T-type Ca2+ channels in normal and abnormal brain functions

Eunji Cheong, Hee Sup Shin

Research output: Contribution to journalReview article

67 Citations (Scopus)

Abstract

Low-voltage-activated T-type Ca2+ channels are widely expressed in various types of neurons. Once deinactivated by hyperpolarization, T-type channels are ready to be activated by a small depolarization near the resting membrane potential and, therefore, are optimal for regulating the excitability and electroresponsiveness of neurons under physiological conditions near resting states. Ca2+ influx through T-type channels engenders low-threshold Ca2+ spikes, which in turn trigger a burst of action potentials. Low-threshold burst firing has been implicated in the synchronization of the thalamocortical circuit during sleep and in absence seizures. It also has been suggested that T-type channels play an important role in pain signal transmission, based on their abundant expression in pain-processing pathways in peripheral and central neurons. In this review, we will describe studies on the role of T-type Ca2+ channels in the physiological as well as pathological generation of brain rhythms in sleep, absence epilepsy, and pain signal transmission. Recent advances in studies of T-type channels in the control of cognition will also be briefly discussed.

Original languageEnglish
Pages (from-to)961-992
Number of pages32
JournalPhysiological Reviews
Volume93
Issue number3
DOIs
Publication statusPublished - 2013 Jul 1

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Absence Epilepsy
Neurons
Pain
Sleep
Brain
Membrane Potentials
Cognition
Action Potentials

All Science Journal Classification (ASJC) codes

  • Physiology
  • Molecular Biology
  • Physiology (medical)

Cite this

Cheong, Eunji ; Shin, Hee Sup. / T-type Ca2+ channels in normal and abnormal brain functions. In: Physiological Reviews. 2013 ; Vol. 93, No. 3. pp. 961-992.
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T-type Ca2+ channels in normal and abnormal brain functions. / Cheong, Eunji; Shin, Hee Sup.

In: Physiological Reviews, Vol. 93, No. 3, 01.07.2013, p. 961-992.

Research output: Contribution to journalReview article

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