ABSTRACT
Recently, our group reported that bradykinin and 5-hydroxytryptamine-induced nociceptive responses were signicantly suppressed by the direct application of GlcN (Kaida et al. 2013, 2014). It has been reported that GlcN reduces the elementary current amplitude and increases the mean channel open time (Marchais and Marty 1980). Because GlcN has a weak binding site in the channel itself, the channel cannot be closed (Marchais and Marty 1980). Voltage-gated sodium channels are necessary for electrogenesis and nerve impulse conduction (Cummins et al. 2007). GlcN may, thus, exhibit an antinociceptive effect by binding to these sodium channels, resulting in a longer open time, which produces the hyperpolarization of nerves in relation to cell membrane stability.
