Abstract
Transient receptor potential vanilloid type 1 (TRPV1) receptor plays an important role as a molecular detector of noxious signals in primary sensory neurons. Activity of TRPV1 can be modulated by the change in the environment such as redox state and extracellular cations. In the present study, we investigated the effect of the mercury chloride (HgCl2) on the activity of TRPV1 in rat dorsal root ganglia (DRG) neurons using whole-cell patch clamp technique. Extracellular HgCl2 reversibly reduced the magnitudes of capsaicin-activated currents (I cap ) in DRG neurons in a dose-dependent manner. The blocking effect of HgCl2 was prevented by pretreatment with the reducing agent dithiothreitol (DTT). Inhibition of I cap by HgCl2 was abolished by point mutation of individual cysteine residues located on the extracellular surface of TRPV1. These results suggest that three extracellular cysteines of TRPV1, Cys616, Cys634 and Cys621, are responsible for the oxidative modulation of I cap by HgCl2.
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