@article {Meder1126, author = {Wolfgang Meder and Klaus Fink and Josef Zentner and Manfred G{\"o}thert}, title = {Calcium Channels Involved in K+- and Veratridine-Induced Increase of Cytosolic Calcium Concentration in Human Cerebral Cortical Synaptosomes }, volume = {290}, number = {3}, pages = {1126--1131}, year = {1999}, publisher = {American Society for Pharmacology and Experimental Therapeutics}, abstract = {Human cerebral cortical synaptosomes were used to study voltage-dependent Ca2+ channels mediating calcium influx in human axon terminals. Synaptosomes were depolarized by elevation of the extracellular K+ concentration by 30 mM or by the addition of veratridine (10 μM). Increase in cytosolic concentration of calcium [Ca2+]i induced by either stimulus was abolished in the absence of extracellular Ca2+ions. ω-Agatoxin IVA inhibited the K+-induced [Ca2+]i increase concentration-dependently (IC50: 113 nM). ω-Conotoxin GVIA (0.1 μM) inhibited K+-induced [Ca2+]iincrease by 20\%. ω-Conotoxin MVIIC (0.2 μM) caused an inhibition by 85\%. Nifedipine (1 μM) had no effect on K+-induced [Ca2+]i increase. Veratridine-induced increase in [Ca2+]i was inhibited by ω-conotoxin GVIA (0.1 μM) and ω-Agatoxin IVA (0.2 μM; by about 25 and 45\%, respectively). Nifedipine inhibited the veratridine-evoked [Ca2+]i increase concentration-dependently (IC50: 4.9 nM); Bay K 8644 (3 μM) shifted the nifedipine concentration-response curve to the right. Mibefradil (10 μM) abolished the increase in [Ca2+]i evoked by K+ and reduced the increase evoked by veratridine by almost 90\%. KB-R7943 (3 μM) an inhibitor of the Na+/Ca2+ exchanger NCX1, decreased the increase in [Ca2+]i evoked by veratridine by approximately 20\%. It is concluded that the increase in [Ca2+]i after K+ depolarization caused by Ca2+ influx predominantly via P/Q-type Ca2+ channels and after veratridine depolarization via N- and P/Q-type, but also by L-type Ca2+ channels. The toxin- and nifedipine-resistant fraction of the veratridine response may result both from influx via R-type Ca2+ channels and by Ca2+ inward transport via Na+/Ca2+exchanger. The American Society for Pharmacology and Experimental Therapeutics}, issn = {0022-3565}, URL = {https://jpet.aspetjournals.org/content/290/3/1126}, eprint = {https://jpet.aspetjournals.org/content/290/3/1126.full.pdf}, journal = {Journal of Pharmacology and Experimental Therapeutics} }