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  Probing the intracellular calcium sensitivity of transmitter release during synaptic facilitation

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.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0012-F144-8 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002E-2772-B
Genre: Journal Article

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 Creators:
Felmy, F.1, Author              
Neher, E.1, Author              
Schneggenburger, R.2, Author              
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1Department of Membrane Biophysics, MPI for biophysical chemistry, Max Planck Society, ou_578579              
2Research Group of Synaptic Dynamics and Modulation, MPI for Biophysical Chemistry, Max Planck Society, ou_578582              

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 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.

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 Dates: 2003-03-06
 Publication Status: Published in print
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 Rev. Method: Peer
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Title: Neuron
Source Genre: Journal
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Pages: - Volume / Issue: 37 (5) Sequence Number: - Start / End Page: 801 - 811 Identifier: -