Abstract

Presynaptic CaV2.2 (N‐type) channels are fundamental for transmitter release across the nervous system. The gene encoding CaV2.2 channels, Cacna1b, contains alternatively spliced exons that result in functionally distinct splice variants (e18a, e24a, e31a, and 37a/37b). Alternative splicing of the cassette exon 18a generates two mRNA transcripts (+e18a‐Cacna1b and ∆e18a‐Cacna1b). In this study, using novel mouse genetic models and in situ hybridization (BaseScope™), we confirmed that +e18a‐Cacna1b splice variants are expressed in monoaminergic regions of the midbrain. We expanded these studies and identified +e18a‐Cacna1b mRNA in deep cerebellar cells and spinal cord motor neurons. Furthermore, we determined that +e18a‐Cacna1b is enriched in cholecystokinin‐expressing interneurons. Our results provide key information to understand cell‐specific functions of CaV2.2 channels.

Highlights

  • Presynaptic CaV2.2 (N-type) channels are key mediators of transmitter release across the nervous system

  • Validation of a mouse model to detect +e18a-Cacna1b mRNA in the central nervous system

  • We found no significant differences in the total amount of Cacna1b mRNA between WT and De18a-only mice

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Summary

Introduction

Presynaptic CaV2.2 (N-type) channels are key mediators of transmitter release across the nervous system. Alternative splicing of the Cacna1b pre-mRNA is thought to provide functional diversification to cells that utilize CaV2.2 channels to release neurotransmitter. To understand the functional role of +e18a-Cacna1b and De18a-Cacna1b splice variants, it is necessary to determine their tissue and cell-type expression.

Results
Conclusion

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