Abstract:
It has been hypothesised for >20 years that there may be NMDA receptor dysfunction in schizophrenia, leading to an imbalance between excitatory and inhibitory function in cortical circuits. The exact nature of this imbalance is unclear, however. Biophysical modelling of M/EEG paradigms can enable us to make inferences about cortical dysfunction: not just regarding connectivity between cortical areas, but also about dysfunction of specific neuronal populations. Using dynamic causal modelling of multiple M/EEG paradigms, I have found evidence for dysfunction of pyramidal cells in schizophrenia, and (perhaps compensatory) loss of inhibition that relates to symptoms. This suggests promising avenues for future work, including how to allocate existing glutamatergic treatments for the disorder.
