Previous studies have shown that mice without AC1 and AC8 have impairments of several kinds of memory, including contextual memory (learning to avoid a specific situation when it is paired with an unpleasant stimulus). However, the mice can perform other kinds of memory tasks without difficulty, and the two proteins do not affect existing memories, Dr. Zhuo says. The potential memory impairment from drugs or gene therapy to inhibit these proteins may be acceptable to patients who otherwise have to live with intense pain, he suggests.
While the researchers do not know of any existing drugs that can inhibit AC1 and AC8, it might be possible to identify or design drugs for this purpose, Dr. Zhuo says. "Our study makes a good argument for drug companies to look at these proteins," he adds. He and his colleagues are now planning experiments to study the proteins and mechanisms that are triggered by AC1 and AC8. Those studies may lead to other potential targets for therapy.
The NINDS is a component of the National Institutes of Health in Bethesda, Maryland, and is the nation's primary supporter of biomedical research on the brain and nervous system.
Reference:
1 Wei F, Chang-Shen Q, Kim SJ, Muglia L, Maas JW Jr., Pineda VV, Xu HM, Chen ZF, Storm DR, Muglia LJ, Zhuo M. "Genetic elimination of behavioral sensitization in mice lacking calmodulin-stimulated adenyl cyclases." Neuron, November 14, 2002, Vol. 36, pp. 713-726.
From the National Institute of Neurological Disorders and Stroke.
