Abstract
NMDA receptor hypofunction in schizophrenia has been inferred by a large number of clinical and preclinical observations; however, whether and how NMDA receptors are exactly involved in the pathogenesis of schizophrenia are still unknown and subject to interpretation. Here we show, in two independent samples of brains from patients with schizophrenia, a significant decrease in the phosphorylation level at serine 897 (S897) of the NMDA receptor type 1 (NR1) subunit. Our finding, together with a previous report that antipsychotics increase phosphorylation of NR1 at S897 in vivo, strongly suggests that insufficient phosphorylation at S897 may contribute to the neuronal pathology underlying schizophrenia.
MeSH terms
-
Antibody Specificity
-
Blotting, Western
-
Brain / metabolism*
-
Brain Chemistry
-
Frontal Lobe / chemistry
-
Frontal Lobe / metabolism
-
Humans
-
PTEN Phosphohydrolase
-
Phosphoric Monoester Hydrolases / analysis
-
Phosphoric Monoester Hydrolases / chemistry
-
Phosphoric Monoester Hydrolases / metabolism
-
Phosphorylation
-
Receptors, AMPA / analysis
-
Receptors, AMPA / metabolism
-
Receptors, N-Methyl-D-Aspartate / analysis
-
Receptors, N-Methyl-D-Aspartate / metabolism*
-
Reference Values
-
Schizophrenia / metabolism*
-
Serine / metabolism*
-
Tumor Suppressor Proteins / analysis
-
Tumor Suppressor Proteins / metabolism
Substances
-
NR1 NMDA receptor
-
Receptors, AMPA
-
Receptors, N-Methyl-D-Aspartate
-
Tumor Suppressor Proteins
-
Serine
-
Phosphoric Monoester Hydrolases
-
PTEN Phosphohydrolase
-
PTEN protein, human
-
glutamate receptor ionotropic, AMPA 1