Summary

The neural cell adhesion molecule, NCAM, belongs to the immunoglobulin superfamily of cell adhesion molecules, and is well recognized as an important regulator of different morphogenetic events, including neural cell proliferation and migration, as well as axonal fasciculation and outgrowth. This chapter highlights synaptic functions of NCAM. At early stages of synaptogenesis in primary hippocampal cultures, clusters of NCAM at the cell surface - linked via spectrin to trans-Golgi network (TGN)-derived organelles - translocate along growing neurites to sites of neurite-to-neurite contacts within several minutes of initial contact formation. There, NCAM mediates an anchoring ("synaptic trap") of the intracellular organelles. At later stages of synaptogenesis, the relative levels of postsynaptic NCAM expression control both the number and strength of synapses in an activity-dependent manner. This process requires polysialylation of NCAM and activity of FGF and NMDA receptors. In mature brains, NCAM is important for induction of NMDA receptor-dependent long-term potentiation (LTP) and depression (LTD) in the CA1 area of the hippocampus, LTP-associated increase in the number of perforated synapses, NMDA receptor-independent mossy fiber LTP, several forms of learning and memory and morphological plasticity in the hypothalamo-neurohypophysial system. Additionally, NCAM was found to be essential for synaptic vesicle trafficking at the neuromuscular junction (NMJ) and for catecholamine release from neuroendocrine chromaffin cells. Thus, NCAM is important for formation and plasticity of synapses and plays a basic role in transmitter release. The significance of NCAM is further underscored by the efficacy of NCAM-derived compounds to affect these processes, and emerging links between NCAM and schizophrenia.

'Department of Neurophysiology and Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany; [email protected]

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