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Nervous inhibitions

If inhibitory neurons are prevented from carrying out their function, this causes major defects early in embryonal development - and these defects can even occur outside the nervous system. These are the results of a study recently published by scientists from the Max Planck Institute for Experimental Medicine in Göttingen (Neuron, May 18, 2006).

The most common inhibitory transmitters in the mammalian central nervous system are GABA and glycine. Nerve cells can release GABA or glycine where they contact other nerve cells at junctions called synapses. This typically prevents further signal transmission by the post-synaptic cell.

Most inhibitory nerve cells release either GABA or glycine. However, some inhibitory nerve cells appear to be "bilingual", releasing a mixture of GABA and glycine. These mixed-release cells are most common during nervous system development and seem to be crucial for normal spinal cord growth. For brain researchers, however, they have proven mysterious. Most nerve cells specialise in releasing only one type of neurotransmitter. They use transport proteins to pump the neurotransmitter into vesicles surrounded by a membrane and store it there until release is triggered.

Sonja Wojcik and Jeong-Seop Rhee, from the Department of Molecular Neurobiology at the Max Planck Institute for Experimental Medicine in Göttingen, Germany, working with colleagues from Kaiserslautern, Germany and Houston, Texas, have discovered what enables nerve cells to release both GABA and glycine. The researchers discovered that one particular transport protein called VIAAT is able to store both GABA and glycine in vesicles; this joint storage is rather unusual for a classical neurotransmitter. The scientists genetically altered mice so that their nerve cells do not produce VIAAT. This change eliminated both GABA and glycine release.

The scientists did not just solve the problem of simultaneous release of GABA and glycine from "bilingual" sp
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Contact: Dr. Sonja M. Wojcik
wojcik@em.mpg.de
49-551-389-9722
Max-Planck-Gesellschaft
29-May-2006


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