NDLI: Perchlorate stimulates insulin secretion by shifting the gating of L-type Ca2+ currents in mouse pancreatic B-cells towards negative potentials

Content Provider	Springer Nature Link
Author	Larsson Nyrén, Gerd Sehlin, Jave Rorsman, Patrik Renström, Erik
Copyright Year	2000
Abstract	The effects of the chaotrophic anion perchlorate (ClO4 –) on glucose-induced electrical activity, exocytosis and ion channel activity in mouse pancreatic B-cells were investigated by patch-clamp recordings and capacitance measurements. ClO4 – stimulated glucose-induced electrical activity and increased the action potential frequency by 70% whilst not affecting the membrane potential when applied in the presence of a subthreshold concentration of the sugar. ClO4 – did not influence ATP-dependent K (KATP) channel activity and voltage-gated delayed K+ current. Similarly, ClO4 – had no effect on Ca2+-dependent exocytosis. The stimulation of electrical activity and insulin secretion was instead attributable to an enhancement of the whole-cell Ca2+ current. This effect was particularly pronounced at voltages around the threshold for action potential initiation and a doubling of the current amplitude was observed at –30 mV. This was due to a 7-mV shift in the gating of the Ca2+ current towards negative voltages. The action of ClO4 – was more pronounced when added in the presence of 0.1 mM BAY K8644, whereas no stimulation was observed when applied at a maximal concentration of the agonist (1 mM). Single-channel recordings revealed that the effect of ClO4 – on whole-cell currents was principally due to a 60% increase in the mean duration of the long openings and the number of active channels. We propose that ClO4 – stimulates insulin secretion and electrical activity by exerting a BAY K8644-like action on Ca2+ channel gating.
Starting Page	587
Ending Page	595
Page Count	9
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	441
Issue Number	5
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	2000-12-02
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Human Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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