Increased Calcium Influx through L-Type Calcium Channels in Hippocampal Neurons with Exogenous Expression of Presenilin-1 ΔE9 Mutant.

Abstract

Mutations in the PSEN1 gene encoding presenilin-1 (PS1) protein are the most common cause of familial Alzheimer's disease. One of these, deletion of exon 9, results in the production of shortened PS1 protein (PS1ΔE9). Neuronal hyperexcitability and hyperactivation of L-type calcium channels were observed in cellular and animal models of familial Alzheimer's disease. However, the effect of PS1ΔE9 on L-type calcium channels has not been studied before. We demonstrate enhanced calcium entry through L-type calcium channels in hippocampal mouse neurons with exogenous expression of PS1ΔE9. Additionally, we show that the same effect of the exogenous PS1ΔE9 can be observed in cells with predominant expression of L-type calcium channels subunit Cav1.2. Further research is required to unravel molecular mechanisms underlying hyperactivation L-type calcium channels caused by PS1ΔE9 expression.

• Authors: K V Skobeleva, М A Ryazantseva, Е V Kaznacheyeva
• Journal: Bulletin of experimental biology and medicine (Bull Exp Biol Med) Vol. 172 Issue 6 Pg. 785-788 (Apr 2022) ISSN: 1573-8221 [Electronic] United States
• PMID: 35503587 (Publication Type: Journal Article)
• Copyright: © 2022. Springer Science+Business Media, LLC, part of Springer Nature.

Chemical References

• Calcium Channels, L-Type
• Presenilin-1
• presenilin 1, mouse
• Calcium

Topics

• Alzheimer Disease (genetics, metabolism, pathology)
• Animals
• Calcium (metabolism)
• Calcium Channels, L-Type (genetics, metabolism)
• Hippocampus (cytology, metabolism)
• Mice
• Mutation
• Neurons (cytology, metabolism)
• Presenilin-1 (biosynthesis, genetics, metabolism)