Journal
NEURON
Volume 37, Issue 5, Pages 801-811Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(03)00085-0
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In nerve terminals, residual Ca2+ remaining from previous activity can cause facilitation of transmitter release by a mechanism that is still under debate. Here we show that the intracellular Ca2+ sensitivity of transmitter release at the calyx of Held is largely unchanged during facilitation, which leaves an increased microdomain Ca2+ signal as a possible mechanism for facilitation. We measured the Ca2+ dependencies of facilitation, as well as of transmitter release, to estimate the required increment in microdomain Ca2+. These measurements show that linear summation of residual and microdomain Ca2+ accounts for only 30% of the observed facilitation. However, a small degree of supra-linearity in the summation of intracellular Ca2+ signals, which might be caused by saturation of cytosolic Ca2+ buffer(s), is sufficient to explain facilitation at this CNS synapse.
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