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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Redox modulation of T-type calcium channels in rat peripheral nociceptors.

Although T-type calcium channels were first described in sensory neurons, their function in sensory processing remains unclear. In isolated rat sensory neurons, we show that redox agents modulate T currents but not other voltage- and ligand-gated channels thought to mediate pain sensitivity. Similarly, redox agents modulate currents through Ca(v)3.2 recombinant channels. When injected into peripheral receptive fields, reducing agents, including the endogenous amino acid L-cysteine, induce thermal hyperalgesia. This hyperalgesia is blocked by the oxidizing agent 5,5'-dithio-bis-(2-nitrobenzoic acid) (DTNB) and the T channel antagonist mibefradil. DTNB alone and in combination with mibefradil induces thermal analgesia. Likewise, L-cysteine induces mechanical DTNB-sensitive hyperalgesia in peripheral receptive fields. These data strongly suggest a role for T channels in peripheral nociception. Redox sites on T channels in peripheral nociceptors could be important targets for agents that modify pain perception.[1]


  1. Redox modulation of T-type calcium channels in rat peripheral nociceptors. Todorovic, S.M., Jevtovic-Todorovic, V., Meyenburg, A., Mennerick, S., Perez-Reyes, E., Romano, C., Olney, J.W., Zorumski, C.F. Neuron (2001) [Pubmed]
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