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Abstract
The synapsins are a family of neuronal phosphoproteins evolutionarily conserved in
invertebrate and vertebrate organisms. Their best-characterised function is to modulate
neurotransmitter release at the pre-synaptic terminal, by reversibly tethering synaptic
vesicles (SVs) to the actin cytoskeleton. However, many recent data have suggested
novel functions for synapsins in other aspects of the pre-synaptic physiology, such
as SV docking, fusion and recycling. Synapsin activity is tightly regulated by several
protein kinases and phosphatases, which modulate the association of synapsins to SVs
as well as their interaction with actin filaments and other synaptic proteins. In
this context, synapsins act as a link between extracellular stimuli and the intracellular
signalling events activated upon neuronal stimulation. Genetic manipulation of synapsins
in various in vivo models has revealed that, although not essential for the basic
development and functioning of neuronal networks, these proteins are extremely important
in the fine-tuning of neuronal plasticity, as shown by the epileptic phenotype and
behavioural abnormalities characterising mouse lines lacking one or more synapsin
isoforms. In this review, we summarise the current knowledge about how the various
members of the synapsin family are involved in the modulation of the pre-synaptic
physiology. We give a comprehensive description of the molecular basis of synapsin
function, as well as an overview of the more recent evidence linking mutations in
the synapsin proteins to the onset of severe central nervous system diseases such
as epilepsy and schizophrenia.
(c) 2010 Elsevier Ltd. All rights reserved.