ScienceDaily (Feb. 28, 2008) — A brain circuit that underlies feelings of stress and anxiety shows promise as a new therapeutic target for alcoholism, according to new studies by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health (NIH).
In preclinical and clinical studies currently reported online in Science Express, NIAAA Clinical Director Markus Heilig, M.D., Ph.D., and colleagues from the NIH, Lilly Research Laboratories, and University College in London found that a brain molecule known as the neurokinin 1 receptor, or NK1R, appears to be a central actor in stress-related drinking.
The researchers first demonstrated that NK1R plays an integral role in alcohol consumption in animals. Mice that were genetically engineered to lack NK1 receptors consumed much less alcohol than did normal mice with fully functional NK1R. Subsequently, in a small clinical study, the researchers showed that an experimental compound designed to block NK1 receptors reduced alcohol craving and improved overall wellbeing among recently detoxified alcohol-dependent individuals who had high levels of anxiety.
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Thursday, February 28, 2008
Common Heart Drug May Reduce Cocaine Cravings
ScienceDaily (Feb. 28, 2008)
Researchers from Boston University School of Medicine and Harvard Medical School have found that diltiazem, a drug used in the treatment of high blood pressure, reduces cocaine cravings in a rat model.
Previous work showed that two brain chemicals, dopamine and glutamate, independently contribute to the development of cocaine addiction. This new research indicates that calcium channels provide critical links between dopamine and glutamate that drives the intense craving associated with cocaine addiction. Diltiazem, one of a class of drugs known as calcium channel blockers, disrupts the connection between dopamine and glutamate formed during chronic cocaine use.
According to the researchers, brain calcium plays an important role in learning and memory in that calcium influences an enzyme known as the "memory molecule." "Our work shows that cocaine increases the levels of this molecule specifically in a brain area that controls motivation. Thus, cocaine use teaches the brain to be addicted, resulting in a dysfunctional form of learning that drives the overwhelming desire to consume more cocaine," said senior author Chris Pierce, a professor of pharmacology and psychiatry at Boston University School of Medicine.
Currently, there are no effective drug therapies for cocaine addiction. Pierce noted that research such as this using animal models could lead to desperately needed medications. "The strength of this work is that it tells us something fundamental about how brain chemistry changes as cocaine addiction takes hold. Importantly, our findings also suggest new strategies for developing cocaine addiction therapies, which thus far remain elusive," he added.
These findings will appear in the March issue of the leading medical journal Nature Neuroscience.
This study was supported by grants from the National Institutes of Health.
Adapted from materials provided by Boston University.
Researchers from Boston University School of Medicine and Harvard Medical School have found that diltiazem, a drug used in the treatment of high blood pressure, reduces cocaine cravings in a rat model.
Previous work showed that two brain chemicals, dopamine and glutamate, independently contribute to the development of cocaine addiction. This new research indicates that calcium channels provide critical links between dopamine and glutamate that drives the intense craving associated with cocaine addiction. Diltiazem, one of a class of drugs known as calcium channel blockers, disrupts the connection between dopamine and glutamate formed during chronic cocaine use.
According to the researchers, brain calcium plays an important role in learning and memory in that calcium influences an enzyme known as the "memory molecule." "Our work shows that cocaine increases the levels of this molecule specifically in a brain area that controls motivation. Thus, cocaine use teaches the brain to be addicted, resulting in a dysfunctional form of learning that drives the overwhelming desire to consume more cocaine," said senior author Chris Pierce, a professor of pharmacology and psychiatry at Boston University School of Medicine.
Currently, there are no effective drug therapies for cocaine addiction. Pierce noted that research such as this using animal models could lead to desperately needed medications. "The strength of this work is that it tells us something fundamental about how brain chemistry changes as cocaine addiction takes hold. Importantly, our findings also suggest new strategies for developing cocaine addiction therapies, which thus far remain elusive," he added.
These findings will appear in the March issue of the leading medical journal Nature Neuroscience.
This study was supported by grants from the National Institutes of Health.
Adapted from materials provided by Boston University.
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