ArticleNeurochemistry international2009
Schizophrenia-like GABAergic gene expression deficits in cerebellar Golgi cells from rats chronically exposed to low-dose phencyclidine.
Article in Neurochemistry international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- Neighborhood social fragmentation and cerebello-thalamo-cortical connectivity in youth at clinical high-risk for psychosis and healthy comparisons.Brain and environment · 2026Article
- New clues for the role of cerebellum in schizophrenia and the associated cognitive impairment.Frontiers in cellular neuroscience · 2024Review
- Why Can Modulation of α6-Containing GABAArchives of pharmacology and therapeutics · 2024Article
- Cerebellar Functional Dysconnectivity in Drug-Naïve Patients With First-Episode Schizophrenia.Schizophrenia bulletin · 2023Article
- Myospryn deficiency leads to impaired cardiac structure and function and schizophrenia-associated symptoms.Cell and tissue research · 2021Article
- Genetic and animal model analyses reveal the pathogenic role of a novel deletion of RELN in schizophrenia.Scientific reports · 2018Article
- Neuronal RNA-binding protein HuD regulates addiction-related gene expression and behavior.Genes, brain, and behavior · 2018Article
- mGluR2/3 agonist LY379268 rescues NMDA and GABAA receptor level deficits induced in a two-hit mouse model of schizophrenia.Psychopharmacology · 2016Article
- GluN2D N-Methyl-d-Aspartate Receptor Subunit Contribution to the Stimulation of Brain Activity and Gamma Oscillations by Ketamine: Implications for Schizophrenia.The Journal of pharmacology and experimental therapeutics · 2016Article
- Molecular substrates of schizophrenia: homeostatic signaling to connectivity.Molecular psychiatry · 2016Review
- The subchronic phencyclidine rat model: relevance for the assessment of novel therapeutics for cognitive impairment associated with schizophrenia.Psychopharmacology · 2015Review
- Exogenous Sonic hedgehog modulates the pool of GABAergic interneurons during cerebellar development.Cerebellum (London, England) · 2015Article
- Impaired limbic cortico-striatal structure and sustained visual attention in a rodent model of schizophrenia.The international journal of neuropsychopharmacology · 2014Article
- Modulation of GABAergic transmission in development and neurodevelopmental disorders: investigating physiology and pathology to gain therapeutic perspectives.Frontiers in cellular neuroscience · 2014Review
- Role of glutamic acid decarboxylase 67 in regulating cortical parvalbumin and GABA membrane transporter 1 expression: implications for schizophrenia.Neurobiology of disease · 2013Article
- Animal models of schizophrenia.British journal of pharmacology · 2011Review
- Opposite effects of acute ethanol exposure on GAP-43 and BDNF expression in the hippocampus versus the cerebellum of juvenile rats.Alcohol (Fayetteville, N.Y.) · 2011Article
- Abnormalities of neuronal oscillations and temporal integration to low- and high-frequency auditory stimulation in schizophrenia.Biological psychiatry · 2011Article
- The role of the cerebellum in schizophrenia: from cognition to molecular pathways.Clinics (Sao Paulo, Brazil) · 2011Review
- Increased expression of axogenesis-related genes and mossy fibre length in dentate granule cells from adult HuD overexpressor mice.ASN neuro · 2011Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
One of the most consistent findings in schizophrenia is the decreased expression of the GABA synthesizing enzymes GAD(67) and GAD(65) in specific interneuron populations. This dysfunction is observed in distributed brain regions including the prefrontal cortex, hippocampus, and cerebellum. In an effort to understand the mechanisms for this GABA deficit, we investigated the effect of the N-methyl-D-aspartate receptor (NMDAR) antagonist phencyclidine (PCP), which elicits schizophrenia-like symptoms in both humans and animal models, in a chronic, low-dose exposure paradigm. Adult rats were given PCP at a dose of 2.58 mg/kg/day i.p. for a month, after which levels of various GABAergic cell mRNAs and other neuromodulators were examined in the cerebellum by qRT-PCR. Administration of PCP decreased the expression of GAD(67), GAD(65), and the presynaptic GABA transporter GAT-1, and increased GABA(A) receptor subunits similar to those seen in patients with schizophrenia. Additionally, we found that the mRNA levels of two Golgi cell selective NMDAR subunits, NR2B and NR2D, were decreased in PCP-treated rats. Furthermore, we localized the deficits in GAD(67) expression solely to these interneurons. Slice electrophysiological studies showed that spontaneous firing of Golgi cells was reduced by acute exposure to low-dose PCP, suggesting that these neurons are particularly vulnerable to NMDA receptor antagonism. In conclusion, our results demonstrate that chronic exposure to low levels of PCP in rats mimics the GABAergic alterations reported in the cerebellum of patients with schizophrenia (Bullock et al., 2008. Am. J. Psychiatry 165, 1594-1603), further supporting the validity of this animal model.
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