Slow-wave activity homeostasis in the somatosensory cortex after spinal cord injury.

The cortical reorganization after spinal cord injury (SCI) involves a series of physiological changes that drive the expansion of the intact cortical area to the deafferented cortical area. These changes have always been studied under a stimulus-response paradigm, which demonstrates that the deafferented cortex becomes more responsive to stimulation of body regions above the level of the lesion. However, less is known about how permanent large-scale deafferentation affects spontaneous activity in the somatosensory cortex, an important physiological feature related to the processing of peripheral inputs and perception. Here we studied the spontaneous activity at two sites of the somatosensory cortex, corresponding to forepaw and hindpaw, and at three different time points after SCI: acute SCI, one week post-SCI and chronic SCI (1-3 months after injury). Electrophysiological recordings from anesthetized rats were obtained in conditions of slow-wave activity in order to compare features of the neural populations in periods of cortical up-states. Our data demonstrate that acute SCI reduces the excitability of cortical neurons during up-states in both the forepaw and the hindpaw cortex. One week after SCI, the properties of cortical neurons were similar to those under control conditions, indicating a homeostatic plasticity. Finally, chronic SCI increased neural activity during up-states, while reduced up-state frequency in the cortex. We conclude that SCI induces different homeostatic changes in cortical slow-wave depending on the time after lesion. This temporal evolution of spontaneous activity could help better understand the cortical plasticity associated with acute or chronic SCI.