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Journal Article

Probing the intracellular calcium sensitivity of transmitter release during synaptic facilitation

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Felmy,  F.
Department of Membrane Biophysics, MPI for biophysical chemistry, Max Planck Society;

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Neher,  E.
Department of Membrane Biophysics, MPI for biophysical chemistry, Max Planck Society;

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Schneggenburger,  R.
Research Group of Synaptic Dynamics and Modulation, MPI for Biophysical Chemistry, Max Planck Society;

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Citation

Felmy, F., Neher, E., & Schneggenburger, R. (2003). Probing the intracellular calcium sensitivity of transmitter release during synaptic facilitation. Neuron, 37(5), 801-811. Retrieved from http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6WSS-483858G-9-1&_cdi=7054&_user=38661&_pii=S0896627303000850&_orig=search&_coverDate=03%2F06%2F2003&_sk=999629994&view=c&wchp=dGLzVzb-zSkzS&md5=9ba2420c7bcea54980d433aea47da820&ie=/sdarticle.pdf.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0012-F144-8
Abstract
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.