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Electrical stimulation of the frog glossopharyngeal (GP) nerve evoked slow  hyperpolarizing potentials (HPs) in taste cells. This study aimed to clarify whether slow  HPs were postsynaptically induced in taste cells. The slow HPs were recorded  intracellularly with a microelectrode. When Ca 2+  concentration in the  blood plasma was decreased to ∼0.5 mM, the amplitude of slow HPs reduced and their  latency lengthened. When the Ca 2+  concentration was increased to ∼20  mM, the amplitude of slow HPs increased and their latency shortened. Addition of  Cd 2+  to the plasma greatly reduced the amplitude of slow HPs and  lengthened their latency. These data suggest that the slow HPs are dependent on  presynaptic activities in the GP nerve terminals in the taste disk. Of various  antagonists injected intravenously for blocking receptors of neurotransmitter biogenic  amines and peptides, only antagonists for substance P blocked the slow HPs at 2–4  mg/kg body wt. Application of substance P of 2 mg/kg to the plasma induced  hyperpolarizing responses in taste cells, whose amplitude was the same as that of the  slow HPs induced by GP nerve stimulation. Application of a nonselective cation channel  antagonist, flufenamic acid, to the plasma blocked the slow HPs. These results suggest  that the slow HPs are generated by closing the nonselective cation channels in the  postsynaptic membrane of taste cells following possible release of substance P from the  GP nerve terminals in the taste disk.

Analysis of Slow Hyperpolarizing Potentials in Frog Taste Cells Induced by Glossopharyngeal Nerve Stimulation