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

• Published in: Neuroscience Vol. 146; no. 1; pp. 190 - 201
• Main Authors: Ishibashi, H, Jang, I.-S, Nabekura, J
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 25-04-2007; Elsevier
• Subjects: Action Potentials - drug effects; Action Potentials - physiology; Action Potentials - radiation effects; Animals; Animals, Newborn; Biological and medical sciences; Calcium - pharmacology; depolarization; Dose-Response Relationship, Drug; Drug Interactions; Electric Stimulation - methods; Enzyme Inhibitors - pharmacology; Fundamental and applied biological sciences. Psychology; Glycine - metabolism; Glycine Agents - pharmacology; In Vitro Techniques; Inhibitory Postsynaptic Potentials - drug effects; Inhibitory Postsynaptic Potentials - physiology; Inhibitory Postsynaptic Potentials - radiation effects; intracellular Ca 2+ release; IPSC; Lumbosacral Region; Neurology; patch-clamp; Peptides, Cyclic - pharmacology; phospholipase C; Posterior Horn Cells - cytology; Posterior Horn Cells - drug effects; Posterior Horn Cells - physiology; Potassium - pharmacology; Presynaptic Terminals - drug effects; Presynaptic Terminals - metabolism; Rats; Spinal Cord - cytology; Strychnine - pharmacology; Vertebrates: nervous system and sense organs; phospholipase C; PIP 2; inhibitory postsynaptic current; phosphatidylinositol-4,5-bisphosphate; patch-clamp; PLC; xestospongin C; PKC; 2-APB; IPSC; depolarization; XeC; IP 3; TTX; intracellular Ca 2+ release; tetrodotoxin; inositol 1,4,5-trisphosphate; protein kinase C; 2-aminoethoxydiphenyl borate; Spinal cord; Calcium; Rat; Central nervous system; Electrophysiology; Patch clamp method; Esterases; Phosphoric diester hydrolases; Posterior spinal horn; Glycine; Depolarization; Release; Enzyme; Inhibitory postsynaptic current; Rodentia; intracellular Ca2+ release; Extracellular; Phospholipase C; Vertebrata; Mammalia; Neuron; Animal; Hydrolases; Intracellular; Potassium
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2007.01.018

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.