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Updated: Jun 2, 2026
Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
Published on: March 12, 2013
Evidence for presence and functional effects of Kv1.1 channels in β-cells: general survey and results from
Zuheng Ma1, Catharina Lavebratt, Malin Almgren
1Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Background:
Voltage-dependent K(+) channels (Kv) mediate repolarisation of β-cell action potentials, and thereby abrogate insulin secretion. The role of the Kv1.1 K(+) channel in this process is however unclear. We tested for presence of Kv1.1 in different species and tested for a functional role of Kv1.1 by assessing pancreatic islet function in BALB/cByJ (wild-type) and megencephaly (mceph/mceph) mice, the latter having a deletion in the Kv1.1 gene.
Methodology/Principal Findings:
Kv1.1 expression was detected in islets from wild-type mice, SD rats and humans, and expression of truncated Kv1.1 was detected in mceph/mceph islets. Full-length Kv1.1 protein was present in islets from wild-type mice, but, as expected, not in those from mceph/mceph mice. Kv1.1 expression was localized to the β-cell population and also to α- and δ-cells, with evidence of over-expression of truncated Kv1.1 in mceph/mceph islets. Blood glucose, insulin content, and islet morphology were normal in mceph/mceph mice, but glucose-induced insulin release from batch-incubated islets was (moderately) higher than that from wild-type islets. Reciprocal blocking of Kv1.1 by dendrotoxin-K increased insulin secretion from wild-type but not mceph/mceph islets. Glucose-induced action potential duration, as well as firing frequency, was increased in mceph/mceph mouse β-cells. This duration effect on action potential in β-cells from mceph/mceph mice was mimicked by dendrotoxin-K in β-cells from wild-type mice. Observations concerning the effects of both the mceph mutation, and of dendrotoxin-K, on glucose-induced insulin release were confirmed in pancreatic islets from Kv1.1 null mice.
Conclusion/Significance:
Kv1.1 channels are expressed in the β-cells of several species, and these channels can influence glucose-stimulated insulin release.
Insights
The Kv1.1 potassium channel is present in pancreatic beta cells and influences insulin secretion. Blocking Kv1.1 increases insulin release, suggesting its role in regulating glucose-stimulated insulin secretion.
Area of Science:
- Endocrinology
- Molecular Biology
- Neuroscience
Background:
- Voltage-dependent potassium channels (Kv) regulate pancreatic beta-cell action potentials and insulin secretion.
- The specific role of the Kv1.1 channel in this process remains unclear.
Purpose of the Study:
- To investigate the presence and function of Kv1.1 channels in pancreatic islets.
- To determine the impact of Kv1.1 on glucose-stimulated insulin secretion.
Main Methods:
- Examined Kv1.1 expression in islets from wild-type and Kv1.1-deficient mice (megencephaly mutation).
- Assessed insulin secretion and action potential characteristics in response to glucose.
- Utilized dendrotoxin-K to block Kv1.1 function.
Main Results:
- Kv1.1 is expressed in beta cells across species, including mice, rats, and humans.
- Kv1.1-deficient mice exhibited higher glucose-induced insulin release and altered beta-cell action potentials.
- Blocking Kv1.1 with dendrotoxin-K enhanced insulin secretion in wild-type but not Kv1.1-deficient islets.
Conclusions:
- Kv1.1 channels are present in pancreatic beta cells and play a role in regulating glucose-stimulated insulin secretion.
- These findings highlight Kv1.1 as a potential target for modulating insulin secretion.
