Aeed, F. | Search bioRxiv

bioRxiv2024

Electrical Coordinated Reset Stimulation Induces Network Desynchronization in an in Vivo Model of Status Epilepticus

Epilepsy, a neurological disorder characterized by recurrent seizures, profoundly impacts individuals worldwide. Various electrical stimulation protocols have been investigated to mitigate epileptic seizures, among which Coordinated Reset (CR) stimulation may have potential for inducing long-lasting neural desynchronization. This study explores the acute effects of CR stimulation on synchronization dynamics during Status Epilepticus (SE) in an in vivo animal model. An electrographically sustained seizure-state was induced via 4-aminopyridine (4AP) administration to CA3. Custom-designed electrode probes were implanted to facilitate simultaneous recording and electrical stimulation. Analytical univariate and bivariate features were constructed from the LFP time-series recording. Feature metrics focused on spike synchronization metrics and continuous signal analysis of amplitude, spectral power and phase synchronization across electrode pairs and frequency bands. Significance of modulation was assessed through permutation testing of the observed differences between the CR-stimulated group (N=5) compared to the control (no stimulation) group (N=3) during SE. Results showed overall decrease in amplitude and power univariate features, and a significant modulation of bivariate synchronization and connectivity measures across the spectrum between the CR stimulation and control group. Our findings underscore the potential effectiveness of CR stimulation in attenuating excessive neural synchronization, paving the way for further exploration of CR stimulation as a viable intervention for network desynchronization of epileptiform activity and subsequently treatment of seizures.

neuroscience↗

bioRxiv2020

Cell-type specific outcome representation in primary motor cortex

Adaptive movements are critical to animal survival. To guide future actions, the brain monitors different outcomes, including achievement of movement and appetitive goals. The nature of outcome signals and their neuronal and network realization in motor cortex (M1), which commands the performance of skilled movements, is largely unknown. Using a dexterity task, calcium imaging, optogenetic perturbations, and behavioral manipulations, we studied outcome signals in murine M1. We find two populations of layer 2-3 neurons, "success"- and "failure" related neurons that develop with training and report end-result of trials. In these neurons, prolonged responses were recorded after success or failure trials, independent of reward and kinematics. In contrast, the initial state of layer-5 pyramidal tract neurons contains a memory trace of the previous trials outcome. Inter-trial cortical activity was needed to learn new task requirements. These M1 reflective layer-specific performance outcome signals, can support reinforcement motor learning of skilled behavior.

neuroscience↗