Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2530670 | Current Opinion in Pharmacology | 2007 | 8 Pages |
Abstract
The pathophysiology of schizophrenia is poorly understood but is likely to involve alterations in excitatory glutamatergic signaling molecules in several areas of the brain. Clinical and experimental evidence has shown that expression of the N-methyl-d-asparate (NMDA) receptor and intracellular NMDA receptor-interacting proteins of the glutaminergic synapse appear to be dysregulated in schizophrenia. It has been suggested that schizophrenia involves molecular changes in the glutamatergic pathways that mediate excitatory communication between multiple brain regions. Recent data also implicate abnormalities in cellular functions such as receptor trafficking and synaptic targeting.
Related Topics
Life Sciences
Neuroscience
Cellular and Molecular Neuroscience
Authors
Lars V Kristiansen, Ibone Huerta, Monica Beneyto, James H Meador-Woodruff,