Role of voltage-gated K+ channels in regulating Ca2+ entry in rat cortical astrocytes

King Chuen Wu, Chang Shin Kuo, Chia Chia Chao, Chieh Chen Huang, Yuan Kun Tu, Paul Chan, Yuk Man Leung

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


Astrocytes have multiple functions such as provision of nourishment and mechanical support to the nervous system, helping to clear extracellular metabolites of neurons and modulating synaptic transmission by releasing gliotransmitters. In excitable cells, voltage-gated K+ (Kv) channels serve to repolarize during action potentials. Astrocytes are considered non-excitable cells since they are not able to generate action potentials. There is an abundant expression of various Kv channels in astrocytes but the functions of these Kv channels remain unclear. We examined whether these astrocyte Kv channels regulate astrocyte “excitability” in the form of cytosolic Ca2+ signaling. Electrophysiological examination revealed that neonatal rat cortical astrocytes possessed both delayed rectifier type and A-type Kv channels. Pharmacological blockade of both delayed rectifier Kv channels by TEA and A-type Kv channels by quinidine significantly suppressed store-operated Ca2+ influx; however, TEA alone or quinidine alone did not suffice to cause such suppression. TEA and quinidine together dramatically enhanced current injection-triggered membrane potential overshoot (depolarization); either drug alone caused much smaller enhancements. Taken together, the results suggest both delayed rectifier and A-type Kv channels regulate astrocyte Ca2+ signaling via controlling membrane potential.

Original languageEnglish
Pages (from-to)171-177
Number of pages7
JournalJournal of Physiological Sciences
Issue number2
Publication statusPublished - Mar 19 2015


  • Astrocyte
  • Ca signaling
  • Membrane potential
  • Voltage-gated K channels

ASJC Scopus subject areas

  • Physiology


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