What question did this study set out to answer?

To determine whether and through which molecular pathways peptide growth factor receptors modulate the cloned voltage-activated potassium channel Kv1.5.

March 1, 1994Journal of NeuroscienceOpen Access

Modulation of a voltage-activated potassium channel by peptide growth factor receptors

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Population

Xenopus oocytes expressing cloned voltage-activated K+ channel Kv1.5 and receptors for platelet-derived…

Comparison

Activation of PDGF or FGF receptors, or… vs Baseline unactivated state, or a mutant FGF…

Design

Preclinical

Authors

LTLC TimpeUniversity of California, San Francisco WFWJ FantlUniversity of California, San Francisco

Discussion

Member takes

Implication

May inform excitability modulation in animal models; leaves open relevance to human channelopathies or arrhythmias.

Key Points

To determine whether and through which molecular pathways peptide growth factor receptors modulate the cloned voltage-activated potassium channel Kv1.5.
Coexpressed cloned Kv1.5 potassium channels and PDGF or FGF receptors in Xenopus oocytes.
Evaluated channel regulation using thrombin receptors, 5-HT1c receptors, a phospholipase C-gamma 1-deficient mutant FGF receptor, and combined inositol trisphosphate injection with phorbol 12-myristate 13-acetate superfusion.
Receptor activation led to a progressive decline in Kv1.5 current amplitude with a half-time of approximately 20 minutes, while activation kinetics and voltage sensitivity remained largely unchanged.
Suppression of Kv1.5 current was mimicked by phospholipase C-activating receptors and combined inositol trisphosphate and phorbol ester treatment, but was completely absent in cells expressing the phospholipase C-gamma 1-deficient FGF receptor.

Structured PICO

Population

Xenopus oocytes expressing cloned voltage-activated K+ channel Kv1.5 and receptors for platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), human thrombin, or rat 5-HT1c

Intervention

Activation of PDGF or FGF receptors, or simultaneous injection of inositol trisphosphate and superfusion of phorbol 12-myristate 13-acetate

Comparator

Baseline unactivated state, or a mutant FGF receptor that does not activate phospholipase C-gamma 1

Outcome

Kv1.5 current amplitudesurrogate

PDGF and FGF receptors can modulate voltage-activated K+ channels by increasing phospholipase C activity, suggesting a mechanism for rapid alteration of electrical excitability.

Cite This Study

Timpe et al. (1994) studied this question.

synapsesocial.com/papers/6a75b7616e15464cba6a40be https://doi.org/10.1523/jneurosci.14-03-01195.1994

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