Gamma oscillations in mouse primary visual cortex as a biomarker of pathological conditions

Neural gamma oscillations are ubiquitous: diverse functions have been associated with gamma oscillations recorded in extracellular potentials from multiple cortical and subcortical regions. Arising from the coherent activity of hundreds of neurons, gamma rhythm emerges from the coordinated and balanced interaction of excitation and inhibition within a neural network. Coherently, gamma is strongly influenced by any alterations of such balance, such as the synaptic dynamic alterations which are often associated with pathological neural dysfunctions. To investigate the extent of this relationship, we present here a collection of works targeting the neural activity of the primary visual cortex (V1) of mice. We combined several methodological tools: spectral analysis, information theory, and computational modeling. We present first a novel computational model (consisting of a leaky-integrate-and-fire neuronal network) reproducing in silico the multiple forms of gamma oscillations observed in V1 of wild-type awake mice. We used then this model to investigate the neural mechanisms underlying migraine. We observed specific alterations of gamma oscillations in the local field potentials of a monogenetic mouse model of migraine. We consequently employed the computational model to investigate the circuital origins of migraine-driven gamma alterations. Specifically, we examined the relative contribution of each synaptic modification known to be associated with migraine to the pathological neuronal activity observed at the network level. Interestingly, we also found gamma oscillations in mice V1 to be efficient in probing pathological information processing of visual stimuli in a focal model of neocortical epilepsy. We additionally analyzed the impact of the presence of glioma cells on visual cortex activity. Resorting to electrophysiological investigations at different scales, we explored the detrimental impact of tumor cells on the processing of sensory information by the spared neuronal circuitry, and (interestingly) vice versa.