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}
}
Investigation of the neuronal marker N-acetylaspartate as a potential biomarker for neurological diseases
TLDR
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.
T-817MA, a novel neurotrophic compound, ameliorates phencyclidine-induced disruption of sensorimotor gating
TLDR
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
TLDR
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
TLDR
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.
TLDR
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
Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs.
TLDR
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.
Recent advances in the phencyclidine model of schizophrenia.
TLDR
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
TLDR
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.
N-acetylaspartylglutamate, N-acetylaspartate, and N-acetylated alpha-linked acidic dipeptidase in human brain and their alterations in Huntington and Alzheimer's diseases.
TLDR
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.
TLDR
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.
TLDR
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.
...
...