Journal article
Ca2+-Binding Protein 1 Regulates Hippocampal-dependent Memory and Synaptic Plasticity
Neuroscience, Vol.380, pp.90-102
06/01/2018
DOI: 10.1016/j.neuroscience.2018.04.004
PMID: 29660444
Abstract
•CaBP1 regulates contextual fear conditioning.•CaBP1 is required for hippocampal long-term potentiation.•CaBP1 enhances the number of adult-born hippocampal neurons.
Ca2+-binding protein 1 (CaBP1) is a Ca2+-sensing protein similar to calmodulin that potently regulates voltage-gated Ca2+ channels. Unlike calmodulin, however, CaBP1 is mainly expressed in neuronal cell-types and enriched in the hippocampus, where its function is unknown. Here, we investigated the role of CaBP1 in hippocampal-dependent behaviors using mice lacking expression of CaBP1 (C-KO). By western blot, the largest CaBP1 splice variant, caldendrin, was detected in hippocampal lysates from wild-type (WT) but not C-KO mice. Compared to WT mice, C-KO mice exhibited mild deficits in spatial learning and memory in both the Barnes maze and in Morris water maze reversal learning. In contextual but not cued fear-conditioning assays, C-KO mice showed greater freezing responses than WT mice. In addition, the number of adult-born neurons in the hippocampus of C-KO mice was ∼40% of that in WT mice, as measured by bromodeoxyuridine labeling. Moreover, hippocampal long-term potentiation was significantly reduced in C-KO mice. We conclude that CaBP1 is required for cellular mechanisms underlying optimal encoding of hippocampal-dependent spatial and fear-related memories.
Details
- Title: Subtitle
- Ca2+-Binding Protein 1 Regulates Hippocampal-dependent Memory and Synaptic Plasticity
- Creators
- Tian Yang - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Neurology, University of Iowa, Iowa City, IA 52242, USAJeremiah K Britt - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Psychiatry, University of Iowa, Iowa City, IA 52242, USACoral J Cintrón-Pérez - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Psychiatry, University of Iowa, Iowa City, IA 52242, USAEdwin Vázquez-Rosa - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Psychiatry, University of Iowa, Iowa City, IA 52242, USAKevin V Tobin - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Neurology, University of Iowa, Iowa City, IA 52242, USAGrant Stalker - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Neurology, University of Iowa, Iowa City, IA 52242, USAJason Hardie - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Neurology, University of Iowa, Iowa City, IA 52242, USARebecca J Taugher - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Psychiatry, University of Iowa, Iowa City, IA 52242, USAJohn Wemmie - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Psychiatry, University of Iowa, Iowa City, IA 52242, USAAndrew A Pieper - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Neurology, University of Iowa, Iowa City, IA 52242, USAAmy Lee - Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Neurology, University of Iowa, Iowa City, IA 52242, USA
- Resource Type
- Journal article
- Publication Details
- Neuroscience, Vol.380, pp.90-102
- DOI
- 10.1016/j.neuroscience.2018.04.004
- PMID
- 29660444
- NLM abbreviation
- Neuroscience
- ISSN
- 0306-4522
- eISSN
- 1873-7544
- Publisher
- Elsevier Ltd
- Language
- English
- Date published
- 06/01/2018
- Academic Unit
- Molecular Physiology and Biophysics; Psychiatry; Iowa Neuroscience Institute; Biology; Radiation Oncology; Neurosurgery; Internal Medicine
- Record Identifier
- 9984003996702771
Metrics
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