Effect of Gap Junction Blocker β-Glycyrrhetinic Acid on Taste Disk Cells in Frog
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A gap junction blocker, 18β-glycyrrhetinic acid (β-GA), increased the membrane resistance of Ia, Ib and II/III cells of frog taste disk by 50, 160, and 300 MΩ, respectively, by blocking the gap junction channels and hemichannels. The amplitudes of gustatory depolarizing potentials in the disk cells for 4 basic taste stimuli were reduced to 40–60% after intravenous injection of β-GA at 1.0 mg/kg. β-GA of 1.0 mg/kg did not affect the resting potentials and the reversal potentials for tastant-induced depolarizing potentials in any taste disk cells. The percentage of cells responding to each of 4 basic taste stimuli and varying numbers of 4 taste qualities did not differ between control and β-GA-treated taste disk cells. This implies that gustatory depolarizing response profiles for 4 basic taste stimuli were very similar in control and β-GA-treated taste disk cells. It is concluded that β-GA at 1.0 mg/kg reduced the amplitude of gustatory depolarizing potentials in taste disk cells by strongly blocking depolarizing currents flowing through the gap junction channels and hemichannels, but probably weakly affected the gustatory transduction mechanisms for 4 taste stimuli.
KeywordsFrog taste disk cell Depolarizing response profile Gap junction blocker Gap junction hemichannel Membrane resistance increase
This work was supported by Japan Society for the Promotion of Science (17570064).
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