75] Other neurotransmitter systems are also involved, especially dopamine, NMDA and glutamate. [37] [76] Severe acute withdrawal symptoms such as delirium tremens and seizures rarely occur after 1-week post cessation of alcohol. The acute withdrawal phase can be defined as lasting between one and three weeks.