synapses between nerve cells are constantly developed, strengthened or dismantled. scientists at the Max Planck Institute of Neurobiology and Yale University have now examined the protein SynCAM1, the synapses as the glue holding together. If the amount increases SynCAM1 experimentally increased the number of synapses - the nerve cells should be more ways to transfer have information. In behavioral tests, however, mice without SynCAM1 learned significantly better than control animals. Not only the structure but also the degradation of synapses seems to be essential for learning and memory. One finding that may be of interest for certain diseases.
The brain is like a construction site. constantly growing on the surface of nerve cells, new processes. Does such an extension to the corresponding structure of a neighboring cell, the extension ends in a mature synapse. Only these contact points make it possible to transfer information from one cell to another. Synapse is an existing inefficient or is no longer needed, they will be dismantled.
scientists agree that the ability to learn to forget or to remember something, based on the permanent alteration of the brain.
synapses with adhesive function?
Despite the small size of synapses, their function is now reasonably well understood. In contrast, the formation of synapses and molecules involved are difficult to research. It has enabled certain proteins to be identified to keep the two sides of the synapse during maturation in position. Whether these proteins but also affect the function of synapses remained unexplained.
scientists at the Max Planck Institute of Neurobiology, Yale University, New Haven could now reveal some of the functions of these proteins.
"SynCAM1 The protein holds the two sides of a synapse as a sort of material together and we were wondering whether the impact on the number and the lifetime of the synapse," says Alexander Krupp of the Max Planck Institute of Neurobiology. These questions went to the researchers by including in genetically modified mice, the amount of SynCAM1 temporarily increased, or the protein completely away. The changes that were to be observed under the microscope and in behavioral tests surprised that neurobiologists.
The results showed that SynCAM1 not only build the synapse plays a role, but also for the preservation of existing synapses is important. Was the amount of SynCAM1 artificially high, according to the neurobiologists discovered a far more synapses. SynCAM1 the amount was then reduced by a genetic trick again, disappeared the additional synapses. This effect was not only to the development of the brain limited form in which most of the synapses, but was also observed in the adult brain.
Easy to learn without SynCAM1
"One might assume that animals are able to process an increased number of synapses retain information better or, considering Valentin Stein, one of two of the study. But exactly the opposite was the case - they got worse. A behavioral test it clear that mice learn faster and remember without SynCAM1 better.
This result seems illogical only at first glance. With SynCAM1 are indeed formed more synapses. However, they are also more stable, so it is difficult unnecessary connections re-dissolve. The neurobiologists suspect therefore that the observed difference is the ability to learn in the removal of unused synapses. Without the contacts SynCAM1 can easily be separated again. "Our results show how important the reduction of synapses for learning and memory," says Stein. This is small in itself a breakthrough. SynCAM1 but could also play in diseases with altered synapse formation, such as autism, a role. Similarly, seems to be a therapeutic role of SynCAM1 not such as in Alzheimer's disease, are excluded. These aspects are the scientists in their further research in mind.
Original publication:
SynCAM an adhesion dynamically regulates synapse number and impacts plasticity and learning Elissa M. Robbins *, Alexander J. Krupp *, Karen Perez de Arce, Ananda K.
Ghosh, Adam I. Fogel, Antony Boucard, Thomas C. Südhof, Valentin Stein **, ** Thomas Biederer [*,** equal contribution] Neuron, online publication of 8 December 2010
Contact:
Dr. Stefanie Merker, Press and Public Relations Max Planck Institute of Neurobiology, Martinsried
Tel: +49 89 8578-3514
Fax: +49 89 8995-0022
E-mail: merker@neuro.mpg.de
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