Synaptic signaling by nitric oxide

https://doi.org/10.1016/S0959-4388(97)80065-7Get rights and content

Abstract

Endogenous nitric oxide (NO) mediates certain aspects of synaptic plasticity and neurotoxicity associated with NMDA-type glutamate receptors. Neuronal NO synthase contains a modular protein—protein interaction motif, termed the PDZ domain, that links the synthase to a synaptic protein complex containing postsynaptic density protein PSD-95 and NMDA receptors. Characterization of this pathway has provided new insights into the role of NO in brain physiology and disease.

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      Avolition, anhedonia and social withdrawal are negative symptoms [224]. NO has been suggested to play a role in the onset of schizophrenia [227,228] and research indicates that impairments of dopaminergic and cholinergic pathways may be partly responsible for the progression of schizophrenia through NMDAR-dependent dys-regulation of NO signalling [229–231]. Additionally, polymorphism of the nNOS gene is a high-risk factor of schizophrenia development [232].

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