Ca²⁺‐Dependent K⁺ Currents Induced by Muscarinic Receptor Activation in Guinea Pig Adrenal Chromaffin Cells

Abstract

Abstract:The characteristics of the outward current (/out) induced by muscarine were examined by using the whole-cell patch-clamp technique with a K~-containing pipette solution in combination with fura-2 microfluorometry in guinea pig chromaffin cells. Muscarine caused a transient increase in the cytosolic Ca2~concentration ([Ca2~])and activated an 'out with a reversal potential close to a Kẽquilibrium potential. Under symmetric K conditions, muscarine produced a transient inward current and an increase in [Ca2~]ãt -60 mV. At -15 mV, apamin and charybdotoxin, respective SK and BK channel blockers, decreased the 'out but scarcely affected the [Ca2~]response to muscarine. Muscarine produced an 1m~and an increase in [Ca2~]ẽven after a removal of external Ca2ã nd in the presence of 002+, indicating that these responses are mediated by Ca2~release from intracellular stores. The 'out evoked by the Ca2~release was much smaller than that evoked by the voltage-dependent Ca2ĩ nflux, even when similar [Ca2~]changes assessed by fura-2 microfluorometry occurred. Inositol 1 ,4,5-trisphosphate (lnsP 3) applied intracellularly and the photolysis of caged lnsP3 each evoked current changes similar to those induced by muscarine. These results indicate that the 'out evoked by muscarinic stimulation is mediated by Ca 2~-dependent Kchannels (probably BK and SK channels), which are activated by Ca2~released from intracellular Ca2~stores in guinea pig chromaffin cells.

Faster kinetics of quantal catecholamine release in mouse chromaffin cells stimulated with acetylcholine, compared with other secretagogues

“…Thus, the [Ca 2+ ] c elevations triggered by ACh and DMPP were fast (times to peak of 10-20 s) while those of muscarine and caffeine were about 3-5 fold slower. This is consistent with rapid Ca 2+ entry through VACCs in the case of ACh and DMPP, and with slower ER Ca 2+ release by histamine (Stauderman and Pruss 1990;Bunn and Boyd 1992) and muscarine Uceda et al 1992;D'Andrea and Thorn 1996;Ohta et al 1998). A somehow surprising finding was the fast increase in [Ca 2+ ] c triggered by histamine (time to peak of 18.1 s) that however was not accompanied by fast secretion (Fig.…”

“…; D'Andrea and Thorn ; Ohta et al . ). A somehow surprising finding was the fast increase in [Ca 2+ ] c triggered by histamine (time to peak of 18.1 s) that however was not accompanied by fast secretion (Fig.…”

Calcium Signaling and Exocytosis in Adrenal Chromaffin Cells

“…InsP 3 -producing agonists (bradykinin, histamine, angiotensin II, PACAP, muscarinic agonists, etc. ), ATP, glutamate, and caffeine produce Ca 2ϩ release from the ER (15,21,91,94,95,97,112,113,212,213,273,297,319,338,(357)(358)(359). The rate of Ca 2ϩ exchange at steady state is ϳ2-3 mol · l cells Ϫ1 · s Ϫ1 at rest, whereas the net leak induced by caffeine or by maximal stimulation with InsP 3 -producing agonists is 10 -20 times faster (15).…”

Cytosolic organelles shape calcium signals and exo–endocytotic responses of chromaffin cells

“…For instance, this [Ca 2+ ] c signal activates small-conductance Ca 2+ -activated K + channels leading to hyperpolarisation of bovine chromaffin cells [33]. In this line is the finding that muscarine produces a [Ca 2+ ] c elevation and an outward K + current, due to activation of Ca 2+ -activated K + channels in guinea-pig chromaffin cells [89]. These channels are regulating the nicotinic and muscarinic secretory response of cat and bovine chromaffin cells [90][91][92].…”