Homocysteine enhances the excitability of cultured hippocampal neurons without altering the gene expression of voltage-gated ion channels
Language English Country Great Britain, England Media electronic
Document type Journal Article
Grant support
2/0081/22
VEGA
2/0081/22
VEGA
2/0081/22
VEGA
2/0081/22
VEGA
2/0081/22
VEGA
START/MED/054
Charles University
START/MED/054
Charles University
START/MED/054
Charles University
START/MED/054
Charles University
PubMed
40211242
PubMed Central
PMC11983933
DOI
10.1186/s13041-025-01205-x
PII: 10.1186/s13041-025-01205-x
Knihovny.cz E-resources
- Keywords
- Hippocampal excitability, Hyperhomocysteinemia, Intracellular calcium, Transcriptomics, Voltage gated ion channels,
- MeSH
- Hippocampus * cytology drug effects MeSH
- Homocysteine * pharmacology MeSH
- Ion Channels * genetics metabolism MeSH
- Rats MeSH
- Cells, Cultured MeSH
- Neurons * drug effects metabolism cytology MeSH
- Rats, Sprague-Dawley MeSH
- Gene Expression Regulation * drug effects MeSH
- Calcium metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Homocysteine * MeSH
- Ion Channels * MeSH
- Calcium MeSH
Elevated plasma homocysteine (Hcy) levels lead to hyperhomocysteinemia, a condition associated with various neurological disorders affecting multiple brain regions, including the hippocampus. In this study, we investigated the effects of exposing cultured rat hippocampal neurons to Hcy concentrations corresponding to mild, moderate, and severe hyperhomocysteinemia. A short 24-hour exposure had minimal effects, whereas prolonged exposure up to 14 days moderately enhanced hippocampal excitability without altering the gene expression of voltage-dependent calcium, sodium, or potassium channels or intracellular calcium levels. These findings suggest that Hcy-induced changes in neuronal excitability may contribute to neuropathologies associated with hyperhomocysteinemia.
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