Non-synaptic transformation of gustatory receptor potential by stimulation of the parasympathetic fiber of the frog glossopharyngeal nerve

When the glossopharyngeal nerve (GP) in the frog was strongly stimulated electrically, slow potentials were elicited from the tongue surface and taste cells in the fungiform papillae. Injection of atropine completely blocked these slow potentials. The present and previous data indicate that the slow potentials induced in the tongue surface and taste cells are due to a liquid junction potential between saliva secreted from the lingual glands due to parasympathetic fiber activity and an adapting solution on the tongue surface. Intracellularly recorded depolarizing receptor potentials in taste cells induced by 0.5 M NaCl and 3 mM acetic acid were enhanced by depolarizing slow potentials induced by GP nerve stimulation, but were depressed by the hyperpolarizing slow potentials. On average, the receptor potential of taste cells for 0.5 M NaCl was increased by 25% by the GP nerve-induced slow potential, but the receptor potential of taste cells for 3 mM acetic acid was decreased by 1% by the slow potential. These transformations of receptor potentials in frog taste cells were not due to a synaptic event initiated between taste cells and the efferent nerve fiber, but due to a non-synaptic event, a lingual junction potential generated in the dorsal lingual epithelium by GP nerve stimulation.     

Taste cell responses in the frog are modulated by parasympathetic efferent nerve fibers

We studied the anatomical properties of parasympathetic postganglionic neurons in the frog tongue and their modulatory effects on taste cell responses. Most of the parasympathetic ganglion cell bodies in the tongue were found in extremely small nerve bundles running near the fungiform papillae, which originate from the lingual branches of the glossopharyngeal (GP) nerve. The density of parasympathetic postganglionic neurons in the tongue was 8000-11,000/mm(3) of the extremely small nerve bundle. The mean major axis of parasympathetic ganglion cell bodies was 21 microm, and the mean length of parasympathetic postganglionic neurons was 1.45 mm. Electrical stimulation at 30 Hz of either the GP nerve or the papillary nerve produced slow hyperpolarizing potentials (HPs) in taste cells. After nicotinic acetyl choline receptors on the parasympathetic ganglion cells in the tongue had been blocked by intravenous (i.v.) injection of D-tubocurarine (1 mg/kg), stimulation of the GP nerve did not induce any slow HPs in taste cells but that of the papillary nerve did. A further i.v. injection of a substance P NK-1 antagonist, L-703,606, blocked the slow HPs induced by the papillary nerve stimulation. This suggests that the parasympathetic postganglionic efferent fibers innervate taste cells and are related to a generation of the slow HPs and that substance P is released from the parasympathetic postganglionic axon terminals. When the resting membrane potential of a taste cell was hyperpolarized by a prolonged slow HP, the gustatory receptor potentials for NaCl and sugar stimuli were enhanced in amplitude, but those for quinine-HCl and acetic acid stimuli remained unchanged. It is concluded that frog taste cell responses are modulated by activities of parasympathetic postganglionic efferent fibers innervating these cells.     

Slow potentials in taste cells induced by frog glossopharyngeal nerve stimulation

Intracellular recordings were made from the taste cells of atropinized bullfrogs while the glossopharyngeal (GP) nerve fibres were electrically stimulated. Two types of slow potential, slow hyperpolarizing potentials (HPs) and slow depolarizing potentials (DPs), were induced in the taste cells. The slow HPs appeared when the lingual capillary blood flow was kept above 0.7 mm/s, whereas the slow DPs appeared when the blood flow was slowed down below 0.7 mm/s. The membrane resistance of a taste cell increased during the generation of a slow HP, but decreased during the generation of a slow DP. The reversal potentials for the slow HPs and the slow DPs were recorded at the same membrane potential (-11 to approximately -13 mV). Activation of non-selective cation channels possibly induced the slow DP and inactivation of those channels possibly induced the slow HP in the taste cell membrane. Electrical stimulation of the GP nerve activated a population of C fibres in the nerve and possibly released neurotransmitters from the nerve terminals. Released neurotransmitters might cause modulation of the membrane conductance in taste cells that leads to generation of the slow potentials. The present data suggest that slow HPs and slow DPs evoked in the taste cells of atropinized frogs by GP nerve stimulation are induced by putative neurotransmitters in the taste disc.     

Analysis of slow hyperpolarizing potentials in frog taste cells induced by glossopharyngeal nerve stimulation

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 Ca2+ concentration in the blood plasma was decreased to approximately 0.5 mM, the amplitude of slow HPs reduced and their latency lengthened. When the Ca2+ concentration was increased to approximately 20 mM, the amplitude of slow HPs increased and their latency shortened. Addition of Cd2+ 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.     

Depression of gustatory receptor potential in frog taste cell by parasympathetic nerve-induced slow hyperpolarizing potential

Parasympathetic nerve (PSN) innervates taste cells of the frog taste disk, and electrical stimulation of PSN elicited a slow hyperpolarizing potential (HP) in taste cells. Here we report that gustatory receptor potentials in frog taste cells are depressed by PSN-induced slow HPs. When PSN was stimulated at 30 Hz during generation of taste cell responses, the large amplitude of depolarizing receptor potential for 1 M NaCl and 1 mM acetic acid was depressed by approximately 40% by slow HPs, but the small amplitude of the depolarizing receptor potential for 10 mM quinine-HCl (Q-HCl) and 1 M sucrose was completely depressed by slow HPs and furthermore changed to the hyperpolarizing direction. The duration of the depolarizing receptor potentials depressed by slow HPs prolonged with increasing period of PSN stimulation. As tastant-induced depolarizing receptor potentials were increased, the amplitude of PSN-induced slow HPs inhibiting the receptor potentials gradually decreased. The mean reversal potentials of the slow HPs were approximately -1 mV under NaCl and acetic acid stimulations, but approximately -14 mV under Q-HCl and sucrose stimulations. This implies that when a slow HP was evoked on the same amplitude of depolarizing receptor potentials, the depression of the NaCl and acetic acid responses in taste cells was larger than that of Q-HCl and sucrose responses. It is concluded that slow HP-induced depression of gustatory depolarizing receptor potentials derives from the interaction between gustatory receptor current and slow hyperpolarizing current in frog taste cells and that the interaction is stronger for NaCl and acetic acid stimulations than for Q-HCl and sucrose stimulations.     

Analysis of slow depolarizing potential in frog taste cell induced by parasympathetic efferent stimulation under hypoxia

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 Ca(2+) in the blood plasma under hypoxia was decreased to approximately 0.5 mM, the slow DPs reduced in amplitude and lengthened in latency. Increasing the normal Ca(2+) to approximately 20 mM increased the amplitude of slow DPs and shortened the latency. Addition of Cd(2+) to the plasma greatly reduced the amplitude of slow DPs and lengthened the latency. These data suggest that the slow DPs depend on Ca(2+) and Cd(2+) concentration at the presynaptic PSN terminals of taste disk. Antagonists, [D-Arg(1), D-Trp(7,9), Leu(11)]-substance P and L-703 606, of neurotransmitter substance P neurokinin(1) receptor completely blocked the slow DPs. Intravenous application of substance P induced a DP of approximately 7 mV and a reduction of membrane resistance of approximately 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.     

Tonic activity of parasympathetic efferent nerve fibers hyperpolarizes the resting membrane potential of frog taste cells

We investigated the relationship between the membrane potential of frog taste cells in the fungiform papillae and the tonic discharge of parasympathetic efferent fibers in the glossopharyngeal (GP) nerve. When the parasympathetic preganglionic fibers in the GP nerve were kept intact, the mean membrane potential of Ringer-adapted taste cells was -40 mV but decreased to -31 mV after transecting the preganglionic fibers in the GP nerve and crushing the postganglionic fibers in the papillary nerve. The same result occurred after blocking the nicotinic acetylcholine receptors on parasympathetic ganglion cells in the tongue and blocking the substance P neurokinin-1 (NK-1) receptors in the gustatory efferent synapses. This indicates that the parasympathetic nerve (PSN) hyperpolarizes the membrane potential of frog taste cells by -9 mV. Repetitive stimulation of a transected GP nerve revealed that a -9-mV hyperpolarization of taste cells maintained under the intact GP nerve derives from an approximately 10-Hz discharge of the PSN efferent fibers. The mean frequency of tonic discharges extracellularly recorded from PSN efferent fibers of the taste disks was 9.1 impulses/s. We conclude that the resting membrane potential of frog taste cells is continuously hyperpolarized by on average -9 mV by an approximately 10-Hz tonic discharge from the parasympathetic preganglionic neurons in the medulla oblongata.     

Characteristics of biphasic slow depolarizing and slow hyperpolarizing potential in frog taste cell induced by parasympathetic efferent stimulation

When the velocity of capillary blood flow in the frog tongue declined to an intermediate range of 0.2-0.7 mm/s, the glossopharyngeal nerve stimulation induced a biphasic slow depolarizing and slow hyperpolarizing potential (HP) in taste cells. The objective of this work was to examine the generative mechanisms of the biphasic slow potentials. The biphasic slow response was always preceded by a slow depolarizing potential (DP) component and followed by a slow HP component. Intravenous injection of tubocurarine completely blocked the biphasic slow responses, suggesting that both components of the biphasic slow potentials are evoked by the parasympathetic nerve (PSN) fibers. Membrane conductance of taste cells increased during slow DPs and decreased during slow HPs. The reversal potential of either component of a biphasic slow response was the almost same value of -12 mV. An antagonist, L-703,606, for neurotransmitter substance P neurokinin(1) receptor completely blocked both components of the biphasic slow responses. An antagonist, flufenamic acid, for nonselective cation channels on the taste cell membrane completely blocked the biphasic slow responses. These results suggest that PSN-induced biphasic slow responses are postsynaptically elicited in taste cells by releasing substance P at the PSN axon terminals. It is concluded that the slow DP component may be generated by opening one type of nonselective cation channel on taste cells and that the slow HP component may be generated by closing the other type of nonselective cation channel. We discussed that a second messenger inositol 1,4,5-trisphosphate might be related to a slow DP component and another second messenger diacylglycerol might be related to a slow HP component.     

Interaction Between Gustatory Depolarizing Receptor Potential and Efferent-Induced Slow Depolarizing Synaptic Potential in Frog Taste Cell

Electrical stimulation of parasympathetic nerve (PSN) efferent fibers in the glossopharyngeal nerve induced a slow depolarizing synaptic potential (DSP) in frog taste cells under hypoxia. The objective of this study is to examine the interaction between a gustatory depolarizing receptor potential (GDRP) and a slow DSP. The amplitude of slow DSP added to a tastant-induced GDRP of 10 mV was suppressed to 60% of control slow DSPs for NaCl and acetic acid stimulations, but to 20–30% for quinine–HCl (Q-HCl) and sucrose stimulations. On the other hand, when a GDRP was induced during a prolonged slow DSP, the amplitude of GDRPs induced by 1 M NaCl and 1 M sucrose was suppressed to 50% of controls, but that by 1 mM acetic acid and 10 mM Q-HCl unchanged. It is concluded that the interaction between GDRPs and efferent-induced slow DSPs in frog taste cells under hypoxia derives from the crosstalk between a gustatory receptor current across the receptive membrane and a slow depolarizing synaptic current across the proximal subsynaptic membrane of taste cells.     

Effects of antidromic activity in gustatory nerve fibers on taste disc cells of the frog tongue

Summary Antidromic electrical stimulation of the lingual branch of the glossopharyngeal (IX) nerve of the frog was carried out while recording intracellular potentials of taste disc cells.Antidromic activation of sensory fibers resulted in depolarization of cells of the upper layer of the disc and most commonly in hyperpolarization of the cells in the lower layer. These changes in potential exhibited latencies greater than 1 s (Fig. 3), and thus cannot be due to electrotonic effects of action potentials in terminals of IX nerve fibers, which have much shorter conduction times. These cell potentials also showed summation, adaptation and post-stimulus rebound (Figs. 3, 4).Depending upon the chemical stimulus used, antidromic activity produced either depression or enhancement of gustatory fiber discharge in response to taste stimuli (Fig. 5).Alteration of the resting membrane potential by current injection did not significantly modify the antidromically evoked potentials (Fig. 8), whereas chemical stimulation of the tongue did (Fig. 7), indicating that these potential changes are not the result of passive electrical processes.These experimental results indicate that the membrane potential of taste disc cells can be modified by antidromic activity in their afferent nerves. This mechanism may be responsible for peripheral interactions among gustatory units of the frog tongue.The research was supported in part by NIH grant NS-09168.     

Multiple sensitivity of single taste cells of the frog tongue to four basic taste stimuli

The electrical response of the taste cells of the frog fungiform papillae to four fundamental taste solutions (NaCl, acetic acid, quinine-HCl and sucrose) was studied by using the intracellular recording technique. The average value of resting membrane potential was 22.5 mV, inside negative. Each of the four taste solutions applied to the tongue produced a slow depolarizing potential, the receptor potential, on which no spike potential was superimposed. The amplitude of the receptor potentials increased linearly as a function of the logarithm of the concentration of the stimulus. Amplitudes of depolarizations to a given taste stimulation varied from one cell to another even within a single taste bud. Most of the cells responded to more than two of the four basic taste solutions. Sensitivity patterns in terms of the number of effective solutions and the relative effectiveness of different kinds of solutions were variable among cells. Statistical analysis suggests that at the receptor membranes of the taste cells, the sensitivities for the four basic stimuli are independent and random.     

Taste-responsive neurons in the nucleus of the solitary tract receive gustatory information from both sides of the tongue in the hamster

Taste receptors on the left and right sides of the anterior tongue are innervated by chorda tympani (CT) fibers, which carry taste information to the ipsilateral nucleus of the solitary tract (NST). Although the anterior tongue is essential for taste, patients with unilateral CT nerve damage often report no subjective change in their taste experience. The standing theory that explains the taste constancy is the "release of inhibition", which hypothesizes that within the NST there are inhibitory interactions between inputs from the CT and glossopharyngeal nerves and that the loss of taste information from the CT is compensated by a release of inhibition on the glossopharyngeal nerve input. However, the possibility of compensation by taste input from the other side of the tongue has never been investigated in rodents. We recorded from 95 taste-responsive neurons in the NST and examined their responsiveness to stimulation of the contralateral CT. Forty-six cells were activated, mostly with excitatory responses (42 cells). Activation of NST cells induced by contralateral CT stimulation was blocked by microinjection of lidocaine into the contralateral NST but was not affected by anesthetization of the contralateral parabrachial nuclei (PbN). In addition, the NST cells that were activated by contralateral CT stimulation showed reduced responsiveness to taste stimulation after microinjection of lidocaine into the contralateral NST. These results demonstrate that nearly half of the taste neurons in the NST receive gustatory information from both sides of the tongue. This "cross talk" between bilateral NST may also contribute to the "taste constancy".     

Membrane resistance change of the frog taste cells in response to water and Nacl

The electrical properties of the frog taste cells during gustatory stimulations with distilled water and varying concentrations of NaCl were studied with intracellular microelectrodes. Under the Ringer adaptation of the tongue, two types of taste cells were distinguished by the gustatory stimuli. One type, termed NaCl-sensitive (NS) cells, responded to water with hyperpolarizations and responded to concentrated NaCl with depolarizations. In contrast, the other type of cells, termed water-sensitive (WS) cells, responded to water depolarizations and responded to concentrated NaCl with hyperpolarizations. The membrane resistance of both taste cell types increased during the hyperpolarizing receptor potentials and decreased during the depolarizing receptor potentials, Reversal potentials for the depolarizing and hyperpolarizing responses in each cell type were a few millivolts positive above the zero membrane potential. When the tongue was adapted with Na-free Ringer solution for 30 min, the amplitude of the depolarizing responses in the NS cells reduced to 50% of the control value under normal Ringer adaptation. On the basis of the present results, it is concluded (a) that the depolarizing responses of the NS and WS cells under the Ringer adaptation are produced by the permeability increase in some ions, mainly Na+ ions across the taste cell membranes, and (b) that the hyperpolarizing responses of both types of taste cells are produced by a decrease in the cell membrane permeability to some ions, probably Na+ ions, which is slightly enhanced during the Ringer adaptation.     

Further Study of the Electrical and Mechanical Responses of Slow Fibers in Cat Extraocular Muscles

Electrical and mechanical responses have been obtained in situ and in vitro from the superior oblique muscle stimulated by single and repetitive electrical pulses, applied to the trochlear nerve. Two different types of muscle fibers are described, the twitch and the slow. The slow type is characterized electrically by the presence of junctional potentials, which have reversal potentials between -10 and -20 mv, and do not show propagated responses or spikes, during nerve stimulation. When the slow muscle fibers are repetitively stimulated in situ, a prolonged contraction is maintained during stimulation. At the time, the recorded electrical activity is produced locally, at the level of the neuromuscular junctions of the slow fibers. These results indicate that the contractile mechanism of the slow muscle fibers is activated locally and segmentally.     

Mode of Operation of Ampullae of Lorenzini of the Skate, Raja

Ampullae of Lorenzini are sensitive electroreceptors. Applied potentials affect receptor cells which transmit synaptically to afferent fibers. Cathodal stimuli in the ampullary lumen sometimes evoke all-or-none "receptor spikes," which are negative-going recorded in the lumen, but more frequently they evoke graded damped oscillations. Cathodal stimuli evoke nerve discharge, usually at stimulus strengths subthreshold for obvious receptor oscillations or spikes. Anodal stimuli decrease any ongoing spontaneous nerve activity. Cathodal stimuli evoke long-lasting depolarizations (generator or postsynaptic potentials) in afferent fibers. Superimposed antidromic spikes are reduced in amplitude, suggesting that the postsynaptic potentials are generated similarly to other excitatory postsynaptic potentials. Anodal stimuli evoke hyperpolarizations of nerves in preparations with tonic activity and in occasional silent preparations; presumably tonic release of excitatory transmitter is decreased. These data are explicable as follows: lumenal faces of receptor cells are tonically (but asynchronously) active generating depolarizing responses. Cathodal stimuli increase this activity, thereby leading to increased depolarization of and increased release of transmitter from serosal faces, which are inexcitable. Anodal stimuli act oppositely. Receptor spikes result from synchronized receptor cell activity. Since cathodal stimuli act directly to hyperpolarize serosal faces, strong cathodal stimuli overcome depolarizing effects of lumenal face activity and are inhibitory. Conversely, strong anodal stimuli depolarize serosal faces, thereby causing release of transmitter, and are excitatory. These properties explain several anomalous features of responses of ampullae of Lorenzini.     

Structure and physiological properties of the taste organs on the ventral side of frog tongue (Rana catesbeiana)

The structure and physiological properties of the non-papillarytaste organs on the ventral side of frog tongue were examined.The taste organs were distributed around the hyoglossal muscleof the tongue. The total number of organs was estimated as about100. The fine structure of the taste organs was similar to thatof the fungiform papilla. Neural responses recorded from theglossopharyngeal nerve by applying chemical stimuli to the ventraltide of the tongue were noticeably smaller than those to thedorsal side of the tongue. The taste cells on the ventral sideof the tongue generated receptor potentials to various chemicalstimuli like those on the dorsal side of the tongue.     

Peptidergic regulation of secretory activity in amphibian olfactory mucosa: Immunohistochemistry,neural stimulation,and pharmacology

Summary The role of substance P in the regulation of secretion from sustentacular cells, Bowman's glands and deep glands in the amphibian olfactory mucosa was investigated using immunohistochemical, electrophysiological, and pharmacological methods. Substance P-like immunoreactive varicose fibers extended through the olfactory epithelium, terminating at or near the surface. In addition, immunoreactive varicose fibers innervated Bowman's glands, deep glands, and blood vessels in the lamina propria. Innervation of Bowman's gland was sparse, with fibers terminating on basal acinar cell membranes; deep gland innervation was abundant, with fibers often extending between acinar cells almost to the lumen. Stimulation of the ophthalmic branch of the trigeminal nerve resulted in slow potentials recorded at the surface of the olfactory epithelium. When the olfactory mucosae from trigeminal-stimulated animals were examined histologically, morphological signs of secretory activity were observed, suggesting that substance P was released from the trigeminal nerve terminals. Topical application of 10^-5 to 10^-3 mol substance P resulted in morphological signs of secretion that were very similar to those seen as a result of trigeminal stimulation. Thus, substance P released from trigeminal fibers may modulate secretory activity within the olfactory mucosa.     

Histochemical study of the cholinergic structures of the frog tongue after chronic administration of ethanol

The chronic ethanol effect on the cholinergic structures of frog's tongue epithelium was studied by means of histochemical method. It was found that the administration of ethanol daily for 14 days resulted in a decrease of reactive reorganization processes of the nerve fibers and nervous band perineurium, arising under stimulation of the tongue by taste solutions. This process was partly restored in a month, in spite of the continuing ethanol administration. The decrease of acetylcholinesterase activity and the appearance of dystrophic and destructive changes both in the nerve fibers and in neurons was observed in the animals subjected to lasting ethanol effect for 60-90 days. Revealed in the course of alcoholization morpho-functional changes of cholinergic tongue structures can be in the basis of the disturbance of the taste.     

Response characteristics of rat taste cells to potassium benzoate

The rat taste cells responded to K-benzoate solutions higher than the threshold concentrations (0.03-0.3 M) with a depolarizing receptor potential, but they responded to K-benzoate lower than the thresholds with a hyperpolarizing receptor potential. In either depolarizing or hyperpolarizing receptor potentials the rise time decreased with increasing amplitude, but the fall time increased with increasing amplitude. During generation of either depolarizing or hyperpolarizing receptor potentials the input resistance of taste cells decreased with increasing amplitude. Application of the mixtures of various concentrations of NaCl and 0.05 M K-benzoate resulted in a reduction of receptor potential amplitude, as compared with that evoked by application of NaCl alone. It is concluded that a depression of gustatory neural impulse frequency by low concentrations of K-benzoate is mainly due to the hyperpolarizing receptor potential of taste cells elicited by the K-benzoate solutions.     

Voltage-dependent ionic currents in taste receptor cells of the larval tiger salamander

Voltage-dependent membrane currents of cells dissociated from tongues of larval tiger salamanders (Ambystoma tigrinum) were studied using whole-cell and single-channel patch-clamp techniques. Nongustatory epithelial cells displayed only passive membrane properties. Cells dissociated from taste buds, presumed to be gustatory receptor cells, generated both inward and outward currents in response to depolarizing voltage steps from a holding potential of -60 or -80 mV. Almost all taste cells displayed a transient inward current that activated at -30 mV, reached a peak between 0 and +10 mV and rapidly inactivated. This inward current was blocked by tetrodotoxin (TTX) or by substitution of choline for Na+ in the bath solution, indicating that it was a Na+ current. Approximately 60% of the taste cells also displayed a sustained inward current which activated slowly at about -30 mV and reached a peak at 0 to +10 mV. The amplitude of the slow inward current was larger when Ca2+ was replaced by Ba2+ and it was blocked by bath applied CO2+, indicating it was a Ca2+ current. Delayed outward K+ currents were observed in all taste cells although in about 10% of the cells, they were small and activated only at voltages more depolarized than +10 mV. Normally, K+ currents activated at -40 mV and usually showed some inactivation during a 25-ms voltage step. The inactivating component of outward current was not observed at holding potentials more depolarized -40 mV. The outward currents were blocked by tetraethylammonium chloride (TEA) and BaCl2 in the bath or by substitution of Cs+ for K+ in the pipette solution. Both transient and noninactivating components of outward current were partially suppressed by CO2+, suggesting the presence of a Ca2(+)-activated K+ current component. Single-channel currents were recorded in cell-attached and outside-out patches of taste cell membranes. Two types of K+ channels were partially characterized, one having a mean unitary conductance of 21 pS, and the other, a conductance of 148 pS. These experiments demonstrate that tiger salamander taste cells have a variety of voltage- and ion-dependent currents including Na+ currents, Ca2+ currents and three types of K+ currents. One or more of these conductances may be modulated either directly by taste stimuli or indirectly by stimulus-regulated second messenger systems to give rise to stimulus-activated receptor potentials. Others may play a role in modulation of neurotransmitter release at synapses with taste nerve fibers.(ABSTRACT TRUNCATED AT 400 WORDS)