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GABA
deficits disturb endocannabinoid system, Research Study.
Changes in the endocannabinoid system may
have important implications for psychiatric and
addiction disorders. This brain
system is responsible for making substances that have effects
on brain function
which resemble those of cannabis products, e.g., marijuana.
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GABA
deficits disturb endocannabinoid system
January 24, 2012
Changes in the endocannabinoid system may have important implications for
psychiatric and addiction disorders. This brain system is responsible for making
substances that have effects on brain function which resemble those of cannabis
products, e.g., marijuana.
The endocannabinoid system is of particular interest in the field of
schizophrenia research because exposure to cannabis products during adolescence
and young adulthood appears to increase the risk for developing schizophrenia.
Also, in studies examining brain tissue collected from people who had
schizophrenia, changes in the endocannabinoid system were highly correlated with
changes in the principal inhibitory chemical messenger system in the brain, the
gamma-aminobutyric acid (GABA) system.
The current study was conducted in order to research the relationship between
changes in the GABA system and changes in the endocannabinoid system. Led by Dr.
David Lewis at the University of Pittsburgh, researchers made genetic
manipulations in mice that selectively reduced the GABA system function by
decreasing the expression of the enzyme that makes GABA, GAD67, or by decreasing
the expression of the principal receptor target for endocannabinoids in the
brain, the cannabinoid 1 receptor (CB1R), in order to determine whether a change
in one is sufficient to cause a change in the other.
Using these techniques, the researchers demonstrated that reduced expression of
GAD67 can lead to reduced expression of CB1R, but not vice versa.
"Because activation of the CB1R suppresses GABA release, lower levels of
CB1R may help augment GABA release from nerve terminals that have below normal
amounts due to reduced GABA synthesis," said Dr. Lewis of the results.
"This evidence suggests that reduced GABA signaling is an 'upstream' event
in the disease process of schizophrenia and that lower CB1R is a compensation to
help normalize GABA signaling."
These findings indicate that GABA abnormalities in schizophrenia are what
trigger the disturbances in the endocannabinoid system. Importantly, cannabis
use also alters GABA activity in the brain.
"While the whole story is still developing, from these data, it looks like
developmental deficits in GABA systems are sufficient to disturb the function of
the endocannabinoid system. This could be an important clue to the link between
cannabis use and psychosis," commented Dr. John Krystal, editor of
Biological Psychiatry.
Additional research will be necessary to further explore such links, including
investigations into whether and/or how cannabis exposure affects the
relationship between GAD67 and CB1R.
More information: The article is "Cortical Glutamic Acid Decarboxylase 67
Deficiency Results in Lower Cannabinoid 1 Receptor Messenger RNA Expression:
Implications for Schizophrenia" by Stephen M. Eggan, Matthew S. Lazarus,
Samuel R. Stoyak, David W. Volk, Jill R. Glausier, Z. Josh Huang, and David A.
Lewis (doi: 10.1016/j.biopsych.2011.09.014) (http://www.biologicalpsychiatryjournal.com/article/S0006-3223%2811%2900911-5/abstract).
The article appears in Biological Psychiatry, Volume 71, Issue 2 (January 15,
2012)
Provided by Elsevier
http://medicalxpress.com/news/2012-01-gaba-deficits-disturb-endocannabinoid.html
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