, 2000). Multiple synaptic mechanisms have been proposed to drive the expansion of spared whisker representations

in a partially deprived barrel cortex (Feldman, 2009). For example an imbalance in sensory input induces forms of synaptic long-term potentiation (LTP) that may strengthen latent intracortical connections (Clem and Barth, 2006; Finnerty et al., 1999; Glazewski et al., 2000), or stimulates the formation of new synapses whose stabilization may in turn depend on LTP-like processes (Cheetham et al., 2008; Hardingham et al., 2011; Linsitinib Wilbrecht et al., 2010). Tactile deprivation has also been shown to decrease the number of cortical inhibitory synapses (Chen et al., 2011; Keck et al., 2011; Micheva and Beaulieu, 1995) and reduce feedforward inhibitory currents in vitro (Chittajallu and Isaac, 2010; House et al., 2011; Jiao et al., 2006). Such ABT-888 nmr disinhibition may allow sensory-driven excitation to spread over a larger population of supragranular pyramidal neurons (Kelly et al., 1999; Li et al., 2002) and to invade neighboring columns (Tremere et al., 2001). Despite strong evidence for each of these synaptic mechanisms separately, the interrelationship remains poorly studied in the context of barrel cortex plasticity. Spike-timing-dependent plasticity (STDP), which is

defined as the bidirectional modification of postsynaptic potentials (PSPs) after repeated coincidence of postsynaptic subthreshold and suprathreshold potentials (Markram et al., 1997), has been postulated as a Hebbian learning rule that could drive surround potentiation (Feldman, 2009; Sjöström et al., 2008). In acute slices of barrel cortex, the paired stimulation of L4-to-L2/3 inputs with back-propagating postsynaptic action potentials (APs) induces LTP in L2/3 neurons of the stimulated barrel column (Banerjee

et al., 2009; Feldman, 2000; Hardingham et al., 2008) and in some occasions in the neighboring barrel column Rapamycin in vivo (Hardingham et al., 2011). Whisker deprivation rapidly changes the spike timing and spike order in barrel cortex (Celikel et al., 2004) and modulates the ability to induce spike-timing-dependent long-term potentiation (STD-LTP) in brain slices (Hardingham et al., 2008, 2011). Together, this suggests that barrel cortex map plasticity could be driven in vivo by a spike-timing-dependent mechanism, similar to retinal injury-induced visual cortex reorganization (Young et al., 2007). However, it is worth noting that most of the evidence for cortical STDP comes from studies in brain slices and that despite successful attempts to induce sensory input-mediated STD-LTP in the visual (Meliza and Dan, 2006) and auditory (Froemke et al., 2007) cortex, as well as STD long-term depression (LTD) in the somatosensory cortex (Jacob et al., 2007), whisker-evoked STD-LTP has not yet been demonstrated convincingly.