Title : Presynaptic calcium and control of vesicle fusion - Schneggenburger_2005_Curr.Opin.Neurobiol_15_266 |
Author(s) : Schneggenburger R , Neher E |
Ref : Current Opinion in Neurobiology , 15 :266 , 2005 |
Abstract :
Vesicle fusion and transmitter release at synapses is driven by a highly localized Ca2+ signal that rapidly builds up around open Ca2+-channels at and near presynaptic active zones. It has been difficult to estimate the amplitude and the kinetics of this 'microdomain' signal by direct Ca2+-imaging approaches. Recently, Ca2+ uncaging at large CNS synapses, among them the calyx of Held, has shown that the intrinsic cooperativity of Ca2+ in inducing vesicle fusion is high, with 4-5 Ca2+ ions needed to trigger vesicle fusion. Given the Ca2+-sensitivity of vesicle fusion as determined by Ca2+-uncaging, it was found that a surprisingly small (10-25 microM) and brief (<1 ms) local Ca2+ signal is sufficient to achieve the amount, and the kinetics of the physiological transmitter release. The high cooperativity of Ca2+ in inducing vesicle fusion and the non-saturation of the Ca2+-sensor for vesicle fusion renders small changes of the local Ca2+-signal highly effective in changing the release probability; an insight that is important for our understanding of short-term modulation of synaptic strength. |
PubMedSearch : Schneggenburger_2005_Curr.Opin.Neurobiol_15_266 |
PubMedID: 15919191 |
Schneggenburger R, Neher E (2005)
Presynaptic calcium and control of vesicle fusion
Current Opinion in Neurobiology
15 :266
Schneggenburger R, Neher E (2005)
Current Opinion in Neurobiology
15 :266