ArticlePsychopharmacology2013
Electrophysiological and behavioral responses to ketamine in mice with reduced Akt1 expression.
Article in Psychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- The Use of Event-Related Potentials in the Study of Schizophrenia: An Overview.Advances in neurobiology · 2024Review
- Parvalbumin Cell Ablation of NMDA-R1 Leads to Altered Phase, But Not Amplitude, of Gamma-Band Cross-Frequency Coupling.Brain connectivity · 2019Article
- Toward the Language Oscillogenome.Frontiers in psychology · 2018Article
- New Repeat Polymorphism in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- PKBγ/AKT3 loss-of-function causes learning and memory deficits and deregulation of AKT/mTORC2 signaling: Relevance for schizophrenia.PloS one · 2017Article
- Sensory encoding in Neuregulin 1 mutants.Brain structure & function · 2016Article
- Alterations of Dopamine D2 Receptors and Related Receptor-Interacting Proteins in Schizophrenia: The Pivotal Position of Dopamine Supersensitivity Psychosis in Treatment-Resistant Schizophrenia.International journal of molecular sciences · 2015Review
- Delayed emergence of behavioral and electrophysiological effects following juvenile ketamine exposure in mice.Translational psychiatry · 2015Article
- Parvalbumin cell ablation of NMDA-R1 causes increased resting network excitability with associated social and self-care deficits.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
rationaleA number of studies have associated reduced Akt1 expression with vulnerability for schizophrenia. Although mice with deletion of a single copy of the Akt1 gene (Akt1(+/-)) show reduced Akt1 expression relative to wild-type (WT) animals, the extent to which these mice show schizophrenia-like phenotypic changes and/or increased susceptibility to epigenetic or non-genetic factors related to schizophrenia is unknown.
objectivesMutant mice were assessed on electroencephalographic/event-related potential (EEG/ERP) and behavioral (acoustic startle and pre-pulse inhibition) measures relevant to schizophrenia. Mice were also assessed following exposure to the NMDA receptor antagonist ketamine, a potent psychotomimetic drug, in order to assess the role of reduced Akt1 expression as a vulnerability factor for schizophrenia. Methods Akt1(+/-), Akt1(-/-), and WT mice received a series of paired-click, white noise stimuli, following ketamine (50 mg/kg) and saline injections. EEG was analyzed for ERPs and event-related power. Akt1(+/-) and WT mice were also assessed on PPI following ketamine (50 mg/kg) or saline injection.
resultsAkt1(+/-) and Akt1(-/-) mice displayed reduced amplitude of the P20 component of the ERP to the first click of a paired-click stimulus, as well as reduced S1-S2 difference for P20 and N40 components, following ketamine. Mutant mice also showed increased reduction in gamma synchrony and theta suppression following ketamine. Akt1(+/-) mice displayed reduced pre-pulse inhibition.
conclusionsReduced genetic expression of Akt1 facilitated ketamine-induced changes of EEG and behavior in mice, suggesting that reduced Akt1 expression can serve as a vulnerability factor for schizophrenia.
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