Abstract：
:In nerve terminals, residual Ca(2+) remaining from previous activity can cause facilitation of transmitter release by a mechanism that is still under debate. Here we show that the intracellular Ca(2+) sensitivity of transmitter release at the calyx of Held is largely unchanged during facilitation, which leaves an increased microdomain Ca(2+) signal as a possible mechanism for facilitation. We measured the Ca(2+) dependencies of facilitation, as well as of transmitter release, to estimate the required increment in microdomain Ca(2+). These measurements show that linear summation of residual and microdomain Ca(2+) accounts for only 30% of the observed facilitation. However, a small degree of supralinearity in the summation of intracellular Ca(2+) signals, which might be caused by saturation of cytosolic Ca(2+) buffer(s), is sufficient to explain facilitation at this CNS synapse.
journal_name
Neuronjournal_title
Neuronauthors
Felmy F,Neher E,Schneggenburger Rdoi
10.1016/s0896-6273(03)00085-0subject
Has Abstractpub_date
2003-03-06 00:00:00pages
801-11issue
5eissn
0896-6273issn
1097-4199pii
S0896627303000850journal_volume
37pub_type
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