Modeling the spontaneous activity of the auditory cortex.
We present a rate model of the spontaneous activity in the auditory cortex, based on synaptic depression. A Stochastic integro-differential system of equations is derived and the analysis reveals two main regimes. The first regime corresponds to a normal activity. The second regime corresponds to epileptic spiking. A detailed analysis of each regime is presented and we prove in particular that synaptic depression stabilizes the global cortical dynamics. The transition between the two regimes is induced by a change in synaptic connectivity: when the overall connectivity is strong enough, an epileptic activity is spontaneously generated. Numerical simulations confirm the predictions of the theoretical analysis. In particular, our results explain the transition from normal to epileptic regime which can be induced in rats auditory cortex, following a specific pairing protocol. A change in the cortical maps reorganizes the synaptic connectivity and this transition between regimes is accounted for by our model. We have used data from recording experiments to fit synaptic weight distributions. Simulations with the fitted distributions are qualitatively similar to the real EEG recorded in vivo during the experiments. We conclude that changes in the synaptic weight function in our model, which affects excitatory synapses organization and reproduces the changes in cortical map connectivity can be understood as the main mechanism to explain the transitions of the EEG from the normal to the epileptic regime in the auditory cortex.
Bart
E
E
Department of Applied Mathematics and Computer Science, Weizmann Institute of Science, Rehovot 76100, Israel.
Bao
S
S
Holcman
D
D
D000465:Algorithms; D001303:Auditory Cortex / Q000502:physiology* / Q000503:physiopathology; D001519:Behavior / Q000502:physiology; D001703:Biophysics / Q000706:statistics & numerical data; D003198:Computer Simulation; D004569:Electroencephalography; D004827:Epilepsy / Q000503:physiopathology / Q000523:psychology; D006801:Humans; D008959:Models, Neurological; D009434:Neural Pathways / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000502:physiology; D013569:Synapses / Q000502:physiology