BACKGROUND: Phencyclidine and ketamine induce a syndrome closely resembling schizophrenia due to their blockade of N-methyl-D-aspartate (NMDA) receptor. These findings suggested that some aspects of schizophrenia are associated with decreased NMDA--glutamatergic function. We hypothesized that structural and symptomatic deficits in schizophrenia are related to glutamatergic neurotransmission. METHODS: We studied the relationships among cerebrospinal fluid (CSF) glutamatergic markers, clinical presentation of schizophrenia, and CT parameters of brain structure in drug-free schizophrenics. RESULTS: We found no significant differences between patients with schizophrenia and controls in CSF glutamatergic markers. When patients with schizophrenia were considered as a group, significant negative correlations between glutamatergic markers and brain structural measures as well as clinical measures were observed. Cluster analysis reveals a group of lower indices of glutamatergic neurotransmission, and more prominent thought disorder as well as ventricular enlargement, and a group with increased glutamate level. CONCLUSIONS: The findings support the hypothesis that altered glutamatergic neurotransmission plays a role in the brain structure and the clinical symptoms of schizophrenia.
BACKGROUND:Phencyclidine and ketamine induce a syndrome closely resembling schizophrenia due to their blockade of N-methyl-D-aspartate (NMDA) receptor. These findings suggested that some aspects of schizophrenia are associated with decreased NMDA--glutamatergic function. We hypothesized that structural and symptomatic deficits in schizophrenia are related to glutamatergic neurotransmission. METHODS: We studied the relationships among cerebrospinal fluid (CSF) glutamatergic markers, clinical presentation of schizophrenia, and CT parameters of brain structure in drug-free schizophrenics. RESULTS: We found no significant differences between patients with schizophrenia and controls in CSF glutamatergic markers. When patients with schizophrenia were considered as a group, significant negative correlations between glutamatergic markers and brain structural measures as well as clinical measures were observed. Cluster analysis reveals a group of lower indices of glutamatergic neurotransmission, and more prominent thought disorder as well as ventricular enlargement, and a group with increased glutamate level. CONCLUSIONS: The findings support the hypothesis that altered glutamatergic neurotransmission plays a role in the brain structure and the clinical symptoms of schizophrenia.
Authors: Eric Plitman; Shinichiro Nakajima; Camilo de la Fuente-Sandoval; Philip Gerretsen; M Mallar Chakravarty; Jane Kobylianskii; Jun Ku Chung; Fernando Caravaggio; Yusuke Iwata; Gary Remington; Ariel Graff-Guerrero Journal: Eur Neuropsychopharmacol Date: 2014-08-01 Impact factor: 4.600
Authors: John R Moffett; Brian Ross; Peethambaran Arun; Chikkathur N Madhavarao; Aryan M A Namboodiri Journal: Prog Neurobiol Date: 2007-01-05 Impact factor: 11.685
Authors: Brian F O'Donnell; Jenifer L Vohs; Giri P Krishnan; Olga Rass; William P Hetrick; Sandra L Morzorati Journal: Suppl Clin Neurophysiol Date: 2013