Muscarinic agonists activate Ca2+ store-operated and -independent ionic currents in insulin-secreting HIT-T15 cells and mouse pancreatic beta-cells.
Autor: | Mears, D., Zimliki, C. L. |
---|---|
Předmět: |
ACETYLCHOLINE
INSULIN PANCREATIC secretions CELLS IONS CALCIUM metabolism ANIMAL experimentation CALCIUM CARRIER proteins CELL culture CELL lines CELL receptors CELLULAR signal transduction COMPARATIVE studies DOSE-effect relationship in pharmacology HAMSTERS HEPARIN HYDROCARBONS ISLANDS of Langerhans ISLANDS of Langerhans tumors RESEARCH methodology MEDICAL cooperation MEMBRANE proteins MICE PARASYMPATHOMIMETIC agents PROTEINS RESEARCH EVALUATION research MUSCARINIC agonists CHEMICAL inhibitors PHARMACODYNAMICS |
Zdroj: | Journal of Membrane Biology; Jan2004, Vol. 197 Issue 1, p59-70, 12p |
Abstrakt: | The neurotransmitter acetylcholine, a muscarinic receptor agonist, augments glucose-induced insulin secretion from pancreatic β-cells by depolarizing the membrane to enhance voltage-gated Ca2+ influx. To clarify the electrical events involved in this process, we measured ionic currents from a clonal β-cell line (HIT-T15) and mouse pancreatic β-cells. In whole-cell recordings, the muscarinic agonist carbachol (CCh) dose-dependently and reversibly activated a voltage-independent, nonselective current (whole-cell conductance 24 pS/pF, reversal potential ~-15 mV). The current, which we refer to as I |
Databáze: | Complementary Index |
Externí odkaz: |