veratrine and Glioma

Depolarization with 50 mM K+ increased 45Ca2+ uptake into neuronal clonal cell lines NG108-15, N1E-115 and NH15-CA2. In each cell line this depolarization-induced uptake was blocked by inorganic and organic blockers of voltage sensitive calcium channels. However, tetrodotoxin (10(-6) M) was ineffective. Moreover, in the presence of tetrodotoxin, neither batrachotoxin nor veratridine inhibited the depolarization-induced uptake. The novel dihydropyridine BAY K8644 enhanced depolarization-induced 45Ca2+ uptake into each cell line in a nitrendipine reversible fashion. In the presence of tetrodotoxin, the BAY K8644/50 mM K+ stimulated uptake could be partially inhibited by batrachotoxin (10(-6) M) and veratridine (5 X 10(-5) M). These effects were not altered by the presence of scorpion venom (1 microgram/ml). The results indicate that both batrachotoxin and veratridine can modulate the effects of dihydropyridines on the gating properties of voltage sensitive calcium channels.

Topics: 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; Batrachotoxins; Calcium; Calcium Channel Blockers; Calcium Radioisotopes; Cell Line; Clone Cells; Electrophysiology; Glioma; Hybrid Cells; Ion Channels; Neuroblastoma; Neurons; Nifedipine; Potassium; Pyridines; Veratridine; Veratrine

The voltage-dependent Na+ ionophore of various neuronal cells is permeable not only to Na+ ions but also to guanidinium ions. Therefore, the veratridine- (or aconitine-)stimulated influx of [14C]guanidinium in neuroblastoma x glioma hybrid cells was measured to characterize the Na+ ionophore of these cells. Half-maximal stimulation of guanidinium uptake was seen at 30 microM veratridine. At 1 mM guanidinium, the veratridine-stimulated uptake of guanidinium was lowered to 50% by approximately 60 mM Li+, Na+, or K+ and by a few millimolar Mn2+, Co2+, or Ni2+. The basal, as well as the veratridine-stimulated, uptake of guanidinium was inhibited by the cholinergic antagonists (+)-tubocurarine (Ki = 50 to 500 nM) and atropine (Ki = 5 to 30 microM) and the adrenergic antagonists phentolamine (Ki = 5 microM) and propranolol (Ki = 60 microM). The specificity of the inhibitory effects of these agents is stressed by the ineffectiveness of various other neurotransmitter antagonists. However, the corresponding ionophore in neuroblastoma cells (clone N1E-115) seems to be regulated differently. While phentolamine and propranolol inhibit the veratridine-activated uptake as in the hybrid cells, (+)-tubocurarine and atropine exert only a slight effect.

Topics: Animals; Atropine; Calcium; Cell Line; Glioma; Guanidine; Guanidines; Hybrid Cells; Ion Channels; Kinetics; Membrane Potentials; Mice; Neuroblastoma; Neurons; Neurotransmitter Agents; Phentolamine; Propranolol; Rats; Tubocurarine; Veratridine; Veratrine

Veratridine induces membrane potential oscillations in non-excitable glioma cells, which are not affected by ouabain (2 mM) or by D600 (0.1 mM). In the presence of veratridine, scorpion toxin causes depolarization of the glioma cells to a positive value of the membrane potential. These effects of veratridine and of scorpion toxin are observed in Na+ but not in choline medium and are inhibited by tetrodotoxin. The response of the glioma cells to bradykinin has also been studied during these experiments. Previously bradykinin has been shown in these cells to induce a hyperpolarizing response caused by an increase in K+ conductance. This response to bradykinin can still be seen during the veratridine-induced oscillations of the membrane potential. In the glioma cells the uptake of guanidinium, a substitute for Na+, is enhanced by veratridine plus scorpion toxin. This stimulation is tetrodotoxin-sensitive. However, in the excitable neuroblastoma X glioma hybrid cells studied for comparison, veratridine causes membrane potential oscillations accompanied at the rising phase by one action potential or a train of action potentials. The results demonstrate that in non-excitable glioma cells tetrodotoxin-sensitive Na+ channels can be activated by veratridine and by scorpion toxin.

Topics: Animals; Biological Transport; Cell Line; Glioma; Guanidine; Guanidines; Hybrid Cells; Ion Channels; Membrane Potentials; Neoplasms, Experimental; Neuroblastoma; Rats; Scorpion Venoms; Sodium; Tetrodotoxin; Veratridine; Veratrine

Topics: Anesthetics, Local; Animals; Cell Line; Glioma; Guanidine; Guanidines; Hybrid Cells; Ion Channels; Kinetics; Mice; Neuroblastoma; Rats; Strychnine; Veratridine; Veratrine

Topics: Amino Acids; Animals; Brain Neoplasms; Calcium; Cells, Cultured; Chloramphenicol; Cycloheximide; Female; Glioma; Membrane Potentials; Nerve Tissue Proteins; Neuroglia; Potassium; Rats; Sodium; Synaptic Membranes; Synaptosomes; Tetrodotoxin; Veratrine