ArticleExperimental brain research2010
Postnatal exposure to MK801 induces selective changes in GAD67 or parvalbumin.
Article in Experimental brain research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Neuroimaging studies of GABA in schizophrenia: a systematic review with meta-analysis.Translational psychiatry · 2017Pooled it
- Effectiveness of positive allosteric modulators of metabotropic glutamate receptor 2/3 (mGluR2/3) in animal models of schizophrenia.Translational psychiatry · 2025Review
- Impact of Dysfunctional Feed-Forward Inhibition on Glutamate Decarboxylase Isoforms and γ-Aminobutyric Acid Transporters.International journal of molecular sciences · 2021Article
- Altered excitatory transmission onto hippocampal interneurons in the IQSEC2 mouse model of X-linked neurodevelopmental disease.Neurobiology of disease · 2020Article
- Short-Term Exposure to Enriched Environment in Adult Rats Restores MK-801-Induced Cognitive Deficits and GABAergic Interneuron Immunoreactivity Loss.Molecular neurobiology · 2018Article
- Repeated Blockade of NMDA Receptors During Adolescence Impairs Reversal Learning and Disrupts GABAergic Interneurons in Rat Medial Prefrontal Cortex.Frontiers in molecular neuroscience · 2016Article
- Postnatal MK-801 treatment of female rats impairs acquisition of working memory, but not reference memory in an eight-arm radial maze; no beneficial effects of enriched environment.Psychopharmacology · 2015Article
- Loss of phenotype of parvalbumin interneurons in rat prefrontal cortex is involved in antidepressant- and propsychotic-like behaviors following acute and repeated ketamine administration.Molecular neurobiology · 2015Article
- Enriched environment prevents cognitive and motor deficits associated with postnatal MK-801 treatment.Psychopharmacology · 2014Article
- Fgfr1 inactivation in the mouse telencephalon results in impaired maturation of interneurons expressing parvalbumin.PloS one · 2014Article
- Impact of ketamine on neuronal network dynamics: translational modeling of schizophrenia-relevant deficits.CNS neuroscience & therapeutics · 2013Review
- Periadolescent exposure to the NMDA receptor antagonist MK-801 impairs the functional maturation of local GABAergic circuits in the adult prefrontal cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- The influence of NMDA and GABA(A) receptors and glutamic acid decarboxylase (GAD) activity on attention.Psychopharmacology · 2013Article
- Strategies to defeat ketamine-induced neonatal brain injury.Neuroscience · 2012Article
- Is age-dependent, ketamine-induced apoptosis in the rat somatosensory cortex influenced by temperature?Neuroscience · 2010Article
- Postnatal expression of GAD67.Neurochemical research · 2010Article
- Neonatal exposure to MK801 promotes prepulse-induced delay in startle response time in adult rats.Experimental brain research · 2009Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Brain injury during the last trimester to the first 1-4 years in humans is now thought to trigger an array of intellectual and emotional problems later in life, including disorders such as schizophrenia. In adult schizophrenic brains, there is a specific loss of neurons that co-express glutamic acid decarboxylase-parvalbumin (GAD67-PV). Loss of this phenotype is thought to occur in mature animals previously exposed to N-methyl-D: -aspartate receptor (NMDAR) antagonists during late gestation or at postnatal day 7 (P7). However, in similarly treated animals, we have previously shown that GAD67 and PV are unaltered in the first 24 h. To more precisely define when changes in these markers first occur, we exposed rat pups (P7 or P6-P10) to the NMDAR antagonist MK801 and at P11 co-stained brain sections for GAD67 or PV. In the cingulate cortex, we found evidence for a reduction in PV (GAD67 levels were very low to undetectable). In contrast, in the somatosensory cortex, we found that expression of GAD67 was reduced, but PV remained stable. Further, repeated but not single doses of MK801 were necessary to see such changes. Thus, depending on the region, NMDAR antagonism appears to influence expression of PV or GAD67, but not both. These observations could not have been predicted by previous studies and raise important questions as to how the GAD67-PV phenotype is lost once animals reach maturity. More importantly, such differential effects may be of great clinical importance, given that cognitive deficits are seen in children exposed to anesthetics that act by blocking the NMDAR.
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Registered trials
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