PMID- 15649442 OWN - NLM STAT- MEDLINE DCOM- 20050707 LR - 20131121 IS - 0006-8993 (Print) IS - 0006-8993 (Linking) VI - 1031 IP - 2 DP - 2005 Jan 21 TI - Transient increases in extracellular K+ produce two pharmacological distinct cytosolic Ca2+ transients. PG - 174-84 AB - Transient increases in extracellular K+ are observed under various conditions, including repetitive neuronal firing, anoxia, ischemia and hypoglycemic coma. We studied changes in cytoplasmic Ca2+ ([Ca2+]cyt) evoked by pulses of KCl in human neuroblastoma SH-SY5Y cells and rat dorsal root ganglia (DRG) neurons at 37 degrees C. A "pulse" of KCl evoked two transient increases in [Ca2+]cyt, one upon addition of KCl (K+on) and the other upon removal of KCl (K+off). The K+on transient has been described in many cell types and is initiated by the activation of voltage-dependent Ca2+ channels followed by Ca2+-evoked Ca2+ release from intracellular Ca2+ stores. The level of KCl necessary to evoke the K+off transient depends on the type of neuron, in SH-SY5Y cells it required 100 mM KCl, in most (but not all) of dorsal root ganglia neurons it could be detected with 100-200 mM KCl and in a very few dorsal root ganglia neurons it was detectable at 20-50 mM KCl. In SH-SY5Y cells, reduction of extracellular Ca2+ inhibited the K+on more strongly than the K+off and slowed the decay of K+off. Isoflurane (1 mM) reduced the K+on)- but not the K+off-peak. However, isoflurane slowed the decay of K+off. The nonspecific cationic channel blocker La3+ (100 microM) had an effect similar to that of isoflurane. Treatment with thapsigargin (TG) at a concentration known to only deplete IP3-sensitive Ca2+ stores did not affect K+on or K+off, suggesting that Ca2+ release from the IP3-sensitive Ca2+ stores does not contribute to K+on and K+off transients and that the thapsigargin-sensitive Ca2+ ATPases do not contribute significantly to the rise or decay rates of these transients. These findings indicate that a pulse of extracellular K+ produces two distinct transient increases in [Ca2+]cyt. FAU - Corrales, Alexandra AU - Corrales A AD - Anesthesiology Department, New York University School of Medicine, 550 First Avenue, RR605, New York, NY 10016, USA. FAU - Montoya G, Jose V AU - Montoya G JV FAU - Sutachan, Jhon-Jairo AU - Sutachan JJ FAU - Cornillez-Ty, Genoveve AU - Cornillez-Ty G FAU - Garavito-Aguilar, Zayra AU - Garavito-Aguilar Z FAU - Xu, Fang AU - Xu F FAU - Blanck, Thomas J J AU - Blanck TJ FAU - Recio-Pinto, Esperanza AU - Recio-Pinto E LA - eng PT - Comparative Study PT - Journal Article PL - Netherlands TA - Brain Res JT - Brain research JID - 0045503 RN - 0 (Calcium Channels) RN - RWP5GA015D (Potassium) RN - SY7Q814VUP (Calcium) SB - IM MH - Animals MH - Calcium/*metabolism MH - Calcium Channels/metabolism MH - Calcium Signaling/*physiology MH - Cytosol/*metabolism MH - Extracellular Fluid/chemistry MH - Ganglia, Spinal/cytology MH - Humans MH - Membrane Potentials/physiology MH - Neuroblastoma MH - Neurons/cytology/*metabolism MH - Potassium/analysis/*metabolism MH - Rats MH - Signal Transduction/*physiology MH - Tumor Cells, Cultured EDAT- 2005/01/15 09:00 MHDA- 2005/07/08 09:00 CRDT- 2005/01/15 09:00 PHST- 2004/10/28 00:00 [accepted] PHST- 2005/01/15 09:00 [pubmed] PHST- 2005/07/08 09:00 [medline] PHST- 2005/01/15 09:00 [entrez] AID - S0006-8993(04)01758-5 [pii] AID - 10.1016/j.brainres.2004.10.031 [doi] PST - ppublish SO - Brain Res. 2005 Jan 21;1031(2):174-84. doi: 10.1016/j.brainres.2004.10.031.