Dual actions of caffeine on voltage-dependent currents and intracellular calcium in taste receptor cells

2002 ◽  
Vol 283 (1) ◽  
pp. R115-R129 ◽  
Author(s):  
Fang-Li Zhao ◽  
Shao-Gang Lu ◽  
Scott Herness
Keyword(s):  
Intracellular Calcium ◽  
Imaging Techniques ◽  
Sodium Current ◽  
Taste Receptor ◽  
Input Resistance ◽  
Ionic Currents ◽  
Receptor Cells ◽  
Voltage Dependent ◽  
Transduction Mechanisms ◽  
Taste Receptor Cells

Although the numerous stimuli representing the taste quality of bitterness are known to be transduced through multiple mechanisms, recent studies have suggested an unpredicted complexity of the transduction pathways for individual bitter stimuli. To investigate this notion more thoroughly, a single prototypic bitter stimulus, caffeine, was studied by using patch-clamp and ratiometric imaging techniques on dissociated rat taste receptor cells. At behaviorally relevant concentrations, caffeine produced strong inhibition of outwardly and inwardly rectifying potassium currents. Caffeine additionally inhibited calcium current, produced a weaker inhibition of sodium current, and was without effect on chloride current. Consistent with its effects on voltage-dependent currents, caffeine caused a broadening of the action potential and an increase of the input resistance. Caffeine was an effective stimulus for elevation of intracellular calcium. This elevation was concentration dependent, independent of extracellular calcium or ryanodine, and dependent on intracellular stores as evidenced by thapsigargin treatment. These dual actions on voltage-activated ionic currents and intracellular calcium levels suggest that a single taste stimulus, caffeine, utilizes multiple transduction mechanisms.

Development of voltage-dependent currents in taste receptor cells

1996 ◽  
Vol 365 (2) ◽  
pp. 278-288 ◽  
Author(s):  
Alan Mackay-Sim ◽  
Rona J. Delay ◽  
Stephen D. Roper ◽  
Sue C. Kinnamon
Keyword(s):  
Taste Receptor ◽  
Receptor Cells ◽  
Voltage Dependent ◽  
Taste Receptor Cells

scholarly journals Ionic currents in intimal cultured synoviocytes from the rabbit

2010 ◽  
Vol 299 (5) ◽  
pp. C1180-C1194 ◽  
Author(s):  
R. J. Large ◽  
M. A. Hollywood ◽  
G. P. Sergeant ◽  
K. D. Thornbury ◽  
S. Bourke ◽  
...  
Keyword(s):  
Ion Channels ◽  
Intracellular Calcium ◽  
Outward Current ◽  
Input Resistance ◽  
Ionic Currents ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Pipette Solution ◽  
Voltage Dependent ◽  
Fibroblast Like Synoviocytes

Hyaluronan, a joint lubricant and regulator of synovial fluid content, is secreted by fibroblast-like synoviocytes lining the joint cavity, and secretion is greatly stimulated by Ca2+-dependent protein kinase C. This study aimed to define synoviocyte membrane currents and channels that may influence synoviocyte Ca2+ dynamics. Resting membrane potential ranged from −30 mV to −66 mV (mean −45 ± 8.60 mV, n = 40). Input resistance ranged from 0.54 GΩ to 2.6 GΩ (mean 1.28 ± 0.57 GΩ; ν = 33). Cell capacitance averaged 97.97 ± 5.93 pF. Voltage clamp using Cs+ pipette solution yielded a transient inward current that disappeared in Ca2+-free solutions and was blocked by 1 μM nifedipine, indicating an L-type calcium current. The current was increased fourfold by the calcium channel activator FPL 64176 (300 nM). Using K+ pipette solution, depolarizing steps positive to −40 mV evoked an outward current that showed kinetics and voltage dependence of activation and inactivation typical of the delayed rectifier potassium current. This was blocked by the nonspecific delayed rectifier blocker 4-aminopyridine. The synoviocytes expressed mRNA for four Kv1 subtypes (Kv1.1, Kv1.4, Kv1.5, and Kv1.6). Correolide (1 μM), margatoxin (100 nM), and α-dendrotoxin block these Kv1 subtypes, and all of these drugs significantly reduced synoviocyte outward current. The current was blocked most effectively by 50 nM κ-dendrotoxin, which is specific for channels containing a Kv1.1 subunit, indicating that Kv1.1 is critical, either as a homomultimeric channel or as a component of a heteromultimeric Kv1 channel. When 50 nM κ-dendrotoxin was added to current-clamped synoviocytes, the cells depolarized by >20 mV and this was accompanied by an increase in intracellular calcium concentration. Similarly, depolarization of the cells with high external potassium solution caused an increase in intracellular calcium, and this effect was greatly reduced by 1 μM nifedipine. In conclusion, fibroblast-like synoviocytes cultured from the inner synovium of the rabbit exhibit voltage-dependent inward and outward currents, including Ca2+ currents. They thus express ion channels regulating membrane Ca2+ permeability and electrochemical gradient. Since Ca2+-dependent kinases are major regulators of synovial hyaluronan secretion, the synoviocyte ion channels are likely to be important in the regulation of hyaluronan secretion.

scholarly journals Estimation of the junctional resistance between electrically coupled receptor cells in Necturus taste buds.

1995 ◽  
Vol 106 (4) ◽  
pp. 705-725 ◽  
Author(s):  
A Bigiani ◽  
S D Roper
Keyword(s):  
Lucifer Yellow ◽  
Electrical Coupling ◽  
Taste Receptor ◽  
Input Resistance ◽  
Taste Buds ◽  
Dye Coupling ◽  
Receptor Cells ◽  
Taste Cells ◽  
Taste Receptor Cells ◽  
Junctional Resistance

Junctional resistance between coupled receptor cells in Necturus taste buds was estimated by modeling the results from single patch pipette voltage clamp studies on lingual slices. The membrane capacitance and input resistance of coupled taste receptor cells were measured to monitor electrical coupling and the results compared with those calculated by a simple model of electrically coupled taste cells. Coupled receptor cells were modeled by two identical receptor cells connected via a junctional resistance. On average, the junctional resistance was approximately 200-300 M omega. This was consistent with the electrophysiological recordings. A junctional resistance of 200-300 M omega is close to the threshold for Lucifer yellow dye-coupling detection (approximately 500 M omega). Therefore, the true extent of coupling in taste buds might be somewhat greater than that predicted from Lucifer yellow dye coupling. Due to the high input resistance of single taste receptor cells (> 1 G omega), a junctional resistance of 200-300 M omega assures a substantial electrical communication between coupled taste cells, suggesting that the electrical activity of coupled cells might be synchronized.

Serotonin Modulates Voltage-Dependent Calcium Current in Necturus Taste Cells

1997 ◽  
Vol 77 (5) ◽  
pp. 2515-2524 ◽  
Author(s):  
Rona J. Delay ◽  
Sue C. Kinnamon ◽  
Stephen D. Roper
Keyword(s):  
Calcium Current ◽  
Taste Receptor ◽  
Cell Voltage ◽  
Nerve Fibers ◽  
Receptor Subtype ◽  
Basal Cells ◽  
Receptor Cells ◽  
Taste Cells ◽  
Voltage Dependent ◽  
Taste Receptor Cells

Delay, Rona J., Sue C. Kinnamon, and Stephen D. Roper. Serotonin modulates voltage-dependent calcium current in Necturus taste cells. J. Neurophysiol. 77: 2515–2524, 1997. Necturus taste buds contain two primary cell types: taste receptor cells and basal cells. Merkel-like basal cells are a subset of basal cells that form chemical synapses with taste receptor cells and with innervating nerve fibers. Although Merkel-like basal cells cannot interact directly with taste stimuli, recent studies have shown that Merkel-like basal cells contain serotonin (5-HT), which may be released onto taste receptor cells in response to taste stimulation. With the use of whole cell voltage clamp, we examined whether focal applications of 5-HT to isolated taste receptor cells affected voltage-activated calcium current ( I Ca). Two different effects were observed. 5-HT at 100 μM increased I Ca in 33% of taste receptor cells, whereas it decreased I Ca in 67%. Both responses used a 5-HT receptor subtype with a pharmacological profile similar to that of the 5-HT1A receptor, but the potentiation and inhibition of I Ca by 5-HT were mediated by two different second-messenger cascades. The results indicate that functional subtypes of taste receptor cells, earlier defined only by their sensitivity to taste stimuli, may also be defined by their response to the neurotransmitter 5-HT and suggest that 5-HT released by Merkel-like basal cells could modulate taste receptor function.

Acid-induced responses in hamster chorda tympani and intracellular pH tracking by taste receptor cells

1998 ◽  
Vol 275 (1) ◽  
pp. C227-C238 ◽  
Author(s):  
Robert E. Stewart ◽  
Vijay Lyall ◽  
George M. Feldman ◽  
Gerard L. Heck ◽  
John A. DeSimone
Keyword(s):  
Voltage Clamp ◽  
Intracellular Ph ◽  
Imaging Techniques ◽  
Taste Receptor ◽  
Channel Blockers ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Linear Change ◽  
Receptor Cells ◽  
Taste Receptor Cells

HCl- and NaCl-induced hamster chorda tympani nerve responses were recorded during voltage clamp of the lingual receptive field. Voltage perturbations did not influence responses to HCl. In contrast, responses to NaCl were decreased by submucosal-positive and increased by submucosal-negative voltage clamp. Responses to HCl were insensitive to the Na+ channel blockers, amiloride and benzamil, and to methylisobutylamiloride (MIA), an Na+/H+exchange blocker. Responses to NaCl were unaffected by MIA but were suppressed by benzamil. Microfluorometric and imaging techniques were used to monitor the relationship between external pH (pHo) and the intracellular pH (pHi) of fungiform papilla taste receptor cells (TRCs) following 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein loading. TRC pHi responded rapidly and monotonically to changes in pHo. This response was unaffected by Na+ removal or the presence of amiloride, benzamil, or MIA. The neural records and the data from isolated TRCs suggest that the principal transduction pathway for acid taste in hamster is similar to that in rat. This may involve the monitoring of changes in TRC pHimediated through amiloride-insensitive H+ transport across TRC membranes. This is an example of cell monitoring of environmental pH through pH tracking, i.e., a linear change in pHi in response to a change in pHo, as has been proposed for carotid bodies. In taste, the H+transport sites may be concentrated on the basolateral membranes of TRCs and, therefore, are responsive to an attenuated H+ concentration from diffusion of acids across the tight junctions.

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