DNA in brain altered with alcohol consumption
Shravan Sarvepalli
Issue date: 5/19/08 Section: Pulse
Booze and brains: two things college students use for survival. Most of us know that alcohol and our brains have a very interesting relationship, to say the least. However, until now, scientists did not know much about what happens in our brains during alcohol consumption.
Recently, Dr. Subhash Pandey and his research team performed pioneering experiments that clue us in on epigenetic changes. These are basically changes in genes that are constant between generations.
"This is the first time anyone has looked for epigenetic changes related to chromatin remodeling in the brain during alcohol addiction," said Dr. Pandey, director of neuroscience alcoholism research at the UIC College of Medicine.
Dr. Pandey is talking about how the DNA, which is packed up in tight knots and twists to conserve space, loosens when exposed to alcohol. The enzyme histone acetyltransferase (HAT) is responsible for unwrapping DNA. While HATs loosen up the DNA, another enzyme, histone deacetylase (HDAC), brings it closer together. All this is important because in its unpacked form, the DNA is coded into the protein Neuropeptide Y that reduces anxiety.
"Neuropeptide Y is an example, but there maybe several other genes getting modified," he said.
At a molecular level, HDACs are responsible for the anxiety and pain we feel during the withdrawal period. Knowing this, the researchers simply used molecules that block HDAC activity. Also known as HDAC inhibitors, they can be used to control withdrawal symptoms.
The researchers injected HDAC inhibitors into rats that were fed a diet supplemented by ethanol, and then deprived of alcohol for 24 hours.
"It is a very good animal model that can mimic human conditions," said Dr. Pandey. The HDAC inhibitors prevented alcohol withdrawal-related anxiety in these rats.
Not only are withdrawal symptoms the main reason why people remain addicted to alcohol, but also "most of the time people suffer with these symptoms," says Dr. Pandey. In fact, alcohol is widely known to be a source of self-medication for addicts. Assuaging anxiety associated with withdrawal could drastically reduce alcoholism.
"Strategies to treat alcoholism should be directed toward the prevention of these withdrawal symptoms that occur after cessation of drinking," writes Dr. Pandey in his article, which was published in the "Journal of Neuroscience" last month.
Dr. Pandey's research certainly can be used to make headway in developing a treatment that focuses on alleviating withdrawal symptoms.
"HDAC inhibitors may be potential therapeutic agents in treating alcohol withdrawal symptoms," he concludes. These findings apply to both temporary exposures to alcohol as well as chronic alcohol abuse.
This research gets us one step closer to eradicating alcoholism. One day, for better or worse, college will be more about enhancing our brains than guzzling down booze.
Recently, Dr. Subhash Pandey and his research team performed pioneering experiments that clue us in on epigenetic changes. These are basically changes in genes that are constant between generations.
"This is the first time anyone has looked for epigenetic changes related to chromatin remodeling in the brain during alcohol addiction," said Dr. Pandey, director of neuroscience alcoholism research at the UIC College of Medicine.
Dr. Pandey is talking about how the DNA, which is packed up in tight knots and twists to conserve space, loosens when exposed to alcohol. The enzyme histone acetyltransferase (HAT) is responsible for unwrapping DNA. While HATs loosen up the DNA, another enzyme, histone deacetylase (HDAC), brings it closer together. All this is important because in its unpacked form, the DNA is coded into the protein Neuropeptide Y that reduces anxiety.
"Neuropeptide Y is an example, but there maybe several other genes getting modified," he said.
At a molecular level, HDACs are responsible for the anxiety and pain we feel during the withdrawal period. Knowing this, the researchers simply used molecules that block HDAC activity. Also known as HDAC inhibitors, they can be used to control withdrawal symptoms.
The researchers injected HDAC inhibitors into rats that were fed a diet supplemented by ethanol, and then deprived of alcohol for 24 hours.
"It is a very good animal model that can mimic human conditions," said Dr. Pandey. The HDAC inhibitors prevented alcohol withdrawal-related anxiety in these rats.
Not only are withdrawal symptoms the main reason why people remain addicted to alcohol, but also "most of the time people suffer with these symptoms," says Dr. Pandey. In fact, alcohol is widely known to be a source of self-medication for addicts. Assuaging anxiety associated with withdrawal could drastically reduce alcoholism.
"Strategies to treat alcoholism should be directed toward the prevention of these withdrawal symptoms that occur after cessation of drinking," writes Dr. Pandey in his article, which was published in the "Journal of Neuroscience" last month.
Dr. Pandey's research certainly can be used to make headway in developing a treatment that focuses on alleviating withdrawal symptoms.
"HDAC inhibitors may be potential therapeutic agents in treating alcohol withdrawal symptoms," he concludes. These findings apply to both temporary exposures to alcohol as well as chronic alcohol abuse.
This research gets us one step closer to eradicating alcoholism. One day, for better or worse, college will be more about enhancing our brains than guzzling down booze.
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victor2008
posted 10/27/08 @ 7:29 AM CST
A study released today reveals a cellular mechanism involved in alcohol dependence. The study, in the May 28 issue of The Journal of Neuroscience, shows that gabapentin, a drug used to treat chronic pain and epilepsy, reduces alcohol intake in alcohol-dependent rats by normalizing chemical communication between neurons, which is altered by chronic alcohol abuse. (Continued…)
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