Journal
JOURNAL OF NEUROSCIENCE
Volume 26, Issue 42, Pages 10796-10807Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2746-06.2006
Keywords
GIN mice; somatostatin; mathematical model; presynaptic; paired; pulse facilitation; release probability; interneuron; CA1; hippocampus
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Funding
- NICHD NIH HHS [P30 HD038985, P01 HD038760, P01-HD38760, P30-HD38985] Funding Source: Medline
- NIMH NIH HHS [R01 MH065328, R01 MH65328] Funding Source: Medline
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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.
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