The<unk>  models the subset of pathologic mechanisms of schizophrenia linked to<unk> rgic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of<unk> rgic signaling via NMDA receptors. While thought to be more proximal to the root causes of schizophrenia, it does not negate the dopamine hypothesis, and the two may be ultimately brought together by circuit-based models. The development of the hypothesis allowed for the integration of the GABAergic and oscillatory abnormalities into the converging disease model and made it possible to discover the causes of some disruptions. Like the dopamine hypothesis, the development of the<unk>  hypothesis developed from the observed effects of mind-altering drugs. However, where dopamine agonists can mimic positive symptoms with significant risks to brain structures during and after use, NMDA antagonists mimic some positive and negative symptoms with less brain harm, when combined with a GABAA activating drug. Likely, both dopaminergic and glutaminergic abnormalities are implicated in schizophrenia, from a profound alteration in the function of the chemical synapses, as well as electrical synaptic irregularities. These form a portion of the complex constellation of factors, neurochemically, psychologically, psychosocially, and structurally, which result in schizophrenia.
Glutamate hypothesis of schizophrenia
Dopamine hypothesis of schizophrenia
Dopamine supersensitivity psychosis
Basic symptoms of schizophrenia
Ion channel hypothesis of Alzheimer's disease
Epigenetics of schizophrenia
Pseudoneurotic schizophrenia
Simple-type schizophrenia