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Downregulation of voltage-gated sodium channels by dexamethasone in clonal rat pituitary cells
Guillermo Avila1, Eduardo Monjaraz, Juan Luis Espinosa
1Department of Biochemistry, Cinvestav-IPN, AP 14-740, DF 07000, Mexico City, Mexico.
Abstract:
The effect of chronic dexamethasone (DEX) treatment (4-5 days) on Na(+) channel expression was examined in a clonal strain of rat pituitary cells secreting growth hormone (GH) and prolactin (GH3 cells). Using whole-cell patch clamp recording, we found that DEX (1 microM) induces an 80% decrease in Na(+) current density. No concomitant changes in current kinetics or voltage dependence of Na(+) channel function were detected. Instead, the decrease in current density was accompanied by a similar reduction in maximal Na(+) conductance, suggesting the loss of Na(+) channels from the plasma membrane. Accordingly, saxitoxin binding assays carried out on intact cells showed that the average number of Na(+) channels per cell is markedly decreased by DEX. Thus, this glucocorticoid inhibits the cell surface expression of Na(+) channels when chronically applied to GH3 cells.
Insights
Chronic dexamethasone treatment significantly reduces sodium channel expression in rat pituitary cells. This glucocorticoid lowers sodium current density and the number of cell surface sodium channels in GH3 cells.
Area of Science:
- Endocrinology
- Neuroscience
- Cell Biology
Background:
- Dexamethasone (DEX) is a potent glucocorticoid with widespread physiological effects.
- Pituitary GH3 cells express sodium channels, crucial for cellular excitability.
- The impact of chronic DEX on ion channel expression in these cells is not fully understood.
Purpose of the Study:
- To investigate the effect of chronic dexamethasone (DEX) on sodium (Na+) channel expression in rat pituitary GH3 cells.
- To determine if DEX alters Na+ channel function or surface expression.
Main Methods:
- Whole-cell patch clamp recordings were used to measure Na+ current density and kinetics.
- Saxitoxin binding assays were performed to quantify cell surface Na+ channel numbers.
- GH3 cells were chronically treated with 1 microM DEX for 4-5 days.
Main Results:
- DEX treatment induced an 80% decrease in Na+ current density.
- No changes in Na+ channel kinetics or voltage dependence were observed.
- Saxitoxin binding assays revealed a marked reduction in the number of cell surface Na+ channels.
Conclusions:
- Chronic dexamethasone treatment inhibits the cell surface expression of Na+ channels in GH3 cells.
- The observed decrease in Na+ current density is attributed to a loss of functional Na+ channels from the plasma membrane.
- DEX alters Na+ channel expression, impacting the electrophysiological properties of pituitary cells.
