Scientists have discovered that mice genetically engineered to lack a particular protein in the brain have profound deafness and seizures. The finding suggests a pathway, they say, for exploring the hereditary causes of deafness and epilepsy in humans.
More broadly, the discovery provides an entry point for gaining new insight into the role of glutamate, the chemical messenger carried by the protein, says the team, led by scientists at the University of California, San Francisco. Glutamate is involved in virtually every brain function, including sensory perception, learning and memory.
The missing protein is a particular vesicular neurotransmitter transporter, a machine within nerve cells that ferries chemical messengers, or neurotransmitters, from the fluid-filled cytoplasm into vesicles that are positioned at the tips of nerve cells and serve to release neurotransmitters onto neighboring cells. Transporters and neurotransmitters work together to make possible essentially all neural communication in the brain.
While the neurotransmitter glutamate is the major excitatory messenger in the brain, the neurotransmitter GABA is the major inhibitory messenger, sending signals that reduce excitation and anxiety. Two other neurotransmitters, dopamine and serotonin, modulate the activity of neural circuits to influence mood, sleep and other aspects of behavior.
Scientists have known for several years about two vesicular glutamate transporters, VGLUT1 and VGLUT2. As would be predicted, they are expressed on nerve cells that release glutamate. More recently, scientists have identified VGLUT3. To their surprise, they have discovered that VGLUT3 is expressed primarily by nerve cells that release GABA, serotonin and acetylcholine, another neurotransmitter. VGLUT3 is also released in some non-nerve cells, in tissues outside the brain. These findings led scientists to suspect that VGLUT3 might support some function other than neurotransm
|Contact: Jennifer O'Brien|
University of California - San Francisco