A study published today in Neuron offers the first evidence that lack of this protein known as RIM1 alpha causes profound deficits in the learning process. The discovery is a major step in understanding the molecular events that underlie learning and memory complex processes that can be impaired in human neuropsychiatric disorders such as Alzheimer's disease, mental retardation and schizophrenia.

"We found that when you delete this molecule, the mice essentially become incredibly stupid," said Dr. Thomas Sdhof, director of both the Center for Basic Neuroscience and the C. Vincent Prothro Center for Research in Basic Neuroscience at UT Southwestern and co-author of the paper.

Researchers hope that further study of the protein's role in learning and memory will lead to potential treatments for some neuropsychiatric disorders.

"This is the first indication that these proteins could be good targets for treatment of specific brain disorders," said Dr. Craig Powell, assistant professor of psychiatry and neurology at UT Southwestern and the study's lead author.

The researchers compared behaviors of normal mice to those of three sets of genetically altered mice each of which was missing a specific protein involved in releasing neurotransmitters. The mice lacking the RIM1 alpha protein, unlike the others, lacked the ability to learn the location of an escape platform in a pool of water despite repeated attempts over several days.

Dr. Eric Nestler, chairman of psychiatry at UT Southwestern and senior author of the study, said another notable finding was that, while the other two sets of genetically altered mice displayed some of the same cellular abnormalities as the RIM1 alpha mice, these other m
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Contact: Rachel Horton
rachel.horton@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center
7-Apr-2004