High potassium-induced facilitation of glycine release from presynaptic terminals on mechanically dissociated rat spinal dorsal horn neurons in the absence of extracellular calcium

H. Ishibashi, I. S. Jang, J. Nabekura

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

The high potassium-induced potentiation of spontaneous glycine release in extracellular Ca2+-free conditions was studied in mechanically dissociated rat spinal dorsal horn neurons using whole-cell patch-clamp technique. Elevating extracellular K+ concentration reversibly increased the frequency of spontaneous glycinergic inhibitory postsynaptic currents (IPSCs) in the absence of extracellular Ca2+. Blocking voltage-dependent Na+ channels (tetrodotoxin) and Ca2+ channels (nifedipine and ω-grammotoxin-SIA) had no effect on this potassium-induced potentiation of glycine-release. The high potassium-induced increase in IPSC frequency was also observed in the absence of extracellular Na+, although the recovery back to baseline levels of release was prolonged under these conditions. The action of high potassium solution on glycine release was prevented by BAPTA-AM, by depletion of intracellular Ca2+ stores by thapsigargin and by the phospholipase C inhibitor U-73122. The results suggest that the elevated extracellular K+ concentration causes Ca2+ release from internal stores which is independent of extracellular Na+- and Ca2+-influx, and may reveal a novel mechanism by which the potassium-induced depolarization of presynaptic nerve terminals can regulate intracellular Ca2+ concentration and exocytosis.

Original languageEnglish
Pages (from-to)190-201
Number of pages12
JournalNeuroscience
Volume146
Issue number1
DOIs
StatePublished - 25 Apr 2007

Keywords

  • depolarization
  • intracellular Ca release
  • IPSC
  • patch-clamp
  • phospholipase C

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