Mice lacking collapsin response mediator protein 1 manifest hyperactivity, impaired learning and memory, and impaired prepulse inhibition

Collapsin response mediator protein 1 (CRMP1) is one of the CRMP family members that are involved in various aspects of neuronal development such as axonal guidance and neuronal migration. Here we provide evidence that crmp1 (-/-) mice exhibited behavioral abnormalities related to schizophrenia. The...

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Bibliographic Details
Published in:Frontiers in behavioral neuroscience 2013-12, Vol.7, p.216
Main Authors: Yamashita, Naoya, Takahashi, Aoi, Takao, Keizo, Yamamoto, Toshifumi, Kolattukudy, Pappachan, Miyakawa, Tsuyoshi, Goshima, Yoshio
Format: Article
Language:English
Subjects:
Alzheimer's disease
Antipsychotics
Axon guidance
Axonogenesis
Behavior
Cell adhesion & migration
Cell migration
Chlorpromazine
Comprehensive behavioral test
CRMP1
Cyclin-dependent kinases
Dopamine
Dopamine receptors
Emotional behavior
Hyperactivity
Kinases
knockout mouse
Long term memory
Mediator protein
Medicine
Mental disorders
mesocortical dopaminergic transmission
Methamphetamine
Microdialysis
Nervous system
Neuroscience
Neurosciences
Phenotypes
Phosphorylation
Prefrontal cortex
Proteins
Schizophrenia
Science
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Summary:Collapsin response mediator protein 1 (CRMP1) is one of the CRMP family members that are involved in various aspects of neuronal development such as axonal guidance and neuronal migration. Here we provide evidence that crmp1 (-/-) mice exhibited behavioral abnormalities related to schizophrenia. The crmp1 (-/-) mice exhibited hyperactivity and/or impaired emotional behavioral phenotype. These mice also exhibited impaired context-dependent memory and long-term memory retention. Furthermore, crmp1 (-/-) mice exhibited decreased prepulse inhibition, and this phenotype was rescued by administration of chlorpromazine, a typical antipsychotic drug. In addition, in vivo microdialysis revealed that the methamphetamine-induced release of dopamine in prefrontal cortex was exaggerated in crmp1 (-/-) mice, suggesting that enhanced mesocortical dopaminergic transmission contributes to their hyperactivity phenotype. These observations suggest that impairment of CRMP1 function may be involved in the pathogenesis of schizophrenia. We propose that crmp1 (-/-) mouse may model endophenotypes present in this neuropsychiatric disorder.
ISSN:1662-5153
1662-5153
DOI:10.3389/fnbeh.2013.00216