| Literature DB >> 19145483 |
Toshihide Sato1, Kazuhisa Nishishita, Yukio Okada, Kazuo Toda.
Abstract
A gap junction blocker, 18beta-glycyrrhetinic acid (beta-GA), increased the membrane resistance of Ia, Ib and II/III cells of frog taste disk by 50, 160, and 300 M Omega, 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 beta-GA at 1.0 mg/kg. beta-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 beta-GA-treated taste disk cells. This implies that gustatory depolarizing response profiles for 4 basic taste stimuli were very similar in control and beta-GA-treated taste disk cells. It is concluded that beta-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.Entities:
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Year: 2009 PMID: 19145483 DOI: 10.1007/s10571-008-9342-6
Source DB: PubMed Journal: Cell Mol Neurobiol ISSN: 0272-4340 Impact factor: 5.046