The research, published in the October issue of The Journal of Clinical Investigation, also showed that blocking the enzyme reduced levels of stress hormones. The same issue of the journal includes a commentary on the research (Anxiolytic Drug Targets: Beyond the Usual Suspects) by Joshua A. Gordon of Columbia University's Center for Neurobiology and Behavior.
Anti-anxiety drugs such as Valium often leave people sedated, less capable at mental tasks, and can become addicting, whereas drugs without these side effects -- such as some antidepressants -- may not reduce anxiety as well, said Robert Messing, MD, UCSF professor of neurology at the Gallo Research Center and senior author on the paper.
But in the new study, mice lacking the enzyme showed reduced anxiety while maintaining normal levels of alertness and learning abilities, the researchers reported.
The enzyme, known as protein kinase C epsilon (PKC epsilon), is present in many neurons in the brain, but its role is not well known. Its ability to affect anxiety but not sedation may stem from indirect, rather than direct action, the researchers found.
When the neurotransmitter GABA binds to proteins on the surface of many neurons, known as GABA-A receptors, the neurons become less active, which tends to reduce anxiety. Drugs such as Valium act by increasing the action of GABA at the GABA-A receptors. A group of brain molecules derived from progesterone, known as neurosteroids, also act to increase the action at the GABA-A receptor, and thereby reduce anxiety. But PKC epsilon appears to make the GA
Contact: Wallace Ravven
University of California - San Francisco