PMC

A. Simultaneous depth-EEG and quadruple intracellular recordings. The electrodes were equally distributed from anterior to posterior parts of suprasylvian gyrus. The intra-cell 1 was in the anterior part of area 5 and the intra-cell 4 was in the posterior part of area 21. Shadowed areas are expanded in B. B. Fragment of intracellular activity during slow oscillation. (1) During slow oscillation neurons oscillate between silent (hyperpolarized) and active (depolarized) states. (2) During paroxysmal spike-wave complexes neurons also reveal alterations of depolarized and hyperpolarized states (modified from ().

A. Cat brain depicting the localization of the undercut (arrows), global view – left, frontal section – middle and sagital section – right. B. Intracellular and field potential recordings during different states of vigilance. Epochs indicated by horizontal bars are expanded below. Note the presence of large amplitude hyperpolarizing potentials, indicated by shadowed area, during REM sleep and waking state. C. Intracellular neuronal recording in the intact cortex (B, modified from (); C, modified from ().

Patterns of connectivity in recorded pairs of neurons. The postsynaptic neuron was recorded intracellularly (IC) and the presynaptic neuron was recorded extracelularly (EC). EPSP and IPSP - direct connection, network excitation (NE) and network inhibition (NI) - indirect connections. B. Variation in time of the number of ictal events. C. Variation in time of the EPSP and NE amplitudes. D. Variation in time of the EPSP's failure rates. E. Coefficient of variation versus EPSP amplitude in control and in injured cortex. F. Variation of direct connection probability at different time delays after cortical injury. G. Incidence of NE and NI in control and after cortical deafferentation. Ctrl - control; Ac - acute; W - weeks. (A, C–G modified from (); B, modified from ().

A. Left and middle panels, sagital section of the suprasylvian gyrus of cat in control conditions and 6 weeks after undercut. Scale bars represent 1 mm. Right panel, reduction of neocortical thickness at different time delays from isolation. B. Double staining GAD & NeuN (left panel) and GABA & NeuN (middle panel). Insets depict the double labelling of inhibitory neurons. Note the nucleus labelled in grey-black (DAB - Ni, Cr enhancement) and the cytoplasm in brown (DAB). Scale bars represent 20 μm (10 μm in the insets). Right panel depicts the relative increase in the excitatory-inhibitory ratio in the late stages of the undercut. CTRL - control, 2W, 4W, 6W – 2, 4 and 6 weeks, respectively. (modified from ().

A. Cortical reorganization from control conditions to chronic stages. B–E. Raster plots of the network activity: neuron index (y-axis) vs. time (x-axis). Each dot represents the spike from a single model neuron. The pyramidal (PY) cells are in the top part of the diagram (cyan) and the inhibitory (IN) cells are shown in the bottom part (violet). These spike rasterplots show network activity after (B) 60% HSP, (C) 63% HSP, (D) 72% HSP. After 72% HSP, a steady state was reached for which PY cells fired on average 5.0 Hz. (E) An expanded spontaneous burst at 72% HSP. (F) Synaptic scaling in intact cortex modulated the average firing rate of PY cells while maintaining a low-amplitude irregular averaged local field potential (LFP) oscillations. Homeostatic synaptic plasticity restored a low-amplitude irregular LFP after partial (<80%) deafferentation. The LFP traces (right panel) are scaled by the reverse of the square root of their means for comparison purposes. (B–F, modified from ().