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Neuroreport ; 5(10): 1256-8, 1994 Jun 02.
Article in English | MEDLINE | ID: mdl-7919177

ABSTRACT

The potassium channel blocker, 4-aminopyridine (4-AP), stimulates neurotransmitter release via plasma membrane depolarization and subsequent activation of voltage-gated calcium channels. The present study assessed the effects of 4-AP on intracellular calcium levels in the human neuroblastoma cell line CHP-100. Blockade of K+ channels with 4-AP significantly increased intracellular calcium concentration ([Ca2+]i). This increase occurred via activation of plasma membrane Ca2+ channels. The 4-AP induced rise in [Ca2+]i was not inhibited by the L-type Ca2+ channel blocker nifedipine but was sensitive to the N-type Ca2+ channel blocker omega-contotoxin GVIA. Tetrodotoxin did not alter the effect of 4-AP. These results suggest that in CHP-100 cells, following inhibition of K+ channels by 4-AP, N-type Ca2+ channels are activated.


Subject(s)
4-Aminopyridine/pharmacology , Calcium Channel Agonists/pharmacology , Calcium Channels/metabolism , Potassium Channels/metabolism , Brain Neoplasms/metabolism , Calcium/metabolism , Cell Membrane/drug effects , Cell Membrane/metabolism , Humans , Neuroblastoma/metabolism , Nifedipine/pharmacology , Peptides/pharmacology , Potassium Channels/drug effects , Rubidium Radioisotopes , Synaptosomes/drug effects , Synaptosomes/metabolism , Tetrodotoxin/pharmacology , Tumor Cells, Cultured , omega-Conotoxin GVIA
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