Authors: Michael Chrostowski Le Yang Hugh R Wilson Ian C Bruce Suzanna Becker
Publish Date: 2010/07/10
Volume: 30, Issue: 2, Pages: 279-299
Abstract
Travelling waves of activity in neural circuits have been proposed as a mechanism underlying a variety of neurological disorders including epileptic seizures migraine auras and brain injury The highly influential WilsonCowan cortical model describes the dynamics of a network of excitatory and inhibitory neurons The WilsonCowan equations predict travelling waves of activity in ratebased models that have sufficiently reduced levels of lateral inhibition Travelling waves of excitation may play a role in functional changes in the auditory cortex after hearing loss We propose that downregulation of lateral inhibition may be induced in deafferented cortex via homeostatic plasticity mechanisms We use the WilsonCowan equations to construct a spiking model of the primary auditory cortex that includes a novel mathematically formalized description of homeostatic plasticity In our model the homeostatic mechanisms respond to hearing loss by reducing inhibition and increasing excitation producing conditions under which travelling waves of excitation can emerge However our model predicts that the presence of spontaneous activity prevents the development of longrange travelling waves of excitation Rather our simulations show shortduration excitatory waves that cancel each other out We also describe changes in spontaneous firing synchrony and tuning after simulated hearing loss With the exception of shifts in characteristic frequency changes after hearing loss were qualitatively the same as empirical findings Finally we discuss possible applications to tinnitus the perception of sound without an external stimulus
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