Anda di halaman 1dari 4

Alcohol The Chemical Hand Grenade: The effects of alcohol on neurotransmitters.

Todd Stephenson 41783743

Introduction For optimal functionality the brain requires a steady equilibrium between inhibitory and excitatory neurotransmission which is the outcome of communication between two cells via neurotransmitters. Neurotransmitters are chemicals that help electrical signals pass from neuron. Each of these neurotransmitters has specific functions such as acetylcholine which inhibits muscular contraction, or serotonin which will control someones mood. Many other drugs only affect a single neurotransmitter due to factors such as size and shape but this is not the case with alcohol which is why it is commonly referred to as the chemical hand grenade. Acetylcholine and serotonin, along with all other neurotransmitters are greatly affected by the consumption of alcohol due to the fact that alcohol is a fat soluble molecule which allows it to easily enter the lipid rich cell membranes of neurons. On these neurons are the receptors of the neurotransmitters that are drastically affected. The invasion of alcohol also alters the release of the neurotransmitter which can result in various short and long-term affects on the neurotransmitters, their receptors and the brain itself. Short-term affects The main neurotransmitters and receptors that are affected by alcohol are the glutamate, gamma-aminobutyric (GABA) and the dopamine and endorphin systems as seen in figure 1.1.

Figure 1.1 The neurotransmitters most affected by the intake of alcohol.

The glutamate receptor function is inhibited from alcohol and will incur in slurred speech and muscular relaxation, staggering and blackouts. This will display many of the noticeable signs of an intoxicated person, It is alcohols effect on the glutamate receptor that will lead to slurred speech and staggering (Anderson, 2010). The GABA system is enhanced as it allows the body to relax and enter a calm anxiousfree state. Dopamine levels are raised as a result of alcohol consumption very similar to the way that cocaine operates. While all this is taking place the endorphins are raised to a level far higher than what is usually is experienced and has a similar affect to that of heroin. This shows how severe the affects of alcohol can be especially in heavy consumption as it mimics many of the same experiences that are present while using dangerous illicit drugs with depressant and stimulant characteristics operating in unison. The raid of alcohol into the cell membranes of neurons will affect different people in different ways. Some may feel sleepy and drowsy after ingesting alcohol where other people may be upbeat an energetic. These findings would suggest that the sleepy drinkers may have experienced more effects on the GABA system whereas the more lively and upbeat type will have found more drastic consequences on their dopamine system. Once the alcohol is metabolised and completely out of the system the body continues to struggle to return to equilibrium due to a side affect called neurotransmitter rebound. While alcohol is in the system and the neurotransmitters are being altered and are fighting against the affects of the alcohol. As a result of this, once the alcohol does leave the system the affected neurotransmitter will surpass equilibrium now producing too much of what was previously required to fight the alcohol. Reasons such as this display why alcohol is not an ideal sleep aid as it will leave the person wide awake in the middle of the night as the GABA system will overshoot stasis leaving them alert and unable to fall back to sleep. When alcohol is in your body you get less of the deep sleep you need to wake up feeling refreshed, Your more likely to wake up during the night (Epstein and Mardon, 2006). The area in the brain that is responsible for these long-term memories is known as the hippocampus. The hippocampus relies on the firing of the neurotransmitters in that area to create long-term potentiation (LTP). For this to function properly, LTP will rely on the firing on glutamate receptors and the inhibition of GABA receptors so as to form these long-term memories. This has been studied and well documented as displayed by Sullivan (1990) who states it has been shown that alcohol administration will block long term potentiation induced by calcium in the hippocampal slice. As it is known that the short-term intake of alcohol is responsible for decreasing the LTP in the hippocampus displaying that alcohol is already eating away at the brain and its long-term memory storage even in short-term use. Long-term affects As mentioned above, the ingestion of alcohol may have many behavioural impacts on the neurotransmitters of the body that mimic the characteristics of other illicit drugs, however the long term effects of alcohol intake on the neurotransmitters will result in greater complications. Once heavy, long-term alcohol intake is abruptly halted the body will experience the same neurotransmitter rebound affects that is evident in light, short-term alcohol intake but will be experienced in a far greater capacity

leading to severe cravings for alcohol with alcohol withdrawal syndrome. These withdrawals come as the body becomes so used to having the alcohol in its system chronic use of alcohol down regulates the GABA system and the neuron actually becomes dependent on the alcohol to function (Frances, 2005). This is a result of the brain decreasing inhibitory neurotransmission and increase excitatory neurotransmission which opposes the affects of short-term alcohol consumption which can be seen also be seen in the GABA system, This decrease in GABA function may result from a decrease in receptor levels or a change in the protein composition of the receptor, leading to decreased sensitivity to neurotransmission (Valenzuela, 1997). The long-term alcoholism will also lead to great deterioration of the brain and the majority of its components as seen in figure 1.2.

Figure 1.2. The effects on the brain of a normal 43 year old compared to a long-term heavy drinking 43 year old. Heavy consumption of alcohol can do great damage to the brain through WernickeKorsakoff syndrome which is more commonly known as wet brain. This syndrome is caused from a vitamin B1 or thiamine deficiency. This is characterised with symptoms such as amnesia, confusion, hallucinations, short-term memory loss and inability to form new memories. This is stated by Knight and Longmore in 1996 when they noted Korsakoff patients appear to have memories from their earlier life but know little of their recent history. This is all a result of the brains inability to absorb thiamine and is in some cases able to be treated with thiamine but is in many cases irreversible. Conclusion The good news for those drinking alcohol is that signs of marked improvement of structure and functioning in the brain are shown within a year of abstinence. This time away from alcohol allows for regeneration of new cells and growth and repair of the existing cells. However the impact of alcohol on the drinkers neurotransmitters and their receptors will have an entirely different effect and may leave the long-term drinker severe damage and brain loss, not to mention the social and psychological degeneration of the life. Alcohol has earned its nickname as the chemical hand grenade and should only ever be consumed in moderation if at all.

References Anderson, K. (2010) How to change your drinking. A harm reduction guide to alcohol. The HAMS harm reduction network. Epstein, L., Mardon, S. (2006) The Harvard Medical School guide to a good nights sleep. Mcgraw-Hill. New York. Frances, R., Miller, S. and Mack, A. (2005) Clinical textbook of addictive disorders. The Guilford Press, New York. Knight, R., G., Longmore, B.,E. (1996) Clinical Neuropsychology of Alcoholism. Laurence Earlbaum Associates LTD. Morrissett, R., A. and Swartzwelder, H., S. (1993) Attenuation of hippocampal longterm potentiation by ethanol: A patch-clamp analysis of glutamatergic and GABAergic mechanisms. Journal of Neuroscience 13:22642272. Sullivan, L. (1990) Alcohol and health: From the secretary and health and human services. US department of health and human services. National institute on alcohol abuse and alcoholism. Tabakoff, B., and Hoffman, P.L. (1996) Alcohol addiction: An enigma among us. Neuron 16:909912. Valenzuela, C., F. (1997) Alcohol and Neurotransmitter Interactions. Journal of Alcohol, Health and Research. Vol 21. No. 2: 144-148.