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Schizophrenia linked to dysfunction in molecular brain pathway activated by marijuana
Date:7/7/2008

aluated levels of CB1R messenger RNA and protein, and also measured levels of glutamic acid decarboxylase (GAD-67), an enzyme that makes GABA, and cholecystokinin (CCK), a neuropeptide released from GABA neurons that, among other actions, regulates the production of the brain's own cannabinoids.

"CB1R levels were significantly 15 percent lower in the subjects with schizophrenia," Dr. Lewis said. "We measured these biochemical messengers using three techniques, and each time got the same answer less CB1R in people with schizophrenia." This reduction, he noted, appears to be the brain's way of compensating for lower levels of GABA, and the use of marijuana defeats this compensation.

"These findings may provide insight into the biological basis of why cannabis use worsens schizophrenia, and, as a result, identify a novel target for new drug development that could improve treatments available for schizophrenia," said Dr. Lewis.


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Contact: Michele Baum
BaumMD@upmc.edu
412-647-3555
University of Pittsburgh Schools of the Health Sciences
Source:Eurekalert

Page: 1 2

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