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Participation of Na+ channels in the potentiation by Tityus serrulatus α-toxin TsTx-V of glucose-induced electrical activity and insulin secretion in rodent islet β-cells

2003; Elsevier BV; Volume: 41; Issue: 8 Linguagem: Inglês

10.1016/s0041-0101(03)00086-2

1879-3150

Antonio Ari Gonçalves, Marcos Hikari Toyama, Everardo M. Carneiro, Sérgio Marangoni, Eliane Candiani Arantes, José R. Giglio, Antônio C. Boschero,

Nicotinic Acetylcholine Receptors Study

The effects of TsTx-V, an α-toxin isolated from Tityus serrulatus venom, on electrical activity and insulin secretion by rodent pancreatic islet cells were studied. TsTx-V (5.6 μg/ml) depolarized mouse pancreatic β-cells, diminished the membrane input resistance and increased the duration of the active phase of glucose-induced electrical activity. Similar results were observed with the Na+ channel agonist veratridine (110 μM). Both agents potentiated glucose (8.3 mM)-induced insulin secretion in rat islet. In the presence of TsTx-V or veratridine, insulin secretion increased 2- and 1.4-fold over basal values, respectively (P<0.001). The Na+ channel antagonist tetrodotoxin (6 μM) significantly decreased glucose- and TsTx-V-induced insulin secretion (P<0.001). TsTx-V also stimulated insulin secretion at low glucose concentrations (2.8 mM) whereas the β-toxin, Ts-γ (gamma toxin), also obtained from Tityus serrulatus venom, significantly reduced TsTx-V-induced secretion at sub- and suprathreshold concentrations of glucose. These results are consistent with a model whereby Na+ channels participate in glucose-induced electrical activity. Alteration in the activity of these channels changes the length of time during which the β-cell depolarizes, thereby altering the secretory behavior of the cell. The construction of a three-dimensional model for TsTx-V revealed a conserved core containing an α-helix and three β-strands, with minor differences when compared with toxins from other scorpion venoms.