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Updated: Jun 25, 2025

Electromechanical Assessment of Optogenetically Modulated Cardiomyocyte Activity
Published on: March 5, 2020
AMPK inhibits voltage-gated calcium channel-current in rat chromaffin cells
A K Fukumoto-Inukai1, K Bermeo2, I Arenas1
1Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, UNAM, Circuito Exterior S/N, Ciudad Universitaria, Coyoacán, 04510, Ciudad de México, Mexico.
Abstract:
Metabolic changes are critical in the regulation of Ca2+ influx in central and peripheral neuroendocrine cells. To study the regulation of L-type Ca2+ channels by AMPK we used biochemical reagents and ATP/glucose-concentration manipulations in rat chromaffin cells. AICAR and Compound-C, at low concentration, significantly induce changes in L-type Ca2+ channel-current amplitude and voltage dependence. Remarkably, an overlasting decrease in the channel-current density can be induced by lowering the intracellular level of ATP. Accordingly, Ca2+ channel-current density gradually diminishes by decreasing the extracellular glucose concentration. By using immunofluorescence, a decrease in the expression of CaV1.2 is observed while decreasing extracellular glucose, suggesting that AMPK reduces the number of functional Ca2+ channels into the plasma membrane. Together, these results support for the first time the dependence of metabolic changes in the maintenance of Ca2+ channel-current by AMPK. They reveal a key step in Ca2+ influx in secretory cells.
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