ArticleProceedings of the National Academy of Sciences of the United States of America2013
Cognitive abnormalities and hippocampal alterations in monoamine oxidase A and B knockout mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 58 citations in OpenAlex.
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- From aggression to autism: new perspectives on the behavioral sequelae of monoamine oxidase deficiency.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
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- Loss of MAOA in epithelia inhibits adenocarcinoma development, cell proliferation and cancer stem cells in prostate.Oncogene · 2018Article
- Perinatal MAO Inhibition Produces Long-Lasting Impairment of Serotonin Function in Offspring.Brain sciences · 2018Article
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- Monoamine oxidase A is highly expressed in classical Hodgkin lymphoma.The Journal of pathology · 2017Article
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- Divergent Roles of Central Serotonin in Adult Hippocampal Neurogenesis.Frontiers in cellular neuroscience · 2017Review
- Emergence in extinction of enhanced and persistent responding to ambiguous aversive cues is associated with high MAOA activity in the prelimbic cortex.Neurobiology of stress · 2016Article
- Association study of MiRSNPs with schizophrenia, tardive dyskinesia and cognition.Schizophrenia research · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The monoamine oxidase isoenzymes (MAOs) A and B play important roles in the homeostasis of monoaminergic neurotransmitters. The combined deficiency of MAO A and B results in significantly elevated levels of serotonin (5-hydroxytryptamine), norepinephrine, dopamine, and β-phenylethylamine; in humans and mice, these neurochemical changes are accompanied by neurodevelopmental perturbations as well as autistic-like responses. Ample evidence indicates that normal levels of monoamines in the hippocampus, amygdala, frontal cortex, and cerebellum are required for the integrity of learning and memory. Thus, in the present study, the cognitive status of MAO A/B knockout (KO) mice was examined with a wide array of behavioral tests. In comparison with male wild-type littermates, MAO A/B KO mice exhibited abnormally high and overgeneralized fear conditioning and enhanced eye-blink conditioning. These alterations were accompanied by significant increases in hippocampal long-term potentiation and alterations in the relative expression of NMDA glutamate receptor subunits. Our data suggest that chronic elevations of monoamines, because of the absence of MAO A and MAO B, cause functional alterations that are accompanied with changes in the cellular mechanisms underlying learning and memory. The characteristics exhibited by MAO A/B KO mice highlight the potential of these animals as a useful tool to provide further insight into the molecular bases of disorders associated with abnormal monoaminergic profiles.
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