inhibitory firing in that column. This unmasks horizontal excitatory connections from adjacent spared columns. This does not explain longer-lasting plastic changes as the unmasking would disappear immediately if the deprived input was reinstated (for example by allowing the whisker to regrow). LTP- and LTD-like processes also seem to be involved. This can be inferred by using transgenic mice where there are changes in the expression of enzymes related to LTP and LTD e.g. calmodulin-dependent protein kinase II (CaMKII) or cyclic-AMP response element binding protein (CREB). In these mice, plasticity is compromised Spike timing rather than frequency may be an important factor. Associative LTP has been demonstrated at layer 4 to layer 2/3 synapses when the layer 4 neuron fires 0-15 ms before the layer 2/3 neuron, and LTD is observed when this timing order is reversed. Such mechanisms could act rapidly to produce plastic changes within hours or days. Sensory deprivation has been demonstrated to cause changes in synaptic dynamics such as EPSP amplitude and frequency. The net effect of these changes is to increase the proportion of synaptic input which layer 2/3 neurons in deprived barrels receive from spared barrels. These observations suggest that other, more specific, mechanisms besides LTP/LTD are at play in experience-dependent plasticity. It seems intuitively likely that structural changes at the level of axons, dendrite branches, and dendrite spines underlie some of the long-term plastic changes in the cortex. Changes in axon structure have been reported in plasticity following lesions and more recently by studies using whisker trimming. Dendritic branching is important during prenatal and neonatal development, is involved in plasticity induced by lesions, but is not involved in experience-dependent plasticity. In vivo two-photon microscopy reveals that dendritic spines in mouse barrel cortex are highly dynamic and subject to continuous turnover, and may be associated with formation or deletion of synapses. It is likely that spine turnover is necessary but not sufficient to produce experience-dependent plasticity, and other mechanisms such as axonal remodelling are also needed to explain features such as savings from prior experience. Plasticity and remodelling of barrel cortex has also been studied in the context of traumatic brain injury, where environmental enrichment of stimuli has been shown to induce plasticity/recovery and patterns of temporal coding have been altered via plasticity and recovery mechanisms. Notes References External links Research groups working on barrel cortex: Ahissar Lab, Israel Barrel cortex group, Cardiff Barth Lab,