Cortical pathways for horizontal transmission of information between barrels. (a) An example of three microlesions placed in between the D2 and D3 barrels. The lesions are not only shown here in layer IV, but also extend vertically into layer III. The lesions are designed to disconnect D2 from D3. In this case, the D2 whisker was spared, the D3 barrel was severed and the other barrels including, for example, D1 were connected. (b) Vibrissae dominance is affected by the type of lesion shown in (a), where the experienced barrel (D2 in that case) is severed from the deprived barrel (D3). Upper three graphs, layer II/III cells; lower three graphs, layer IV. (i) Severed: almost all the cells respond to the principal whisker and hardly any to the spared ‘experienced whisker’. (ii) Connected: this is similar to the case of the animals with no lesion shown to the right. (iii) No lesion: in a normal animal with single whisker experience most cells respond to the spared whisker (1) compared with the deprived principal whisker (0). A vibrissa dominance of 1 indicates only responses to the spared whisker, 0.5 equals response to spared and principal whisker and 0 only responses to the principal whisker. (Adapted from Fox (1994) by permission of the Society for Neuroscience.)

Spine plasticity is affected by stroke and somatosensory experience. (a) Golgi-Cox labelled layer V pyramidal cells; (i) and (ii), control (Ctrl); (iii) and (iv), cells in the peri-infarct region 6 hours following stroke. (b) Quantification of spine length and (c) spine density measured 0, 2, 6 and 24 hours after stroke in the peri-infarct region (peri-infarct (M1)), the ipsilateral secondary motor cortex (M2) and the contralateral barrel field (contra-S1BF). (Adapted from Brown et al. (2008) by permission of Lippincott & Williams.) (d) The pattern of barrel deprived in chessboard deprivation (black, deprived; grey, spared). (e) Spine lifetimes are plotted over 4 days for dendrites located (i) inside and (ii) outside the barrel cortex. The black circles are data means for deprived cortex and open circles for undeprived cortex. Note that transient (1 day) spines increase and persistent (4 days) spines decrease following deprivation (asterisk). (f)(i) Spine density is relatively unaffected by deprivation while (ii) spine turnover increases immediately following deprivation (note that first 4 days are undeprived). (Reprinted by permission from Macmillan Publishers Ltd: Nature, Trachtenberg et al. (2002), © 2002.)

Cortical map plasticity. (a–c) 2-Deoxyglucose mapping in barrel cortex shows expansion of the cortical domain activated by a single whisker in horizontal sections through barrel cortex. (a) Control condition showing the effect of stimulating the C3 whisker. (b) Vibrissectomy condition (follicle lesion) showing that the C3 whisker domain has expanded two months after ablating all but the C3 follicle (Kossut et al. 1988). (c) A similar expansion occurs after two-month whisker deprivation of all but the C3 whisker (Hand 1982). (d) Activation of layer II/II produced by stimulating the D1 whisker is largely confined to the D1 barrel in a normal animal (the D1 barrel is darker grey). Each circle represents the response in an electrode penetration in mouse barrel cortex grey-coded for average intensity of response (white greater than or equal to 1 spike per stimulus; light grey greater than or equal to 0.5 spikes per stimulus; black less than 0.5 spikes per stimulus). (e) The D1 domain in layer II/III after 18 days single whisker experience, i.e. the D1 whisker is spared and all the other whiskers deprived (adapted with permission from Barrel cortex, 2008, Cambridge University Press (Fox 2008)). (f) Plasticity in human somatosensory cortex following amputation of the right arm below the elbow is revealed using magnetic encephalography. In the left hemisphere the hand representation is missing and only present in the right hemisphere (green). The left hemisphere hand cortex has remodelled to respond to face (red) and upper arm (blue). (Adapted from Ramachandran & Hirstein (1998) by permission of Oxford University Press.)

Dependence of cortical LTP on NO. (a) In wild-type mice, stimulation of the IV to II/III pathway diagonally between barrels causes LTP when a presynaptic spike is timed to occur 10 ms before a post-synaptic spike (the arrow indicates the time at which the forward pairing (FP) protocol was applied). However, plasticity is reduced if a NOS antagonist (L-N^G-nitroarginine, L-NNA) is included post-synaptically via the electrode solution. Open circles, L-NNA, n=22; filled circles, control, n=24. (b) The same data in (a) are shown in 10 min averages. Note that only time points beyond 30 min are significantly different between drug treated and control, indicating the slower onset of NOS-dependent LTP in cortical neurons. (c) In GluR1 knockout mice, early LTP (less than 10 min) is reduced compared with wild types, but slowly developing LTP is intact (filled circles). However, the residual LTP present in GluR1 knockouts is completely prevented by post-synaptic NOS antagonism with intracellular L-NNA (open circles). Open circles, L-NNA, n=18; filled circles, control, n=18. (d) The 60 min average values (± s.e.m.) for the four cases shown in (a) and (c) are plotted for comparison. Filled square, control; open square, L-NNA. (Adapted from Hardingham & Fox (2006) by permission of the Society for Neuroscience.)