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The Journal of Neuroscience, October 18, 2006, 26(42):10796-10807; doi:10.1523/JNEUROSCI.2746-06.2006
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Development/Plasticity/Repair
Presynaptic Kainate Receptor Activation Is a Novel Mechanism for Target Cell-Specific Short-Term Facilitation at Schaffer Collateral Synapses
Hua Yu Sun andLynn E. Dobrunz Department of Neurobiology, Civitan International Research Center, and Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, Alabama 35294
Correspondence should be addressed to Lynn E. Dobrunz, 1825 University Boulevard, SHEL 902, Birmingham, AL 35294. Email: dobrunz{at}uab.edu
Target cell-specific differences in short-term plasticity have been attributed to differences in the initial release probability of synapses. Using GIN (GFP-expressing inhibitory neurons) transgenic mice that express enhanced green fluorescent protein (EGFP) in a subset of interneurons containing somatostatin, we show that Schaffer collateral synapses onto the EGFP-expressing somatostatin interneurons in CA1 have very large short-term facilitation, even larger facilitation than onto pyramidal cells, in contrast to the majority of interneurons that have little or no facilitation. Using a combination of electrophysiological recordings and mathematical modeling, we show that the large short-term facilitation is caused both by a very low initial release probability and by synaptic activation of presynaptic kainate receptors that increase release probability on subsequent stimuli. Thus, we have discovered a novel mechanism for target cell-specific short-term plasticity at Schaffer collateral synapses in which the activation of presynaptic kainate receptors by synaptically released glutamate contributes to large short-term facilitation, enabling selective enhancement of the inputs to a subset of interneurons.
Key words: GIN mice; somatostatin; mathematical model; presynaptic; paired-pulse facilitation; release probability; interneuron; CA1; hippocampus
Received June 28, 2006; revised Sept. 8, 2006; accepted Sept. 8, 2006.
Correspondence should be addressed to Lynn E. Dobrunz, 1825 University Boulevard, SHEL 902, Birmingham, AL 35294. Email: dobrunz{at}uab.edu
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