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New Mechanism Controls Efficacy of Marijuana-like Substance in Brain

by Kathy Jones on Aug 7 2010 7:58 PM

 New Mechanism Controls Efficacy of Marijuana-like Substance in Brain
New research indicates that a newly discovered molecular mechanism helps control the amount and effectiveness of a substance that mimics an active ingredient in marijuana.
However, this substance is produced by the body's own nerve cells.

William R. Marrs of the Neurobiology and Behavior program at the University of Washington (UW) and Dr. Nephi Stella, UW professor of pharmacology and psychiatry conducted the study.

The find may improve treatment in people with multiple sclerosis, Huntington's disease and other neurological disorders.

Specifically targeted treatments, for example, might give cancer and AIDS patients the same medicinal benefits as marijuana without its mind-altering properties.

Cannabinoid signalling systems use signals called endocannabinoids - chemicals that mimic the effect of marijuana.

They are common throughout the body and affect a variety of functions.

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Stella's team looked at an enzyme called ABHD6 that degrades 2-AG nerve signalling substance by splitting it with water. 2-AG is an endocannabinoid that is also implicated in brain cell migration and brain tissue inflammation.

The broken down 2-AG was less effective in stimulating the microglia - the brain defenders-to get moving.

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"The enzymatic steps that control the production and inactivation of endocannabinoids constitute promising molecular targets for indirectly modulating the activity of cannabinoid receptors," the authors noted.

Designing treatments that manage the production and inactivation of important enzymes like ABHD6 could thereby control such conditions as brain inflammation or overactive brain signals.

For example, blocking a specific enzyme to heighten a certain signal might ameliorate pain and also act as anti-anxiety and antidepressant therapy, the authors explained.

Drugs that reduce the activity of the ABDH6 enzyme might prevent brain damage from an overactive response to a virus.

The results were reported in the latest Nature Neuroscience.

Source-ANI


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