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Chemical Senses Advance Access originally published online on February 13, 2007
Chemical Senses 2007 32(4):329-336; doi:10.1093/chemse/bjm003
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© The Author 2007. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Analysis of Slow Depolarizing Potential in Frog Taste Cell Induced by Parasympathetic Efferent Stimulation under Hypoxia

Toshihide Sato1, Kazushisa Nishishita2, Yukio Okada1 and Kazuo Toda1

1 Divisions of Integrated Sensory Physiology 2 Oral Pathopharmacology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan

Correspondence to be sent to: Toshihide Sato, Division of Integrated Sensory Physiology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan. e-mail: toshi{at}net.nagasaki-u.ac.jp


  Abstract

Strong electrical stimulation (ES) of the frog glossopharyngeal (GP) efferent nerve induced slow depolarizing potentials (DPs) in taste cells under hypoxia. This study aimed to elucidate whether the slow DPs were postsynaptically induced in taste cells. After a block of parasympathetic nerve (PSN) ganglia by tubocurarine, ES of GP nerve never induced slow DPs in the taste cells, so slow DPs were induced by PSN. When Ca2+ in the blood plasma under hypoxia was decreased to ~0.5 mM, the slow DPs reduced in amplitude and lengthened in latency. Increasing the normal Ca2+ to ~20 mM increased the amplitude of slow DPs and shortened the latency. Addition of Cd2+ to the plasma greatly reduced the amplitude of slow DPs and lengthened the latency. These data suggest that the slow DPs depend on Ca2+ and Cd2+ concentration at the presynaptic PSN terminals of taste disk. Antagonists, [D-Arg1, D-Trp7,9, Leu11]-substance P and L-703 606, of neurotransmitter substance P neurokinin1 receptor completely blocked the slow DPs. Intravenous application of substance P induced a DP of ~7 mV and a reduction of membrane resistance of ~48% in taste cells. A nonselective cation channel antagonist, flufenamic acid, completely blocked the slow DPs. These findings suggest that the slow DPs are postsynaptically initiated in frog taste cells under hypoxia by opening nonselective cation channels on the postsynaptic membrane after substance P is probably released from the presynaptic PSN axon terminals.

Key words: frog taste cell, gustatory efferent synapse, hypoxia, presynaptic modulation, slow depolarizing potential

Accepted 15 January 2007


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