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Neuron. 2001 Jul 19;31(1):75-85.

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

Author information

1
Department of Anesthesiology, Washington University School of Medicine, 63110, St Louis, MO, USA. todorovs@msnotes.wustl.edu

Abstract

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.

PMID:
11498052
DOI:
10.1016/s0896-6273(01)00338-5
[Indexed for MEDLINE]
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