ArticleBrain research2010
Increased sensitivity to kainic acid in a genetic model of reduced NMDA receptor function.
Article in Brain research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Common Genomic and Proteomic Alterations Related to Disturbed Neural Oscillatory Activity in Schizophrenia.International journal of molecular sciences · 2025Review
- Drug-Responsive Inhomogeneous Cortical Modulation by Direct Current Stimulation.Annals of neurology · 2020Article
- Effect of NMDA on proliferation and apoptosis in hippocampal neural stem cells treated with MK-801.Experimental and therapeutic medicine · 2018Article
- Effect of developmental NMDAR antagonism with CGP 39551 on aspartame-induced hypothalamic and adrenal gene expression.PloS one · 2018Article
- Metabolic and Homeostatic Changes in Seizures and Acquired Epilepsy-Mitochondria, Calcium Dynamics and Reactive Oxygen Species.International journal of molecular sciences · 2017Review
- Dopamine Receptors and Neurodegeneration.Aging and disease · 2015Review
- Integrative proteomic analysis of the NMDA NR1 knockdown mouse model reveals effects on central and peripheral pathways associated with schizophrenia and autism spectrum disorders.Molecular autism · 2014Article
- Effects of the selective kainate receptor antagonist ACET on altered sensorimotor gating in a genetic model of reduced NMDA receptor function.Brain research · 2012Article
- Genetic models of sensorimotor gating: relevance to neuropsychiatric disorders.Current topics in behavioral neurosciences · 2012Review
- The relevance of individual genetic background and its role in animal models of epilepsy.Epilepsy research · 2011Review
- Synaptic drive at developing synapses: transient upregulation of kainate receptors.Developmental neurobiology · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The pathophysiology of schizophrenia may involve reduced NMDA receptor function and experimental models of NMDA receptor hypofunction have proven useful for characterizing neurobiological abnormalities potentially relevant to schizophrenia. The present study assessed behavioral responses and induction of Fos after administration of kainic acid to wild type mice (NR1(+/+)) and mice with genetically reduced NMDA receptor expression (NR1(neo/neo)). At a dose of 20 mg/kg, kainic acid induced lethal seizures in 100% of the NR1(neo/neo) mice tested but produced no lethal seizures in the wild type mice. The NR1(neo/neo) mice also exhibited enhanced behavioral responses to kainic acid at a dose of 15 mg/kg but no lethal seizures were produced by this dose. A greater induction of Fos was observed in neocortical and limbic cortical regions of the NR1(neo/neo) compared to NR1(+/+) mice after administration of 15 mg/kg kainic acid. In contrast, there were no differences between the genotypes in kainic acid induced Fos in the amygdala, hippocampus, lateral septum, and nucleus accumbens. In order to determine if altered behavioral phenotypes of the NR1(neo/neo) mice could be related to increased sensitivity of kainate receptors to endogenous glutamate, effects of the highly selective kainate antagonist LY382884 were examined. The kainate antagonist reduced the exaggerated acoustic startle responses, deficits in prepulse inhibition of acoustic startle, and motor hyperactivity in the NR1(neo/neo) mice. These findings suggest that selective kainate receptor antagonists could be novel therapeutic candidates for schizophrenia.
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