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The Journal of Neuroscience, February 7, 2007, 27(6):1271-1284; doi:10.1523/JNEUROSCI.4264-06.2007

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Behavioral/Systems/Cognitive
Spike Timing-Dependent Synaptic Depression in the In Vivo Barrel Cortex of the Rat

Vincent Jacob,1 Daniel J. Brasier,2 Irina Erchova,1 Dan Feldman,2,3 and Daniel E. Shulz1

1Unité de Neurosciences Intégratives et Computationnelles, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France, and 2Neurosciences Program and 3Neurobiology Section, Division of Biology, University of California, San Diego, La Jolla, California 92093-0357

Correspondence should be addressed to Daniel E. Shulz, Unité de Neurosciences Intégratives et Computationnelles, Centre National de la Recherche Scientifique, 1 Avenue de la Terrasse, 91198 Gif sur Yvette, France. Email: shulz{at}iaf.cnrs-gif.fr

Spike timing-dependent plasticity (STDP) is a computationally powerful form of plasticity in which synapses are strengthened or weakened according to the temporal order and precise millisecond-scale delay between presynaptic and postsynaptic spiking activity. STDP is readily observed in vitro, but evidence for STDP in vivo is scarce. Here, we studied spike timing-dependent synaptic depression in single putative pyramidal neurons of the rat primary somatosensory cortex (S1) in vivo, using two techniques. First, we recorded extracellularly from layer 2/3 (L2/3) and L5 neurons, and paired spontaneous action potentials (postsynaptic spikes) with subsequent subthreshold deflection of one whisker (to drive presynaptic afferents to the recorded neuron) to produce "post-leading-pre" spike pairings at known delays. Short delay pairings (<17 ms) resulted in a significant decrease of the extracellular spiking response specific to the paired whisker, consistent with spike timing-dependent synaptic depression. Second, in whole-cell recordings from neurons in L2/3, we paired postsynaptic spikes elicited by direct-current injection with subthreshold whisker deflection to drive presynaptic afferents to the recorded neuron at precise temporal delays. Post-leading-pre pairing (<33 ms delay) decreased the slope and amplitude of the PSP evoked by the paired whisker, whereas "pre-leading-post" delays failed to produce depression, and sometimes produced potentiation of whisker-evoked PSPs. These results demonstrate that spike timing-dependent synaptic depression occurs in S1 in vivo, and is therefore a plausible plasticity mechanism in the sensory cortex.

Key words: spike-timing dependent plasticity; STDP; somatosensory cortex; plasticity; rat; synaptic depression; LTP; LTD; barrel


Received Jan. 17, 2006; revised Dec. 20, 2006; accepted Dec. 23, 2006.

Correspondence should be addressed to Daniel E. Shulz, Unité de Neurosciences Intégratives et Computationnelles, Centre National de la Recherche Scientifique, 1 Avenue de la Terrasse, 91198 Gif sur Yvette, France. Email: shulz{at}iaf.cnrs-gif.fr




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