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A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate

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NMDA receptors and schizophrenia.

Lars V Kristiansen¹, Ibone Huerta, Monica Beneyto

¹University of Alabama at Birmingham, Department of Psychiatry and Behavioral Neurobiology, SC560, 1530 3rd Avenue South, Birmingham, AL 35294-0017, USA. larsk@uab.edu

Current Opinion in Pharmacology

|November 14, 2006

Summary

Schizophrenia pathophysiology may involve altered N-methyl-D-aspartate (NMDA) receptor signaling. Dysregulation of glutamatergic pathways and synaptic functions are implicated in this complex brain disorder.

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Area of Science:

Neuroscience
Psychiatry
Molecular Biology

Background:

Schizophrenia pathophysiology remains largely unknown.
Alterations in excitatory glutamatergic signaling are suspected.
N-methyl-D-aspartate (NMDA) receptor dysregulation is observed in schizophrenia.

Purpose of the Study:

To investigate the role of glutamatergic signaling in schizophrenia.
To explore NMDA receptor and interacting protein dysregulation.
To understand molecular changes in excitatory brain communication.

Main Methods:

Analysis of NMDA receptor expression.
Investigation of intracellular NMDA receptor-interacting proteins.
Examination of glutamatergic pathway molecular changes.

Main Results:

Evidence suggests dysregulated NMDA receptor and associated protein expression.
Schizophrenia is linked to molecular changes in glutamatergic pathways.
Abnormalities in receptor trafficking and synaptic targeting are implicated.

Conclusions:

Glutamatergic system alterations are central to schizophrenia pathophysiology.
NMDA receptor dysfunction is a key feature.
Further research into synaptic mechanisms is warranted.