Deep Brain Stimulation (DBS) is an established clinical treatment for a variety of neurological disorders, including Parkinson’s Disease where it has been shown to reduce motor symptoms as well as disrupt pathological beta oscillations in the basal ganglia. The mechanisms of action of DBS on the collective activity of neuronal circuits is not fully understood. We use a recurrently-connected excitatory-inhbitory network based on the Brunel network architecture that can produce activity in a variety of states. Using a model of DBS that can reproduce observed effects such as antidromic activation, local somatic suppression, and axonal activation, we characterize the effect of stimulation across the entire parameter space of the network. We show that the effects of stimulation are dependent on the baseline state of the network, with the level of beta suppression dependent on the level of inhibition and the external drive. Specifically, networks with higher inhibition and lower drive show greater disruption of beta oscillations. We further show that networks in different states are preferentially sensitive to different frequencies of stimulation, suggesting that alternative protocols to the clinically standard high-frequency stimulation may have therapeutic efficacy.
Spandan Sengupta, Shervin Safavi, T. Knösche et al.· bioRxiv· 0 citations
A comprehensive phenomenological computational model is proposed that accounts for the impact of electrical stimulation parameters on neuronal circuits while incorporating experimentally-validated synaptic and cellular constraints and provides a mechanistic framework for understanding DBS representation and propagation in neuronal networks.
D. Crompton, L. Milosevic, M. Lankarany· bioRxiv· 0 citations