Interactions between presynaptic Ca2+ channels, cytoplasmic messengers and proteins of the synaptic vesicle release complex.
Influx of Ca(2+) through presynaptic voltage-gated Ca(2+) channels is a key step in rapid neurotransmitter release. The amount of Ca(2+) entering through these channels is modulated by a plethora of intracellular messenger molecules, including betagamma-subunits of G proteins, and protein kinases. In addition, Ca(2+) channels bind physically to proteins of the vesicle-release machinery in a Ca(2+)-dependent manner, which can, in turn, regulate the activity of Ca(2+) channels. Recent evidence suggests that second messengers and presynaptic vesicle-release proteins do not regulate Ca(2+) channel activity as independent entities, but that there is extensive crosstalk between these two mechanisms. The complex interactions between second messengers, vesicle-release proteins and voltage-gated Ca(2+) channels might provide multiple avenues for fine-tuning Ca(2+) entry into the presynaptic terminal and, consequently, neurotransmission.
Jarvis
S E
SE
Dept. of Physiology and Biophysics, University of Calgary, 3330 Hospital Drive NW, T2N 4N1, Calgary, Canada.
Zamponi
G W
GW
D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism*; D003593:Cytoplasm / Q000378:metabolism*; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism*; D017729:Presynaptic Terminals / Q000378:metabolism*; D050600:SNARE Proteins; D015290:Second Messenger Systems / Q000502:physiology*; D013572:Synaptic Vesicles / Q000378:metabolism*; D033921:Vesicular Transport Proteins
D015220:Calcium Channels; D008565:Membrane Proteins; D050600:SNARE Proteins; D033921:Vesicular Transport Proteins; D002118:Calcium