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- Title
Cx36-Mediated Coupling Reduces β-Cell Heterogeneity, Confines the Stimulating Glucose Concentration Range, and Affects Insulin Release Kinetics.
- Authors
Speier, Stephan; Gjinovci, Asllan; Charollais, Anne; Meda, Paolo; Rupnik, Marjan
- Abstract
We studied the effect of gap junctional coupling on the excitability of β-cells in slices of pancreas, which provide a normal environment for islet cells. The electrophysiological properties of β-cells from mice (C57B1/6 background) lacking the gap junction protein connexin36 (Cx36[sup -/-]) were compared with heterozygous (Cx36[sup +/-]) and wild-type littermates (Cx36[sup +/+]) and with frequently used wild-type NMRI mice. Most electrophysiological characteristics of β-cells were found to be unchanged after the knockout of Cx36, except the density of Ca[sup 2+] channels, which was increased in uncoupled cells. With closed ATP-sensitive K[sup +] (K[sup ATP]) channels, the electrically coupled β-cells of Cx36[sup +/+] and Cx36[sup +/-] mice were hyperpolarized by the membrane potential of adjacent, inactive cells. Additionally, the hyperpolarization of one β-cell could attenuate or even stop the electrical activity of nearby coupled cells. In contrast, β-cells of Cx36[sup -/-] littermates with blocked K[sup ATP] channels rapidly depolarized and exhibited a continuous electrical activity. Absence of electrical coupling modified the electrophysiological properties of β-cells consistent with the reported increase in basal insulin release and altered the switch on/off response of β-cells during an acute drop of the glucose concentration. Our data indicate an important role for Cx36-gap junctions in modulating stimulation threshold and kinetics of insulin release. Diabetes 56:1078-1086, 2007
- Subjects
B cells; GLUCOSE; INSULIN; ELECTROPHYSIOLOGY; LABORATORY mice
- Publication
Diabetes, 2007, Vol 56, Issue 4, p1078
- ISSN
0012-1797
- Publication type
Article
- DOI
10.2337/db06-0232