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}
}
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53 Citations
Highly Influential Citations
2
Background Citations
18
Methods Citations
9
Results Citations
2

53 Citations

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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
Differential regional N-acetylaspartate deficits in postmortem brain in schizophrenia, bipolar disorder and major depressive disorder.
Schizophrenia-like GABAergic gene expression deficits in cerebellar Golgi cells from rats chronically exposed to low-dose phencyclidine
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.
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References

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TLDR
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TLDR
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TLDR
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