Abstract
A hallmark of synaptic specializations is their dependence on highly organized complexes of proteins that interact with each other. The loss or modification of key synaptic proteins directly affects the properties of such networks, ultimately impacting synaptic function. SNAP-25 is a component of the SNARE complex, which is central to synaptic vesicle exocytosis, and, by directly interacting with different calcium channels subunits, it negatively modulates neuronal voltage-gated calcium channels, thus regulating intracellular calcium dynamics. The SNAP-25 gene has been associated with distinct brain diseases, including Attention Deficit Hyperactivity Disorder (ADHD), schizophrenia and bipolar disorder, indicating that the protein may act as a shared biological substrate among different “synaptopathies”. The mechanisms by which alterations in SNAP-25 may concur to these psychiatric diseases are still undefined, although alterations in neurotransmitter release have been indicated as potential causative processes. This review summarizes recent work showing that SNAP-25 not only controls exo/endocytic processes at the presynaptic terminal, but also regulates postsynaptic receptor trafficking, spine morphogenesis, and plasticity, thus opening the possibility that SNAP-25 defects may contribute to psychiatric diseases by impacting not only presynaptic but also postsynaptic functions.
Highlights
A hallmark of synaptic specializations is their dependence on highly organized complexes of proteins that interact with each other
The SNAP-25 gene has been associated with distinct brain diseases, including Attention Deficit Hyperactivity Disorder (ADHD), schizophrenia and bipolar disorder, indicating that the protein may act as a shared biological substrate among different “synaptopathies”
This review summarizes recent work showing that SNAP-25 controls exo/endocytic processes at the presynaptic terminal, and regulates postsynaptic receptor trafficking, spine morphogenesis, and plasticity, opening the possibility that SNAP-25 defects may contribute to psychiatric diseases by impacting presynaptic and postsynaptic functions
Summary
Oyler et al, 1989; Söllner et al, 1993a,b; Chapman et al, 1994; Poirier et al, 1998; Raciborska et al, 1998; Sutton et al, 1998; Washbourne et al, 2002; Sørensen et al, 2003; Jeans et al, 2007; Mohrmann et al., 2010; Shen et al, 2014
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