Publication |
2002
Abstract
Recent findings of increased levels of N-acetyl-aspartyl-glutamate in some regions of schizophrenic brains support the hypothesis of dysfunction of glutamatergic neurotransmission in this psychosis, but at the same time, they keep most pathophysiological questions unanswered. We demonstrated that the interaction with NMDA receptors may be responsible later for neuronal damage, which was especially evident in the neonatal rat brain.
Pathophysiologic importance of this model and its validity as a "heuristic" model of psychosis is discussed.