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Kv3 Assays

Kv3 Channel Introduction

Potassium channels are one the most widely distributed ion channels of the ion channel family, in which the voltage-gated potassium (Kv) channel is a subfamily of transmembrane channels sensitive to the voltage change of cell membrane potential. Kv3 channel, also known as Shaw, is an important Kv channel initially isolated from Drosophila. Kv3 channels are significant players in the regulation of action potential duration and neurotransmitter release.

Kv3 Channel Members

Totally four Kv3 channels have been reported in rodents and humans, Kv3.1, Kv3.2, Kv3.3, and Kv3.4. Different from other Kv subfamilies, the four Kv3 encoded genes can generate multiple Kv3 isoforms (about 13 different Kv3 proteins) with different intracellular C-terminal sequences after extensive alternative mRNA splicing. Structurally, the four Kv3 channels are highly similar to other Kv subfamilies, which consist of homotetrameric α subunits and auxiliary beta subunits. And each α subunit is composed of a voltage-sensing domain (VSD) and pore domain (PD), flanked by intracellular -NH2 and -COOH terminus on both sides.

The Kv3 channels have different expressions, of which Kv3.1, Kv3.2, and Kv3.3 channels are primarily expressed in the central nervous system while the Kv3.4 channel is weakly expressed in the brain but mainly expressed in skeletal muscle and sympathetic neurons. Although also expressed in T lymphocytes, Kv3.1 is highly enriched in neurons with high-frequency discharge and exerts a key role in rapid repolarization. Kv3.2 is highly expressed in the dorsal thalamus project to the cerebral cortex. Kv3.3 tends to be expressed in the soma and proximal apical dendrites.

Schematic diagram of a Kv3.1 subunit. Fig.1 Schematic diagram of a Kv3.1 subunit. (Kaczmarek, 2017)

Kv3 Channel Functions

Subtype Gene Pathways Function
Kv3.1 KCNC1
  • Potassium channels
  • Dopamine-DARPP32 Feedback onto cAMP Pathway
An important regulator in the rapid repolarization of fast-firing brain neurons.
Mediate the voltage-dependent potassium ion permeability on excitable membranes.
Kv3.2 KCNC2
  • Potassium channels
  • Integration of energy metabolism
Regulates the fast action potential repolarization.
Mediates transmembrane K+ transportation.
Kv3.3 KCNC3
  • Potassium channels
  • Dopamine-DARPP32 Feedback onto cAMP Pathway
An important regulator in the rapid repolarization of fast-firing brain neurons.
Regulates the frequency, shape, and duration of action potentials in Purkinje cells.
Kv3.4 KCNC4
  • Potassium channels
  • Dopamine-DARPP32 Feedback onto cAMP Pathway
Mediates the voltage-dependent K+ permeability of excitable membranes.

Assay List of Kv3 Channel

Creative Biolabs can provide a range of assays of Kv3 channels. You can choose the assay in the list or contact us for more information:

Kv3 Channels
Assay No. Assay Name Host Cell Assay Type Datasheet
S01YF-0722-KX223 Magic™ Human KCNC1 In Vitro Electrophysiology Assay, HEK293 HEK293 Electrophysiology Assay
S01YF-0722-KX224 Magic™ Human KCNC4 In Vitro Electrophysiology Assay, HEK293 HEK293 Electrophysiology Assay
S01YF-0722-KX260 Magic™ Human KCNC2 In Vitro Electrophysiology Assay Electrophysiology Assay

Published Data

Paper Title Kv3.3 subunits control presynaptic action potential waveform and neurotransmitter release at a central excitatory synapse
Journal Neuroscience
Published 2022
Abstract The specific presynaptic roles of Kv3 in the calyx of Held presynaptic terminal have been investigated in the mouse since Kv3 channels, especially Kv3.1 and Kv3.3, were widely expressed in the auditory brainstem.
Result Assays in transgenic mice showed that it was Kv3.3, not Kv3.1, played important roles in action potential repolarisation at the calyx of Held terminal. And Kv3.3 deletion could increase the duration of the presynaptic action potential, promote the release of excitatory transmitter, boost the short-term depression, decrease the precision and signal-to-noise ratios in the response to sound.

Kv3.3 deletion increases EPSC amplitude and occludes block by TEA.Fig.2. Kv3.3 deletion increases EPSC amplitude and occludes block by TEA. (Richardson,2022)

References

  1. Kaczmarek L. K, and Zhang Y. Kv3 channels: enablers of rapid firing, neurotransmitter release, and neuronal endurance. Physiological reviews. 2017, 97(4): 1431-1468.
  2. Richardson, A.; et al. Kv3.3 subunits control presynaptic action potential waveform and neurotransmitter release at a central excitatory synapse. Neuroscience. 2022, 11: e75219.
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