Activation of Ca(2+)-dependent K(+) channels contributes to rhythmic firing of action potentials in mouse pancreatic beta cells
Författare
Summary, in English
We have applied the perforated patch whole-cell technique to beta cells within intact pancreatic islets to identify the current underlying the glucose-induced rhythmic firing of action potentials. Trains of depolarizations (to simulate glucose-induced electrical activity) resulted in the gradual (time constant: 2.3 s) development of a small (<0.8 nS) K(+) conductance. The current was dependent on Ca(2+) influx but unaffected by apamin and charybdotoxin, two blockers of Ca(2+)-activated K(+) channels, and was insensitive to tolbutamide (a blocker of ATP-regulated K(+) channels) but partially (>60%) blocked by high (10-20 mM) concentrations of tetraethylammonium. Upon cessation of electrical stimulation, the current deactivated exponentially with a time constant of 6.5 s. This is similar to the interval between two successive bursts of action potentials. We propose that this Ca(2+)-activated K(+) current plays an important role in the generation of oscillatory electrical activity in the beta cell.
Avdelning/ar
Publiceringsår
1999
Språk
Engelska
Sidor
759-770
Publikation/Tidskrift/Serie
Journal of General Physiology
Volym
114
Issue
6
Dokumenttyp
Artikel i tidskrift
Förlag
Rockefeller Institute for Medical Research
Ämne
- Endocrinology and Diabetes
Nyckelord
- Ca2+-activated K+ channel
- pancreas
- insulin
- Ca2+
- membrane potential
Status
Published
Forskningsgrupp
- Islet cell physiology
ISBN/ISSN/Övrigt
- ISSN: 0022-1295