Please help, research about alchohol effecting brain....

[Kingpin]

i was given a topic on research about ethanol affecting our brain. fortunately i just have to do a little 10 minute speech, can someone knowledgeable here please sum up the effects of ethanol on our brains. thanks alot.

[Stars]

I've been assigned to do research on topic like this one in a U before, and luckily for you I have it saved in Word format on my PC.

It is a common assumption that light drinking can stimulate thinking and that heavier drinking has only temporary harmful effects on brain function. Brain damage to alcoholics is attributed to malnutrition rather than to neurotoxicity of ethanol. However, these assumptions should be questioned.

Even low doses (blood alcohol concentration 0.4%) of alcohol reduces response-time and error-rate of performance. And moderate doses of ethanol induce "a significant deterioration of capacity to detect the activation of erroneous responses." Even blood alcohol levels of 0.1% markedly impair visuospatial skills (for driving, flying or operating machinery) associated with the right parietal region of the brain.

Animal experiments have demonstrated that bouts of binge drinking can produce necrotic neurodegeneration in the areas of the brain most closely associated with the hippocampus. The demonstration of such gross damage should raise the suspicion of brain damage below the threshold of laboratory detection with lesser amounts of alcohol. Cumulative permanent neurological damage on repeated bouts of drinking -- even if small -- should be of particular concern for those who strive for longevity.

Light drinking increases social conversation and reduces inhibition among virtually all people who consume alcoholic beverages on social occasions. The effects are particularly dramatic for some people suffering from high anxiety. Light drinking can also increase violent aggression in some people. Yet the same doses of ethanol producing these seemingly stimulant effects usually reduce performance on complex tasks.

Ethanol exerts its primary effects through modulation of action of a number of brain neurotransmitters, notably subtypes of receptors for GABA, glutamate, serotonin and acetylcholine, among others (particularly the first two). Ethanol also reversibly reduces sodium transport in neurotransmission.

"GABA (Gamma-AminoButyric Acid) is the major inhibitory neurotransmitter in the brain. By increasing the inflow of chloride (Cl-) across neural membranes, GABA opposes the tendency of neurons to depolarize. Ethanol augments the influx of chlorine ions due to GABA, which has much to do with the sedative, tranquilizing and/or anaesthetic properties of beverage alcohol. Yet ethanol does not have this effect on all GABA receptors, only the GABA A subtypes containing subunits that can be phosphorylated with Protein Kinase C (PKC)." [BRAIN RESEARCH]

The second brain neurotransmitter receptor most strongly affected by ethanol is the NMDA (N-Methyl-D-Aspartate) receptor for glutamic acid (glutamate). Ethanol, especially in high doses associated with heavy drinking, is a potent inhibitor of the NMDA receptor. NMDA function in the hippocampus is associated with memory formation through a process known as LTP (Long-Term Potentiation). Ethanol produces a dose-dependent suppression of the magnitude of LTP. Ethanol produces a dose-dependent suppression of the magnitude of LTP. In high doses ethanol can block LTP almost entirely. LTP blockage is the likely explanation for the fact that after an evening of heavy drinking, 30-40% of males in their late teens or early twenties experience a blackout which eliminates all or part of their memory of what occurred while drinking.

Serotonin, a braint neurotransmitter, regulates slow-wave sleep, but serotonin activity is reduced during Rapid Eye Movement (REM) sleep (which is regulated by noradrenalin). Ethanol potentiates serotonin activity, thereby suppressing REM sleep. Low doses of ethanol can enhance acetylcholine's muscarinic activation of the hippocampus (thereby opposing some of the NMDA blockage), but higher doses depress the acetylcholine effect. Ethanol increases dopamine release in the nucleus accumbens, a brain "pleasure center" similarly activated by *******. Ethanol also acts on voltage-gated calcium channels and adenosine receptors.

Pharmacological disruptions in brain signalling probably lead to erroneous thoughts & memories which accumulate and may be hard to remove -- even if there is no permanent physiological damage. Such effects would be difficult to detect unless they were gross, in part because no individual person has a control subject.

[Stars]

Ethanol is known to produce both tolerance and withdrawal. Tolerance refers to the fact that an increasingly higher dose of the drug is required to produce the same effect. Dependence refers to the fact that withdrawal of the drug produces unpleasant physiological effects. Ethanol withdrawal symptoms include tremor, anxiety, aberrations in body temperature and potentially fatal convulsions.

Alcohol tolerance & withdrawal can be attributed to compensatory synaptic plasticity, particularly an adaptive increase in NMDA receptors. Hyperexcitablility of NMDA receptors is associated with the withdrawal convulsions and an increase in ischemic excitotoxicity.

Nutritional deficiency is certainly a factor in alcoholic brain damage. Alcohol amnesic disorder (Korsakoff's Disease) is usually associated to a deficiency of Vitamin B1 (Thiamine). Lesions are found in the thalamus and mammillary bodies as well as in the hippocampus.

But even in the absence of nutritional deficiency, chronic alcoholics show significant reduction of white matter and reduction of neuron density, particularly in the prefrontal cortex, the cerebellum and the amygdala. Reductions in cerebral blood flow & brain function (observed when not under the immediate influence of alcohol) have been demonstrated in heavy drinkers with no nutritional deficiencies and whose ethanol consumption was less than that typically seen in alcoholics.

Females are more sensitive to brain damage by ethanol than are males. The unborn foetus is also highly sensitive to brain damage by ethanol -- in the extreme cases leading to Fetal Alcohol Syndrome (FAS), a condition characterized by facial disfigurement, growth retardation and brain damage (particularly to the corpus callosum, basal ganglia and cerebellum). Although clinically obvious FAS only occurs in a small percentage of alcoholic mothers, pregnant women are well advised to abstain from drinking ethanol. Serotonin is a trophic factor for brain development -- and serotonin is significantly decreased in a foetus exposed to ethanol. Experiments on neonatal rats indicate that the combination of aspirin & ethanol results in a greater reduction of brain weight than either aspirin or ethanol alone.

Acetaldehyde in the brain & liver forms adducts (attachments) to DNA, thiamine (worstening Korsakoff's Disease), enzymes (inactivating them) and tubulin. By binding the lysine of tubulin protein, acetaldehyde prevents the polymerization necessary for microtubule formation. Microtubules in neurons are essential for transport of proteins, nutrients and organelles along the long axons.

Binding of reduced glutathione (GSH) and/or cysteine by acetaldehyde causes marked decreases in GSH after acute or chronic ethanol intoxication. But increases in free-radical production with ethanol is not simply due to reduction in GSH. Ethanol has been shown to increase lipid peroxidation by 21.8% in the brain, but higher increases are seen in the heart (28.8%), lung (35.9%) and testes (45.3%). Isolated synaptosomes (presynaptic membrane-containing vesicles) subjected to ethanol show considerable oxidative damage.