Short Paper on Gaba & Alcoholism
GABA
Gamma-aminobutyric acid , also known as GABA for short is a neurotransmitter found in the human nervous system. GABA is known to cause nerves to “calm down” due to its inhibitory function.
GABA, incidentally, cannot be taken orally or assist the brain GABA levels to increase due to the blood-brain barrier, which prohibits it from entering the central nervous system. Instead, there is a class of drug, called the benzodiazepine-receptor-agonist (BzRA) family that can assist GABA to bind to receptor sites in the brain. This class of drugs includes the well known valium, and related drugs such as Ambien and Lunesta, sleep medications. Despite the blood-brain barrier issue, orally ingested GABA is suggested to cause physiological changes that can benefit hypertension.
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Scientists have known for several years that alcohol produces many of its intoxicating actions through facilitation of GABA receptor function, and preclinical studies of alcohol dependence have shown that GABAergic activity decreases during alcohol withdrawal and protracted abstinence--the initial post-acute withdrawal period after the cessation of drinking during which a person is especially vulnerable to relapse. These GABAergic activity changes are probably a major cause of relapse to alcoholism in individuals undergoing treatment.
Previous studies have also shown that alcohol enhances GABA neurotransmission in the amygdala, the so-called pleasure center of the brain. Interestingly, the brain corticotropin releasing factor (CRF) stress system also increases GABA transmission in the amygdala.
A team of scientists at The Scripps Research Institute has described the cellular mechanism underlying the brain's response to alcohol, which suggests a possible method for treating alcoholism.
This work, published in the latest issue of the journal Science, ties together the effect of the brain peptide corticotropin releasing factor (CRF) with alcohol. Both appear to influence
Gamma-aminobutyric acid , also known as GABA for short is a neurotransmitter found in the human nervous system. GABA is known to cause nerves to “calm down” due to its inhibitory function.
GABA, incidentally, cannot be taken orally or assist the brain GABA levels to increase due to the blood-brain barrier, which prohibits it from entering the central nervous system. Instead, there is a class of drug, called the benzodiazepine-receptor-agonist (BzRA) family that can assist GABA to bind to receptor sites in the brain. This class of drugs includes the well known valium, and related drugs such as Ambien and Lunesta, sleep medications. Despite the blood-brain barrier issue, orally ingested GABA is suggested to cause physiological changes that can benefit hypertension.
------------------
Scientists have known for several years that alcohol produces many of its intoxicating actions through facilitation of GABA receptor function, and preclinical studies of alcohol dependence have shown that GABAergic activity decreases during alcohol withdrawal and protracted abstinence--the initial post-acute withdrawal period after the cessation of drinking during which a person is especially vulnerable to relapse. These GABAergic activity changes are probably a major cause of relapse to alcoholism in individuals undergoing treatment.
Previous studies have also shown that alcohol enhances GABA neurotransmission in the amygdala, the so-called pleasure center of the brain. Interestingly, the brain corticotropin releasing factor (CRF) stress system also increases GABA transmission in the amygdala.
A team of scientists at The Scripps Research Institute has described the cellular mechanism underlying the brain's response to alcohol, which suggests a possible method for treating alcoholism.
This work, published in the latest issue of the journal Science, ties together the effect of the brain peptide corticotropin releasing factor (CRF) with alcohol. Both appear to influence