• Tian Yang, Jeremiah K Britt, Coral J Cintrón-Pérez, Edwin Vázquez-Rosa, Kevin V Tobin, Grant Stalker, Jason Hardie, Rebecca J Taugher, John Wemmie, Andrew A Pieper, and Amy Lee.
• Departments of Molecular Physiology and Biophysics, Otolaryngology Head-Neck Surgery, Neurology, University of Iowa, Iowa City, IA 52242, USA.
• Neuroscience. 2018 Jun 1; 380: 90-102.

AbstractCa2+-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.Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.

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