Studies have tied the hyperfunctioning of the dopaminergic system to hyperexcitability in the hippocampus,77, 78 one of the potential drivers of which is the reduced number of GABAergic interneurons providing tonic inhibitory control.79, 80 Human studies also suggest a major role for GABAergic dysfunction in SCZ. Post-mortem studies of SCZ brains reveals a 40% reduction in GABAergic synapses,81 which is a deficiency that may originate during development.82 Indeed, grafting GABAergic neurons into the ventral hippocampus in the rodent model of SCZ restored normal hippocampal functioning, corrected downstream dopaminergic dysregulation and rescued behavioral deficits.54, 83
