scholarly journals The ionic basis of the receptor potential of frog taste cells induced by water stimuli.

1993 ◽  
Vol 174 (1) ◽  
pp. 1-17
Author(s):  
Y Okada ◽  
T Miyamoto ◽  
T Sato
Keyword(s):  
Basolateral Membrane ◽  
Reversal Potential ◽  
Receptor Potential ◽  
Input Resistance ◽  
Deionized Water ◽  
Glossopharyngeal Nerve ◽  
Equilibrium Potential ◽  
Induced Response ◽  
Control Value ◽  
Taste Cells

The ionic mechanism underlying the receptor potential induced by a deionized water stimulus was studied in frog taste cells with conventional microelectrodes. The taste cells located in the proximal portion of the tongue generated a depolarizing receptor potential which averaged 10mV in response to stimulation with deionized water. The cell membrane of the water-sensitive taste cell could be divided into the taste-receptive (apical) and basolateral membranes and the cells were classified into two types: Cl(-)-dependent and Cl(-)-independent. In Cl(-)-dependent cells whose input resistance was decreased or unchanged by deionized water, the magnitude of the water-induced depolarization decreased with an increase in concentration of superficial Cl- in contact with the receptive membrane and with addition of blockers of anion channels (0.1 mmol l-1 SITS and 0.1 mmol l-1 DIDS) to deionized water. The reversal potential for the depolarization in this type shifted according to the concentration of superficial Cl-. These properties of the responses were consistent with those of the glossopharyngeal nerve which innervates the taste disc. In Cl(-)-independent cells whose input resistance was increased by deionized water, the reversal potential was approximately equal to the equilibrium potential for K+ at the basolateral membrane. The water-induced response of the glossopharyngeal nerve was decreased to about 60% of the control value by addition of interstitial 2 mmol l-1 Ba2+. It is concluded that the water-induced receptor potential is produced by Cl- secretion through the taste-receptive membrane in about 70% of water-sensitive frog taste cells, while it is generated by an inhibition of the resting K+ conductance of the basolateral membrane in the remaining 30% of the cells.

The ionic basis of the receptor potential of frog taste cells induced by sugar stimuli

1992 ◽  
Vol 162 (1) ◽  
pp. 23-36
Author(s):  
Y. Okada ◽  
T. Miyamoto ◽  
T. Sato
Keyword(s):  
Interstitial Fluid ◽  
Basolateral Membrane ◽  
Reversal Potential ◽  
Receptor Potential ◽  
Input Resistance ◽  
Fold Increase ◽  
Taste Cell ◽  
Control Value ◽  
Taste Cells ◽  
Decreasing Ph

The ionic mechanism underlying the receptor potential in frog taste cells induced by sugar stimuli was studied with conventional microelectrodes by replacing the superficial and interstitial fluids of the tongue with modified solutions. The taste cell generated a depolarizing receptor potential accompanying a remarkable reduction of input resistance in response to stimulation with galactose and sucrose. The magnitude of the receptor potential in response to galactose solution increased linearly with decreasing pH in the pH range 6–8, but remained constant above pH8. The reversal potential was increased by only 29 mV by a 10-fold increase in the H+ concentration of the stimulus, suggesting that there are pH-dependent and pH-independent components in the mechanism generating the receptor potential. The use of Na(+)-free, Ca(2+)-free and K(+)-free interstitial fluids did not affect the receptor potential, but the elimination of Cl- from the interstitial fluid largely abolished it. Interstitial 0.1 mmol l-1 N,N'-dicyclohexyl-carbodiimide (DCCD) completely inhibited the receptor potential and interstitial 0.1 mmol l-1 N-ethylmaleimide (NEM) decreased the potential to 40% of the control value. Lowering the pH of interstitial fluid from 7.2 to 6.3 decreased the receptor potential to 30% of the control value. It is concluded that part of the receptor potential in frog taste cells induced by sugar stimuli may be produced by an inflow of H+ through the taste-receptive membrane. The intracellular pH of the taste cell may be regulated by a Cl(−)-dependent H+ pump in the basolateral membrane.

Cholecystokinin-gated currents in neurons of the rat solitary complex in vitro

1993 ◽  
Vol 70 (6) ◽  
pp. 2584-2595 ◽  
Author(s):  
P. Branchereau ◽  
J. Champagnat ◽  
M. Denavit-Saubie
Keyword(s):  
Voltage Clamp ◽  
Potassium Current ◽  
Reversal Potential ◽  
Input Resistance ◽  
Calcium Currents ◽  
Equilibrium Potential ◽  
Potassium Ions ◽  
Nernst Equation ◽  
Membrane Hyperpolarization ◽  
Cckb Receptor

1. Ionic conductances controlled by type A and type B cholecystokinin (CCK) receptors were studied in neurons of the rat nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus (DMNV), using intracellular and whole-cell patch clamp recordings in current or voltage clamp configuration during bath application of agonists (CCK8, CCK4, BC 264) and antagonists. 2. CCKA receptor-related inhibition was associated with a membrane hyperpolarization and a decrease in input resistance that developed 2-6 min after the arrival of drug into the extracellular medium. These effects were induced by 5 nM CCK8 but not BC 264 and they were blocked by the CCKA antagonist, L-364,718, but not by the CCKB antagonist, L-365,260. 3. CCKA receptor-related inhibition was generated by a potassium current that reversed at a reversal potential E(rev) of -73 +/- 1 (mean +/- SE) mV with bathing potassium concentration [K+]o = 6 mM and at -88 +/- 1 with [K+]o = 3 mM, in agreement with the Nernst equation for potassium ions. 4. CCKB receptor-related excitation was associated with a membrane depolarization and an increase of the input resistance induced by the following agonists at threshold concentrations: CCK8 (0.2 nM) > or = BC 264 (0.4 nM) > CCK4 (10.9 nM). The increase of input resistance was abolished by L-365,260 and was maintained after blockade of the CCKA current by L-364,718. 5. CCKB receptor-related excitation, in the neurons (30% of cases) in which clear response reversal was observed, appeared to be generated by a decrease of a potassium conductance. Responses showed a reversal potential E(rev) of -68 +/- 4 mV with [K+]o = 6 mM and -89 +/- 1 mV with [K+]o = 3 mM, verifying predictions from the Nernst equation applied to potassium ions. However, in 70% of cases, clear reversal was not observed at membrane potentials negative to the theoretical potassium equilibrium potential EK. 6. In voltage clamp studies, CCK8 induced a 181 +/- 17 pA inward current associated with a 26 +/- 4% decrease in the instantaneous current (I(ins)) generated by hyperpolarizing voltage steps. This effect on I(ins) was demonstrated in the absence of effects on the outward noninactivating potassium current (IM) and on the inward noninactivating cationic current (IQ). 7. CCKB receptor-mediated excitation was not suppressed by cobalt, a blocker of calcium currents, and was not associated with a change of the calcium-dependent potassium current (IK(Ca)).(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of norepinephrine upon superficial layer neurons in the superior colliculus of the hamster: In vitro studies

1999 ◽  
Vol 16 (3) ◽  
pp. 557-570 ◽  
Author(s):  
HONGJING TAN ◽  
RICHARD D. MOONEY ◽  
ROBERT W. RHOADES
Keyword(s):  
Superior Colliculus ◽  
Optic Tract ◽  
Reversal Potential ◽  
Outward Current ◽  
Input Resistance ◽  
Superficial Layer ◽  
Membrane Properties ◽  
Induced Response

Intracellular recording techniques were used to evaluate the effects of norepinephrine (NE) on the membrane properties of superficial layer (stratum griseum superficiale and stratum opticum) superior colliculus (SC) cells. Of the 207 cells tested, 44.4% (N = 92) were hyperpolarized by ≥3 mV and 8.7% (N = 18) were depolarized by ≥3 mV by application of NE. Hyperpolarization induced by NE was dose dependent (EC50 = 8.1 μM) and was associated with decreased input resistance and outward current which had a reversal potential of −94.0 mV. Depolarization was associated with a very slight rise in input resistance and had a reversal potential of −93.1 mV for the single cell tested. Pharmacologic experiments demonstrated that isoproterenol, dobutamine, and p-aminoclonidine all hyperpolarized SC cells. These results are consistent with the conclusion that NE-induced hyperpolarization of SC cells is mediated by both α2 and β1 adrenoceptors. The α1 adrenoceptor agonists, methoxamine and phenylephrine, depolarized 35% (6 of 17) of the SC cells tested by ≥3 mV. Most of the SC cells tested exhibited responses indicative of expression of more than one adrenoceptor. Application of p-aminoclonidine or dobutamine inhibited transsynaptic responses in SC cells evoked by electrical stimulation of optic tract axons. Inhibition of evoked responses by these agents was usually, but not invariably, associated with a hyperpolarization of the cell membrane and a reduction in depolarizing potentials evoked by application of glutamate. The present in vitro results are consistent with those of the companion in vivo study which suggested that NE-induced response suppression in superficial layer SC neurons was primarily postsynaptic and chiefly mediated by both α2 and β1 adrenoceptors.

Electrical properties of frog motoneurons in the in situ spinal cord

1976 ◽  
Vol 39 (3) ◽  
pp. 459-473 ◽  
Author(s):  
P. C. Magherini ◽  
W. Precht
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Rana Temporaria ◽  
Reversal Potential ◽  
Input Resistance ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Spike Initiation

Electrical properties of the spinal motoneurons of Rana temporaria and R. esculenta were investigated in the in situ spinal cord at 20-22 degrees C by means of intracellular recording and current injection. Input resistance values depended on the method of measurement in a given cell but were generally inversely related to axon conduction velocity. The membrane-potential response to a subthreshold current pulse was composed of at least two exponentials with mean time constants of 2.5 and 20 ms. The membrance potential reached by the peak of a spike depended on the mode of spike initiation and membrane potential. Preceding a suprathreshold depolarization by a hyperpolarizing pulse could delay and eliminate spike initiation, similar to effects reported in certain invertebrate neurons. Antidromic invasion frequently failed in motoneurons of normal resting potential. Antidromic spike components (m,IS, SD) were similar to those of cat motoneurons. The delayed depolarization and the long afterhyperpolarization following an antidromic spike had many properties in common with the analogous afterpotentials of cat motoneurons. The reversal potential of the short afterhyperpolarization occurring immediately after the spike varied with resting potential and could not be used to determine potassium equilibrium potential. Sustained rhythmic firing could be evoked by continuous synaptic drive or long pulses of injected current. The plot of firing rate versus current strength had a substantial linear region. Both steady firing and adaptation properties varied markedly with motoneuron input resistance.

Activation of a cation conductance by acetic acid in taste cells isolated from the bullfrog.

1994 ◽  
Vol 187 (1) ◽  
pp. 19-32 ◽  
Author(s):  
Y Okada ◽  
T Miyamoto ◽  
T Sato
Keyword(s):  
Acetic Acid ◽  
Earth Metal ◽  
Cell Voltage ◽  
Induced Response ◽  
Control Value ◽  
Cation Conductance ◽  
Bath Application ◽  
Na Currents ◽  
Taste Cells ◽  
Gustatory Neural Response

The ionic mechanism of the conductance activated by acetic acid was analyzed in isolated bullfrog taste cells under whole-cell voltage-clamp. Bath-application of acetic acid (pH 3.9-4.7) induced an inward current in about 80% of the taste cells. The current occurred in external 80 mmol l-1 Ba2+ and internal 100 mmol l-1 Cs+, which completely blocked the delayed outward K+ current. The concentration-response relationship for the acid-activated current was consistent with that of the gustatory neural response. Prolonged adaptation of the surface of the tongue to HCl prior to taste cell isolation decreased the acid-induced current to about 20% of the control value without decreasing NaCl-induced neural responses and voltage-activated Na+ currents. The results suggest that the transduction mechanism of the acid response might be different from that of the response to salt. The I-V relationship of the acid-induced response was nearly linear at membrane potentials between -80 and 80 mV. The acid-induced conductance was permeable to alkali metal and alkali earth metal ions. The permeability ratios were PCa:PBa:PSr:PNa:PCs = 1.87:1.17:0.73:0.99:1.00. The present study suggests that the acid-induced receptor current in bullfrog taste cells is generated by an increase in a cation conductance in the apical taste membrane.

Acid-Activated Cation Currents in Rat Vallate Taste Receptor Cells

2002 ◽  
Vol 88 (1) ◽  
pp. 133-141 ◽  
Author(s):  
Weihong Lin ◽  
Tatsuya Ogura ◽  
Sue C. Kinnamon
Keyword(s):  
Taste Receptor ◽  
Reversal Potential ◽  
Equilibrium Potential ◽  
Patch Clamp Technique ◽  
Sour Taste ◽  
Whole Cell Patch Clamp ◽  
Current Voltage ◽  
Taste Cells ◽  
Stimulation Current ◽  
Current Voltage Relationship

Sour taste is mediated by acids with the degree of sourness a function of proton concentration. Recently, several members of the acid-sensing ion channel subfamily (ASICs) were cloned from taste cells and proposed to mediate sour taste. However, it is not known whether sour responses in taste cells resemble the responses mediated by ASICs. Using the whole cell patch-clamp technique and Na+ imaging, we have characterized responses to acid stimuli in isolated rat vallate taste cells. Citric acid (pH 5) induced a large, rapidly activating inward current in most taste cells tested. The response showed various degrees of desensitization with prolonged stimulation. Current amplitudes were pH dependent, and adapting with acidic bath solutions reduced subsequent responses to acid stimulation. Amiloride (100–500 μM) partially and reversibly suppressed the acid-induced current. The current-voltage relationship showed reversal potential near the Na+equilibrium potential, suggesting that the current is carried predominantly by Na+. These data were consistent with Na+ imaging experiments showing that acid stimulation resulted in increases in intracellular Na+. Taken together, these data indicate that acid-induced currents in vallate taste cells share general properties with ASICs expressed in heterologous cells and sensory neurons that express ASIC subunits. The large amplitude of the current and its existence in a high percentage of taste cells imply that ASICs or ASIC-like channels may play a prominent role in sour-taste transduction.

Angiotensin II receptor activation depolarizes rat supraoptic neurons in vitro

1992 ◽  
Vol 263 (6) ◽  
pp. R1333-R1338 ◽  
Author(s):  
C. R. Yang ◽  
M. I. Phillips ◽  
L. P. Renaud
Keyword(s):  
Angiotensin Ii ◽  
Supraoptic Nucleus ◽  
Reversal Potential ◽  
Input Resistance ◽  
Receptor Activation ◽  
Induced Response ◽  
Angiotensin Ii Receptor ◽  
Functional Studies

Functional studies indicate that hypothalamic magnocellular neurosecretory neurons are a target for angiotensin. The present investigation used intracellular recordings to characterize the nature and type of angiotensin II receptors on rat supraoptic nucleus neurons maintained in superfused hypothalamic explants. Of 68 cells transiently exposed to either Val5- or Ile5-angiotensin II (maximum peak concentration 1-25 microM), 34 responded with a gradual membrane depolarization (1-15 mV) that peaked in 2.2 +/- 0.4 (SD) min and was accompanied by a 17.6 +/- 4.8% reduction of input resistance. Responses persisted (and were actually enhanced) in media containing tetrodotoxin (0.5-1.0 microM) and/or nominally zero calcium, indicating a direct postsynaptic action. In 19 responsive cells, the mean reversal potential for the angiotensin-induced response was -26.4 +/- 2 mV. Bath application of the nonpeptide type-1 angiotensin receptor antagonist DuP753 (5-20 microM) reversibly blocked the angiotensin-induced depolarization in all of 11 cells tested. By contrast, equimolar applications of the type-2 antagonist PD123177 were ineffective in all seven angiotensin-responsive cells tested. These observations provide novel evidence for the existence of functional type-1 receptors on rat supraoptic nucleus neurons. The reversal potential for the angiotensin-induced response suggests mediation through a nonselective cationic conductance.

scholarly journals Ion permeation through light-activated channels in rhabdomeric photoreceptors. Role of divalent cations.

1996 ◽  
Vol 107 (6) ◽  
pp. 715-730 ◽  
Author(s):  
M D Gomez ◽  
E Nasi
Keyword(s):  
Time Course ◽  
Light Adaptation ◽  
Single Channel ◽  
Divalent Cations ◽  
Reversal Potential ◽  
Receptor Potential ◽  
Equilibrium Potential ◽  
Positive Equilibrium ◽  
Kinetics Of

The receptor potential of rhabdomeric photoreceptors is mediated primarily by a Na influx, but other ions must also permeate through light-dependent channels to account for some properties of the photoresponse. We examined ion conduction in macroscopic and single-channel light-induced currents of slug and scallop photoreceptors. In the absence of Na, a fivefold change in extracellular K shifted the reversal voltage of the photocurrent (Vrev) by approximately 27 mV. Because the dependency of Vrev on [K]o was sub-Nernstian, and Vrev in each condition was more positive than Ek, some other ion(s) with a positive equilibrium potential must be implicated, in addition to K. We assessed the participation of calcium, an important candidate because of its involvement in light adaptation. Three strategies were adopted to minimize the impairments to cytosolic Ca homeostasis and loss of responsiveness that normally result from the required ionic manipulations: (a) Internal dialysis with Na-free solutions, to prevent reverse operation of the Na/Ca exchanger. (b) Rapid solution changes, temporally limiting exposure to potentially detrimental ionic conditions. (c) Single-channel recording, exposing only the cell-attached patch of membrane to the test solutions. An inward whole-cell photocurrent could be measured with Ca as the only extracellular charge carrier. Decreasing the [Ca]o to 0.5 mM reduced the response by 43% and displaced the reversal potential by -4.3 mV; the shift was larger (delta Vrev = -44 mV) when intracellular permeant cations were also removed. In all cases, however, the current carried by Ca was < 5% of that measured with normal [Na]o. Unitary light-activated currents were reduced in a similar way when the pipette contained only divalent cations, indicating a substantial selectivity for Na over Ca. The fall kinetics of the photoresponse was slower when external Ca was replaced by Ba, or when the membrane was depolarized; however, dialysis with 10 mM BAPTA failed to antagonize this effect, suggesting that mechanisms other than the Ca influx participate in the modulation of the time course of the photocurrent.

Mechanisms of Afterhyperpolarization in Lobster Olfactory Receptor Neurons

1998 ◽  
Vol 80 (3) ◽  
pp. 1268-1276 ◽  
Author(s):  
Frank S. Corotto ◽  
William C. Michel
Keyword(s):  
Voltage Clamp ◽  
Olfactory Receptor ◽  
Reversal Potential ◽  
Input Resistance ◽  
Olfactory Receptor Neurons ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Pipette Solution ◽  
Cation Current ◽  
Receptor Neurons

Corotto, Frank S. and William C. Michel. Mechanisms of afterhyperpolarization in lobster olfactory receptor neurons. J. Neurophysiol. 80: 1268–1276, 1998. In lobster olfactory receptor neurons (ORNs), depolarizing responses to odorants and current injection are accompanied by the development of an afterhyperpolarization (AHP) that likely contributes to spike-frequency adaptation and that persists for several seconds after termination of the response. A portion of the AHP can be blocked by extracellular application of 5 mM CsCl. At this concentration, CsCl specifically blocks the hyperpolarization-activated cation current ( I h) in lobster ORNs. This current is likely to be active at rest, where it provides a constant, depolarizing influence. Further depolarization deactivates I h, thus allowing the cell to be briefly hyperpolarized when that depolarizing influence is removed, thus generating an AHP. Reactivation of I h would terminate the AHP. The component of the AHP that could not be blocked by Cs+ (the Cs+-insensitive AHP) was accompanied by decreased input resistance, suggesting that this component is generated by increased conductance to an ion with an equilibrium potential more negative than the resting potential. The Cs+-insensitive AHP in current clamp and the underlying current in voltage clamp displayed a reversal potential of approximately –75 mV. Both E K and E Cl are predicted to be in this range. Similar results were obtained with the use of a high Cl– pipette solution, although that shifted E Cl from –72 mV to –13 mV. However, when E K was shifted to more positive or negative values, the reversal potential also shifted accordingly. A role for the Ca2+-mediated K+ current in generating the Cs+-independent AHP was explored by testing cells in current and voltage clamp while blocking I K(Ca) with Cs+/Co2+-saline. In some cells, the Cs+-independent AHP and its underlying current could be completely and reversibly blocked by Cs+/Co2+ saline, whereas in other cells some fraction of it remained. This indicates that the Cs+-independent AHP results from two K+ currents, one that requires an influx of extracellular Ca2+ and one that does not. Collectively, these findings indicate that AHPs result from three phenomena that occur when lobster ORNs are depolarized: 1) inactivation of the hyperpolarization-activated cation current, 2) activation of a Ca2+-mediated K+ current, and 3) activation of a K+ current that does not require influx of extracellular Ca2+. Roles of these processes in modulating the output of lobster ORNs are discussed.

scholarly journals Equilibrium Potential for the Postsynaptic Response in the Squid Giant Synapse

1974 ◽  
Vol 64 (5) ◽  
pp. 519-535 ◽  
Author(s):  
R. Llinás ◽  
R. W. Joyner ◽  
C. Nicholson
Keyword(s):  
Time Course ◽  
Reversal Potential ◽  
Input Resistance ◽  
Equilibrium Potential ◽  
Minimal Amount ◽  
Synaptic Potential ◽  
Synaptic Current ◽  
Isolated Segment ◽  
Squid Giant Synapse ◽  
Giant Synapse

The reversal potential for the EPSP in the squid giant synapse has been studied by means of an intracellular, double oil gap technique. This method allows the electrical isolation of a portion of the axon from the rest of the fiber and generates a quasi-isopotential segment. In order to make the input resistance of this nerve segment as constant as possible, the electroresponsive properties of the nerve membrane were blocked by intracellular injection of tetraethylammonium (TEA) and local extracellular application of tetrodotoxin (TTX). Thus, EPSP's could be evoked in the isolated segment with a minimal amount of electroresponsive properties. The reversal potential for the EPSP (EEPSP) was measured by recording the synaptic potential or the synaptic current during voltage clamping. The results indicate that EEPSP may vary from +15 to +25 mV, which is more positive than would be expected for a 1:1 conductance change for Na+ and K+ (approximately -15 mV) and too negative for a pure Na+ conductance (+40 mV). This latter value (ENa) was directly determined in the voltage clamp experiments. The results suggest that the synaptic potential is probably produced by a permeability change to Na+ to K+ in a 4:1 ratio. No change in time-course was observed in the synaptic current at clamp levels of -100 and +90 mV. The implications of a variable ratio for Na+-K+ permeability in subsynaptic-postsynaptic membranes are discussed.

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