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Rogue states: altered dimensionality of neural circuit activity in Fragile-X mice

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If you have a question about this talk, please contact Guillaume Hennequin.

Brain disorders such as autism and schizophrenia have been hypothesized to arise from an imbalance in excitation/inhibition in neural circuits. Why or how such an imbalance would be detrimental for neural coding remains unclear. We approached the problem by analysing two-photon in vivo neural population recordings from the cortex of both wild-type and Fragile-X Syndrome model mice at different stages of development. We developed a new statistical model for the probability distribution of all 2N possible neural population activity patterns that required only N2 parameters, where N is the number of neurons. Using this model we found that the dimensionality of population activity was lower in Fragile-X than wild-type mice at adolescence, but surprisingly switched in adulthood so that Fragile-X dimensionality was higher than wild-type. Finally we used a computational model of layer 2/3 somatosensory cortex to show which neural circuit components can give rise to these alterations in dimensionality. Our findings show how small changes in neural circuit parameters can have dramatic consequences for information processing.

This talk is part of the Computational Neuroscience series.

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