Control of IsAHP in mouse hippocampus CA1 pyramidal neurons by RyR3-mediated calcium-induced calcium release

Y. van de Vrede, P. Fossier, G. Baux, M. Joels, P. Chameau*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

18 Citations (Scopus)

Abstract

In several neuronal preparations, the ryanodine-sensitive calcium store was reported to participate in the generation of slow afterhyperpolarization currents (IsAHP) involved in spike frequency adaptation. We show that calcium release from the ryanodine-sensitive calcium store is a major determinant of the triggering of IsAHP in mouse CA1 pyramidal neurons. Whole-cell patch clamp recordings in hippocampus slices show that the intracellular calcium stores depletion using an inhibitor of the endoplasmic reticulum Ca2+-ATPase (5 mu M cyclopiazonic acid), as well as the specific blockade of ryanodine receptors (100 mu M ryanodine) both reduced the IsAHP by about 70%. Immunohistology, using an anti-RyR3 specific antibody, indicates that RyR3 expression is particularly enriched in the CA1 apical dendrites (considered as the most important site for sAHP generation). We show that our anti-RyR3 antibody acts as a functional RyR3 antagonist and induced a reduction in IsAHP by about 70%. The additional ryanodine application (100 mu M) did not further affect IsAHP, thus excluding RyR2 in IsAHP activation. Our results argue in favor of a specialized function of RyR3 in CA1 pyramidal cells in triggering IsAHP due to their localization in the apical dendrite.

Original languageEnglish
Pages (from-to)297-308
Number of pages12
JournalPflugers archiv-European journal of physiology
Volume455
Issue number2
DOIs
Publication statusPublished - Nov-2007
Externally publishedYes

Keywords

  • CA1 pyramidal neurons
  • IsAHP
  • calcium-induced calcium release
  • ryanodine receptors
  • RyR3
  • SLOW AFTERHYPERPOLARIZATION CURRENT
  • MUSCLE SARCOPLASMIC-RETICULUM
  • CA2+-ACTIVATED K+-CURRENTS
  • CHANNEL RYANODINE RECEPTOR
  • CA2+-INDUCED CA2+ RELEASE
  • CYCLOPIAZONIC ACID
  • IN-VITRO
  • BRAIN
  • ACTIVATION
  • CELLS

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