Characterization of ethosuximide reduction of low-threshold calcium current in thalamic neurons

Ann Neurol. 1989 Jun;25(6):582-93. doi: 10.1002/ana.410250610.


The mechanism by which ethosuximide reduces thalamic low-threshold calcium current (LTCC) was analyzed using voltage-clamp techniques in acutely isolated ventrobasal complex neurons from rats and guinea pigs. The ethosuximide-induced reduction of LTCC was voltage dependent: it was most pronounced at more-hyperpolarized potentials and did not affect the time course of activation or inactivation of the current. Ethosuximide reduced LTCC without altering the voltage dependence of steady-state inactivation or the time course of recovery from inactivation. Dimethadione reduced LTCC by a similar mechanism, while valproic acid had no effect on LTCC. We conclude that ethosuximide reduction of LTCC in thalamic neurons is consistent with a reduction in the number of available LTCC channels or in the single LTCC channel conductance, perhaps indicating a direct channel-blocking action of this drug. Given the importance of LTCC in thalamic oscillatory behavior, a reduction in this current by ethosuximide would be a mechanism of action compatible with the known anticonvulsant effects of this drug in typical absence seizures.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Calcium Channels / drug effects
  • Dimethadione / pharmacology
  • Ethosuximide / pharmacology*
  • Guinea Pigs
  • Neurons / drug effects*
  • Rats
  • Thalamus / cytology*
  • Thalamus / drug effects
  • Valproic Acid / pharmacology


  • Calcium Channels
  • Ethosuximide
  • Valproic Acid
  • Dimethadione