High potassium-induced facilitation of glycine release from presynaptic terminals on mechanically dissociated rat spinal dorsal horn neurons in the absence of extracellular calcium.
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 omega-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.
Ishibashi
H
H
Department of Bio-signaling Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan. isibasi@nips.ac.jp
Jang
I-S
IS
Nabekura
J
J
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004558:Electric Stimulation / Q000379:methods; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005998:Glycine / Q000378:metabolism*; D018684:Glycine Agents / Q000494:pharmacology; D066298:In Vitro Techniques; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D008161:Lumbosacral Region; D010456:Peptides, Cyclic / Q000494:pharmacology; D020671:Posterior Horn Cells / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000494:pharmacology*; D017729:Presynaptic Terminals / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D013116:Spinal Cord / Q000166:cytology*; D013331:Strychnine / Q000494:pharmacology
D004791:Enzyme Inhibitors; D018684:Glycine Agents; D010456:Peptides, Cyclic; C082807:omega-grammotoxin SIA; D013331:Strychnine; D011188:Potassium; D002118:Calcium; D005998:Glycine