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.
Highlights
The Cav3.2 (Cacna1h) gene encodes the pore-forming subunit of the low voltage activated α1H T-type calcium channel [1], which is highly expressed in the hippocampal formation and has been implicated in a variety of physiological processes [2,3,4]
We have reported that the Cav3.2-/- knockout mice (Cacna1htm1Kcam) are impaired in maintenance of late-phase longterm potentiation (L-LTP) and in retrieval of hippocampal-dependent contextual memory, while their locomotion function and ability of learning spatial cues are normal [19]
In order to reconfirm the phenotype of the Cav3.2 knockout mice, we analyzed their behavioral data after trace fear conditioning (TFC)
Summary
The Cav3.2 (Cacna1h) gene encodes the pore-forming subunit of the low voltage activated α1H T-type calcium channel [1], which is highly expressed in the hippocampal formation and has been implicated in a variety of physiological processes [2,3,4]. The neuronal α1H T-type calcium channel can generate low-threshold spikes that lead to burst firing and oscillatory behavior [5,6,7]. Alterations in these oscillations have been found in a wide range of neurological disorders including schizophrenia [8,9], Parkinson’s disease [10,11], and chronic atypical absence seizures [12]. TFC Reverses Gene Expression of Cav3.2 Knockout disrupt channel function have been associated with autism spectrum disorders [18]. These findings suggest a critical role of the Cav3.2 in the central nervous system (CNS)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
