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PLoS One. 2015 Mar 13;10(3):e0118832. doi: 10.1371/journal.pone.0118832. eCollection 2015.

Behavior training reverses asymmetry in hippocampal transcriptome of the cav3.2 knockout mice.

Author information

1
Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien, Taiwan.
2
Institute of Biomedical Informatics, National Yang-Ming University, Taipei, Taiwan.
3
Department of Chemical and Biomolecular Engineering, University of California Los Angeles, Los Angeles, California, United States of America.
4
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
5
Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien, Taiwan; Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.

Abstract

Homozygous Cav3.2 knockout mice, which are defective in the pore-forming subunit of a low voltage activated T-type calcium channel, have been documented to show impaired maintenance of late-phase long-term potentiation (L-LTP) and defective retrieval of context-associated fear memory. To investigate the role of Cav3.2 in global gene expression, we performed a microarray transcriptome study on the hippocampi of the Cav3.2-/- mice and their wild-type littermates, either naïve (untrained) or trace fear conditioned. We found a significant left-right asymmetric effect on the hippocampal transcriptome caused by the Cav3.2 knockout. Between the naive Cav3.2-/- and the naive wild-type mice, 3522 differentially expressed genes (DEGs) were found in the left hippocampus, but only 4 DEGs were found in the right hippocampus. Remarkably, the effect of Cav3.2 knockout was partially reversed by trace fear conditioning. The number of DEGs in the left hippocampus was reduced to 6 in the Cav3.2 knockout mice after trace fear conditioning, compared with the wild-type naïve mice. To our knowledge, these results demonstrate for the first time the asymmetric effects of the Cav3.2 and its partial reversal by behavior training on the hippocampal transcriptome.

Comment in

PMID:
25768289
PMCID:
PMC4358833
DOI:
10.1371/journal.pone.0118832
[Indexed for MEDLINE]
Free PMC Article

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