Abstract
Cortical spreading depression (SD) is a spreading disruption of ionic homeostasis in the brain during which neurons experience complete and prolonged depolarizations. SD is the basis of migraine aura and is increasingly associated with many other brain pathologies. Here, we study the role of glutamate and NMDA receptor dynamics in the context of an ionic electrodiffusion model. We perform simulations in one (1D) and two (2D) spatial dimension. Our 1D simulations reproduce the "inverted saddle" shape of the extracellular voltage signal for the first time. Our simulations suggest that SD propagation depends on two overlapping mechanisms; one dependent on extracellular glutamate diffusion and NMDA receptors and the other dependent on extracellular potassium diffusion and persistent sodium channel conductance. In 2D simulations, we study the dynamics of spiral waves. We study the properties of the spiral waves in relation to the planar 1D wave, and also compute the energy expenditure associated with the recurrent SD spirals.
Highlights
Cortical Spreading Depression (SD) is a pathophysiological phenomenon in the central nervous system characterized by a local breakdown in ionic homeostasis resulting in a temporary silencing of neuronal electrical activity
Cortical spreading depression is a wave of neuronal silencing and ion concentration changes that sweeps slowly through the brain
We study the mechanisms by which cortical spreading depression travels as a wave through the brain
Summary
Cortical Spreading Depression (SD) is a pathophysiological phenomenon in the central nervous system characterized by a local breakdown in ionic homeostasis resulting in a temporary silencing of neuronal electrical activity. This local ionic disruption propagates at speeds of 2-7 mm/min [1]. SD was first discovered by Leao in 1944 [5], and has since been intensively studied from both experimental and theoretical points of view [6]. Many aspects of SD still remain elusive [6,7,8,9,10]
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