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Science  14 Jan 2011:
Vol. 331, Issue 6014, pp. 126
DOI: 10.1126/science.331.6014.126-c

In the vertebrate central nervous system, intercellular junctions (synapses) that form between neurons control the transmission of information associated with learning, memory, and behavior. Forging this network is a dynamic process, involving proteins at the synaptic cleft that function in the formation, maturation, and remodeling of these connections. Robbins et al. genetically engineered mice to overexpress or lack SynCAM1, a cell adhesion molecule that links synaptic neurons. Electron microscopy revealed a decrease in the number of excitatory synapses that formed in the forebrain of postnatal and adult SynCAM1-deficient mice as compared to normal mice. Conversely, an increase in excitatory synapses in the same region was observed in animals overexpressing Syn-CAM1. The surprise was that activity-dependent decreases in synaptic strength were impaired when SynCAM1 expression was increased, indicating a loss of this plasticity mechanism when there are more neuronal connections. Mice overexpressing SynCAM1 also performed poorly in spatial learning and memory tests. The authors propose that too much SynCAM1 may stabilize synapses to an extent that prevents the elimination of ineffective connections, a pruning process that supports synaptic plasticity.

Neuron 68, 894 (2010).

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