We have studied brain connectivity using a biologically inspired in silico model of the visual pathway consisting of the lateral geniculate nucleus (LGN) of the thalamus, and layers 4 and 6 of the primary visual cortex. The connectivity parameters in the model are informed by the existing anatomical parameters from mammals and rodents. In the base state, the LGN and layer 6 populations in the model oscillate with dominant alpha frequency, while the layer 4 oscillates in the theta band. By changing intra-cortical hyperparameters, specifically inhibition from layer 6 to layer 4, we demonstrate a transition to alpha mode for all the populations. Furthermore, by increasing the feedforward connectivities in the thalamo-cortico-thalamic loop, we could transition into the beta band for all the populations. On looking closely, we observed that the origin of this beta band is in the layer 6 (infragranular layers); lesioning the thalamic feedback from layer 6 removed the beta from the LGN and the layer 4. This agrees with existing physiological studies where it is shown that beta rhythm is generated in the infragranular layers. Lastly, we present a case study to demonstrate a neurological condition in the model. By changing connectivities in the network, we could simulate the condition of significant (P < 0.001) decrease in beta band power and a simultaneous increase in the theta band power, similar to that observed in Schizophrenia patients. Overall, we have shown that the connectivity changes in a simple visual thalamocortical in silico model can simulate state changes in the brain corresponding to both health and disease conditions.
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