The Effects Of Alcohol Abuse

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Alcohol dependence and alcohol abuse involve drinking patterns in which periods of heavy drinking followed with periods of abstinence. Alcohol generally has a suppressive effect on the central nervous system (CNS): It reduces the activity of excitatory neurotransmitters and enhances the activity of inhibitory neurotransmitters and thus their receptors. After long-term alcohol exposure, the body activates a set of mechanisms to counteract the effects of alcohol’s persistent presence in the brain. These mechanisms promote the activity of excitatory neurotransmitter systems and suppress the activity of inhibitory neurotransmitter systems, thereby attempting to return brain function to a “normal” state in the presence of alcohol. When the individual stops drinking, however, these adaptive changes result in an imbalance in inhibitory and excitatory neurotransmission, resulting in CNS hyperexcitability that produces as alcohol withdrawal (AW) symptoms. This essay will focus on the main inhibitory and excitatory neurotransmission systems and the symptoms produced in AW due to the imbalance in the brain. Followed by outlining other physiological changes alterations that are associated with AW. The primary inhibitory neurotransmitter in the brain is the gamma-aminobutyric acid (GABA), which exerts its effects mainly through the GABAAreceptor. Alcohol exposure results in activation of the GABAAreceptor, which in turn leads to reduced postsynaptic nerve excitability and thus contribute to alcohol’s sedative effects. In response to chronic alcohol exposure, the CNS adapts to the alcohol-induced GABAA activation by reducing GABA-mediated neurotransmission. Thus after chronic alcohol exposure and during withdrawal, GABA activity at the synapse... ... middle of paper ... ...e levels can affect seizure susceptibility, and produce neural damage. Another neurochemical perturbation as a result of AW is decreased dopamine function. Dopamine-mediated neurotransmissions in various regions plays a key role in mediating the dysphoria associated withdrawal from alcohol and thus reduced function alters perception of alcohol effects. These physiological changes result in withdrawal symptoms, including seizures, anxiety, toxic effects on nerve cells, and altered perception of alcohol’s effects. Any of those symptoms may increase the patient’s potential for relapse and vulnerability to brain damage. With a drinking pattern of repeated bingeing and abstaining, the imbalance occurring during withdrawal may intensify with each successive episode and may culminate in a state of persistent CNS hyperexcitability seen as a augmented withdrawal response.

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