The Glutamate Hypothesis of Schizophrenia

Recent research into the pathophysiology and treatment of schizophrenia has led to moving beyond the dopamine dysfunction hypothesis—which involves an overstimulation of dopaminergic D2 receptors in certain parts of the brain, leading to hallucinations, delusions, and other symptoms of the disorder—to potentially targeting other neurotransmitter systems to enhance the therapeutic response. The glutamate hypothesis of schizophrenia posits that the disorder may be at least partially caused by deficient activity at glutamate synapses, which may in turn account for negative and cognitive symptoms. Glutamate neurotransmission is complex at the circuit level, and an understanding of actions at the receptor level can help our understanding of those glutamate circuits associated with schizophrenia.

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