LFP based analysis of brain injured anesthetized animals undergoing closed-loop intracortical stimulation

Acquired brain injuries, such as stroke, are a major cause of long-term disability worldwide. When an injury occurs within primary motor cortex (M1) there is both a loss of descending information to the spinal cord and a disruption in the communication within and between spared regions, which can lead to hemiparesis and other motor dysfunctions. Recently, activity-dependent stimulation (ADS), a closed loop intracortical neurostimulation technique, was shown to significantly improve behavioural recovery in rodent models following a unilateral traumatic brain injury in the primary motor cortex. While behavioural benefits of this approach have been described, the neurophysiological changes have not yet been fully characterized. In this study, we investigated how neural activity in the form of local field potential (LFP) was impacted by an ischemic lesion and how it changed following prolonged ADS sessions. Intracortical microelectrodes arrays were used to record and stimulate from the rostral forelimb area (RFA) and the primary somatosensory cortex (S1) of 12 rats (Long Evans). An ischemic injury induced with Endothelin-1 microinjections in the caudal forelimb area (CFA) was used as an injury model. We found that the ET-1 caused lesion led to widespread drop of LFP power across all the frequency bands in both the monitored areas. The lesion did not change the functional connectivity within the brain areas, while it increased the synchronization between them. Following stimulation, LFP power generally increased in both areas. Stimulation also led to a decrement in connectivity between S1 and RFA, while causing the within S1 connectivity to increase.