Chronic phencyclidine administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain
@article{Reynolds2005ChronicPA, title={Chronic phencyclidine administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain}, author={Lindsay M. Reynolds and Susan M. Cochran and Brian J. Morris and Judith A. Pratt and Gavin P. Reynolds}, journal={Schizophrenia Research}, year={2005}, volume={73}, pages={147-152} }
53 Citations
Reduced n-acetylaspartate in the temporal cortex of rats reared in isolation
- Biology, PsychologyBiological Psychiatry
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Increased N-acetylaspartate in rat striatum following long-term administration of haloperidol
- Psychology, BiologySchizophrenia Research
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Investigation of the neuronal marker N-acetylaspartate as a potential biomarker for neurological diseases
- Psychology, Biology
- 2015
The present studies suggest that NAA shows promise as a biomarker for neuronal dysfunction in neurological diseases that can be used in pre-clinical and clinical setting with both in vivo and ex vivo applications.
Phencyclidine animal models of schizophrenia: Approaches from abnormality of glutamatergic neurotransmission and neurodevelopment
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Differential regional N-acetylaspartate deficits in postmortem brain in schizophrenia, bipolar disorder and major depressive disorder.
- Psychology, MedicineJournal of psychiatric research
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Schizophrenia-like GABAergic gene expression deficits in cerebellar Golgi cells from rats chronically exposed to low-dose phencyclidine
- Biology, PsychologyNeurochemistry International
- 2009
T-817MA, a novel neurotrophic compound, ameliorates phencyclidine-induced disruption of sensorimotor gating
- Psychology, BiologyPsychopharmacology
- 2007
Results suggest that T-817MA is effective in ameliorating sensorimotor gating deficits caused by chronic PCP treatment, possibly via neuroprotective actions, and provide a novel therapeutic approach for patients with schizophrenia.
Striatal N-Acetylaspartate Synthetase Shati/Nat8l Regulates Depression-Like Behaviors via mGluR3-Mediated Serotonergic Suppression in Mice
- Biology, ChemistryThe international journal of neuropsychopharmacology
- 2017
The findings indicate that the striatal expression of N-acetylaspartate synthetase Shati/Nat8l plays a role in major depressive disorder via the metabotropic glutamate receptor 3-mediated functional control of the serotonergic neuronal system.
The subchronic phencyclidine rat model: relevance for the assessment of novel therapeutics for cognitive impairment associated with schizophrenia
- Psychology, BiologyPsychopharmacology
- 2015
The multi-site study confirmed that scPCP impaired NOR and ASST only and demonstrated the reproducibility and usefulness of the touchscreen approach and recommended further work is required to understand the neurochemical changes and specificity of the cognitive deficits.
Overexpression of Shati/Nat8l, an N-acetyltransferase, in the nucleus accumbens attenuates the response to methamphetamine via activation of group II mGluRs in mice.
- BiologyThe international journal of neuropsychopharmacology
- 2014
Results indicate that Shati/Nat8l in the NAc, but not in the dS, plays an important suppressive role in the behavioral responses to METH by controlling the dopaminergic system via activation of group II mGluRs.
References
SHOWING 1-10 OF 37 REFERENCES
The effect of treatment with antipsychotic drugs on brain N-acetylaspartate measures in patients with schizophrenia
- Psychology, MedicineBiological Psychiatry
- 2001
Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs.
- Biology, PsychologyScience
- 1989
These findings raise new questions regarding the safety of these agents in the clinical management of neurodegenerative diseases and reinforce concerns about the potential risks associated with illicit use of PCP.
Distribution of N-acetylaspartylglutamate immunoreactivity in human brain and its alteration in neurodegenerative disease
- BiologyBrain Research
- 1997
N-acetylaspartate and N-Acetylaspartylglutamate deficits in superior temporal cortex in schizophrenia and bipolar disorder: a postmortem study
- Psychology, MedicineBiological Psychiatry
- 2003
Recent advances in the phencyclidine model of schizophrenia.
- Psychology, MedicineThe American journal of psychiatry
- 1991
It was found that PCP-induced psychotomimetic effects are associated with submicromolar serum concentrations of PCP and the findings suggest that endogenous dysfunction of NMDA receptor-mediated neurotransmission might contribute to the pathogenesis of schizophrenia.
Induction of Metabolic Hypofunction and Neurochemical Deficits after Chronic Intermittent Exposure to Phencyclidine: Differential Modulation by Antipsychotic Drugs
- Psychology, BiologyNeuropsychopharmacology
- 2003
It is demonstrated that chronic intermittent exposure to PCP elicits a metabolic hypofunction, as demonstrated by reductions in the rates of glucose utilization, and proposed that reversal of PCP-induced reductions in parvalbumin expression in the prefrontal cortex may be a potential marker of atypical antipsychotic activity in relation to amelioration of cognitive deficits and negative symptoms of schizophrenia.
The Neuropsychopharmacology of Phencyclidine: From NMDA Receptor Hypofunction to the Dopamine Hypothesis of Schizophrenia
- Psychology, BiologyNeuropsychopharmacology
- 1999
N-acetylaspartylglutamate, N-acetylaspartate, and N-acetylated alpha-linked acidic dipeptidase in human brain and their alterations in Huntington and Alzheimer's diseases.
- Biology, PsychologyMolecular and chemical neuropathology
- 1997
It is shown that the decreases in the levels of NAAG and NAA and in the activity of NAALADase in AD and HD brain correlate primarily with neuronal loss, and that there is a close relationship between N AAG and the dipeptidase NAALadase in populations of affected neurons.
Glutamate receptor dysfunction and schizophrenia.
- Psychology, MedicineArchives of general psychiatry
- 1995
It is proposed that since N-methyl-D-aspartate receptor hypofunction can cause psychosis in humans and corticolimbic neurodegenerative changes in the rat brain, and since these changes are prevented by certain antipsychotic drugs, including atypical neuroleptic agents, a better understanding of this mechanism may lead to improved pharmacotherapy in schizophrenia.
Abnormal excitatory neurotransmitter metabolism in schizophrenic brains.
- Psychology, MedicineArchives of general psychiatry
- 1995
The hypothesis that schizophrenia results from a hypofunction of certain glutamatergic neuronal systems is supported and the therapeutic efficacy of neuroleptics may be related to increased glutamatorgic activity.