DALLAS Researchers at UT Southwestern Medical Center at Dallas are a step closer to defining the function of two proteins involved in neurotransmitter release, which initiates communication between neurons in the brain.

Findings from the two-part study, published in todays issue of Nature, provides new insight in understanding how the brain functions, which ultimately has broad implications for the development of drug therapy to treat neurological diseases such as Alzheimers and Parkinsons, as well as learning and memory disorders.

This is pure, fundamental research, said Dr. Thomas Sdhof, director of the Center for Basic Neuroscience at UT Southwestern and senior author of the first part of the study. It is essential for understanding various diseases of the nervous system. The premise of our work is the understanding of neurotransmitter release, which is a necessity for understanding brain function and how the brain works.

The researchers bred mice that lacked the brain proteins RIM1a or Rab3A. In part one of the study, the researchers report a change in short-term plasticity in the mice lacking the RIM1α protein compared to other types of mutant mice. In part two of the study, the researchers report a correlation between the RIM1a protein and long-term plasticity. The terms short- and long-term plasticity refer to changes that occur during neurotransmitter release.

We found that the mice lacking the protein were still viable, but there were some deficits in short-term plasticity when changes occur at the synapses for a short period of time. The strength of synaptic transmission determines how we process information. It affects everything from memory to thinking and feeling, said Dr. Susanne Schoch, a postdoctoral research fellow and lead author of the two-part study.

We also found that RIM1a has a central function in neurotransmitter release and is required for long-term plasticity, which is similar to short-term
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Contact: Amy Shields
Amy.Shields@UTSouthwestern.edu
214-648-3404
UT Southwestern Medical Center
16-Jan-2002