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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

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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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