Journal article
VMAT1 Deletion Causes Neuronal Loss in the Hippocampus and Neurocognitive Deficits in Spatial Discrimination
Neuroscience, Vol.232, pp.32-44
03/01/2013
DOI: 10.1016/j.neuroscience.2012.11.023
PMCID: PMC4364608
PMID: 23201251
Abstract
Vesicular monoamine transporters (VMAT) are involved in presynaptic storage and release of neurotransmitters. While it was thought initially that only VMAT2 is brain expressed and VMAT1 is present only in the periphery, recent data has challenged the exclusive expression of VMAT2 in brain. To further elucidate the role of VMAT1 brain expression and its potential role in neuropsychiatric disorders, we have investigated mice lacking VMAT1. Comparison of wildtype and knock-out (KO) mice using qPCR and immunohistochemistry documents the expression of VMAT1 in the brain. Deletion of VMAT1 leads to increased hippocampal apoptosis and reduced neurogenesis as assessed by caspase-3-labeling and BrdU-labeling. Behavioral data show that mice lacking VMAT1 have neurocognitive deficits. VMAT2 expression is not altered in VMAT1 KO mice, suggesting a distinct role of VMAT1. Our data support VMAT1 brain expression and suggest that VMAT1 plays a key role in survival of hippocampal neurons and thus might contribute to neurocognitive deficits observed in neuropsychiatric disorders.
Details
- Title: Subtitle
- VMAT1 Deletion Causes Neuronal Loss in the Hippocampus and Neurocognitive Deficits in Spatial Discrimination
- Creators
- Pushpinder K Multani - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PARachel Hodge - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PAMarcel A Estévez - Department of Biology, University of Pennsylvania, Philadelphia, PATed Abel - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PAHank Kung - Departments of Pharmacology and Radiology, University of Pennsylvania School of Medicine, Philadelphia, PAMark Alter - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PABethany Brookshire - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PAIrwin Lucki - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PAAleksandra H Nall - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PAKonrad Talbot - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PAGlenn A Doyle - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PAFalk W Lohoff - Center for Neurobiology and Behavior, Department of Psychiatry University of Pennsylvania School of Medicine Translational Research Laboratories, Philadelphia, PA
- Resource Type
- Journal article
- Publication Details
- Neuroscience, Vol.232, pp.32-44
- DOI
- 10.1016/j.neuroscience.2012.11.023
- PMID
- 23201251
- PMCID
- PMC4364608
- NLM abbreviation
- Neuroscience
- ISSN
- 0306-4522
- eISSN
- 1873-7544
- Language
- English
- Date published
- 03/01/2013
- Academic Unit
- Molecular Physiology and Biophysics; Psychiatry; Psychological and Brain Sciences; Iowa Neuroscience Institute; Neuroscience and Pharmacology; Biochemistry and Molecular Biology
- Record Identifier
- 9984065832902771
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