Veratridine modifies the TTX-resistant Na+ channels in rat vagal afferent neurons
Fabiana Vasconcelos Campos1, Thaís Helena Moreira, Paulo Sérgio Lacerda Beirão
1Excitable Membranes Laboratory, Department of Biochemistry and Immunology, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av. Antonio Carlos 6627, Belo Horizonte, MG CEP 31970-901, CP 486, Brazil.
Abstract:
A number of neurotoxins from venoms of invertebrates and plants are ligands for voltage-gated Na+ channels and are useful tools for studying Na+ channel function and structure. Using whole-cell recordings from vagal afferent nodose neurons, we studied neurotoxins that target Na+ channels. We asked whether Ts3 (an alpha-scorpion toxin) and/or veratridine (a lipid-soluble toxin), could modify the TTX-resistant Na+ current generated by vagal afferent nodose neurons. Nodose TTX-resistant current was not affected by Ts3, whereas Ts3 slowed inactivation of the current generated by TTX-sensitive current component. We found that veratridine inhibited the TTX-resistant Na+ currents on rat nodose neurons. Interestingly, veratridine-modified Na+ channels developed a persistent current that accounted for the large tail current observed. We propose that veratridine modifies TTX-resistant Na+ channels through a mechanism distinct from its actions on other voltage-gated Na+ channels.
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