Interaction of anionic and cationic currents leads to a voltage dependence in the odor response of olfactory receptor neurons

1995 ◽  
Vol 73 (2) ◽  
pp. 562-567 ◽  
Author(s):  
S. Firestein ◽  
G. M. Shepherd
Keyword(s):  
Olfactory Receptor ◽  
Voltage Dependence ◽  
Reversal Potential ◽  
Outward Current ◽  
Olfactory Receptor Neurons ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Ambystoma Tigrinum ◽  
Induced Current ◽  
Receptor Neurons

1. We recorded odor-induced currents from isolated olfactory receptor neurons of the land phase tiger salamander (Ambystoma tigrinum) with the whole cell patch clamp. 2. In a subset of cells the current-voltage relation for the odor-induced current showed a strong rectification with, in some cells, a negative resistance slope between about -45 and -25 mV. In these cells there was little or no odor-induced current at -55 mV, the average resting potential of olfactory neurons. 3. Depolarizing the membrane to +20 mV revealed a large outward current, and on repolarizing the membrane to -55 mV we could observe a large inward current. This current was not observed in the absence of the depolarizing step or in the absence of odor stimuli. 4. This odor-induced tail current was dependent on extracellular Ca2+ and voltage, activating with increased depolarization. The reversal potential was sensitive to the chloride equilibrium potential and it could be significantly blocked by niflumic acid, a blocker of calcium-activated chloride currents. The voltage dependence could result from either the voltage-dependent block of adenosine 3',5'-cyclic monophosphate-gated cation channels known to be activated by odorants and permeable to Ca2+, or from an inherent voltage dependence in the chloride channel gating. 5. The current appears to function as a regenerative mechanism that might increase the amplitude and duration of the odor-induced current, especially to low concentrations of stimulus.

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.

Persistence of the olfactory receptor current in a wide variety of extracellular environments

1996 ◽  
Vol 75 (4) ◽  
pp. 1386-1391 ◽  
Author(s):  
S. J. Kleene ◽  
R. Y. Pun
Keyword(s):  
Olfactory Receptor ◽  
Rana Pipiens ◽  
Olfactory Receptor Neurons ◽  
Resting Potential ◽  
Induced Current ◽  
Olfactory Cilia ◽  
Inward Current ◽  
Cyclic Monophosphate ◽  
Cationic Current ◽  
Receptor Neurons

We measured the current activated by cytoplasmic adenosine 3':5'-cyclic monophosphate (cAMP) in olfactory cilia from the frog Rana pipiens. The odorant-induced current in frog olfactory receptor neurons was also measured for comparison. In both cases, recordings were performed near the neuronal resting potential in a variety of extracellular bath solutions. 2. In Ca(2+)-free baths, cAMP activated an inward current in excised olfactory cilia that was carried entirely by cations. As extracellular Ca2+ was increased, the cationic current decreased while a second current, carried by C1-, increased. Total cAMP-activated current decreased with increasing extracellular CA2+. When external Na+ but not Ca2+ was eliminated, only the C1- component of the current persisted. When external Na+ and Ca2+ were both removed, there was no cAMP-activated current. 3. In receptor neurons, the total odorant-induced receptor current varied in a similar way with the extracellular ionic environment. Under conditions favoring the anionic receptor current, the response amplitude decreased and the latency increased. 4. It is known that olfactory receptor currents persist in a wide variety of extracellular environments. This persistence can be sufficiently explained by the balance between cationic and anionic currents demonstrated here.

scholarly journals α2-Adrenergic autoreceptors in A5 and A6 neurons of neonate rats

1997 ◽  
Vol 273 (5) ◽  
pp. H2290-H2295 ◽  
Author(s):  
Donghai Huangfu ◽  
Patrice G. Guyenet
Keyword(s):  
Adrenergic Receptors ◽  
Reversal Potential ◽  
Outward Current ◽  
Locus Ceruleus ◽  
Equilibrium Potential ◽  
Induced Current ◽  
Noradrenergic Neurons ◽  
Membrane Oscillations ◽  
Inwardly Rectifying ◽  
Whole Cell Recordings

A5 noradrenergic neurons control sympathetic outflow, nociception, and respiration. The presence of α2-adrenergic receptors (α2-ARs) in A5 cells has been suggested by immunohistochemistry. In the present experiments, we analyze the response of spinally projecting A5 cells to α2-AR agonists, and we compare it with that of locus ceruleus (A6) neurons. Whole cell recordings were obtained from 52 spinally projecting neurons in the ventrolateral pons of neonate rats. Immunohistochemistry showed that 60% of the recorded cells were A5 cells. In A5 cells clamped at −55 mV, norepinephrine (NE) in the presence of the α1-AR antagonist prazosin produced a Ba2+-sensitive outward current (20.4 ± 2.6 pA; n = 28). The α2-AR-induced current reversed at the K+ equilibrium potential ( E K) at three different extracellular K+ concentrations. Replacement of 82% of the extracellular Na concentration with N-methyl-d-glucamine did not change the reversal potential. The 19 presumably noncatecholaminergic neurons responded weakly or not at all to NE (2.5 ± 0.6 pA outward current). Pontospinal A6 neurons ( n = 11) were also recorded. Six A6 cells displayed large tetrodotoxin (TTX)-resistant membrane oscillations. In these cells, the current induced by α2-AR stimulation did not reverse over the voltages tested (−50 to −130 mV) or reversed at potentials more negative than E K (less than −114 mV). In A6 neurons that did not display large oscillations ( n = 5), the α2-AR-induced current reversed at or close to the E K (−90 ± 1.6 mV). In conclusion, A5 cells, like locus ceruleus neurons, have α2-ARs that may function as autoreceptors. In both cases, α2-AR activation increases an inwardly rectifying K+conductance. In A5 cells, we found no evidence that α2-AR activation decreases a resting Na+ conductance. The inhibition of A5 cells by clonidine and other agents with α2-AR agonist activity is likely to contribute to the ability of these drugs to decrease sympathetic tone and arterial pressure.

Odor-induced currents in Xenopus olfactory receptor cells measured with perforated-patch recording

1995 ◽  
Vol 74 (1) ◽  
pp. 479-483 ◽  
Author(s):  
A. B. Zhainazarov ◽  
B. W. Ache
Keyword(s):  
Olfactory Receptor ◽  
Reversal Potential ◽  
Olfactory Receptor Neurons ◽  
Whole Cell ◽  
Time To Peak ◽  
Olfactory Receptor Cells ◽  
Whole Cell Recording ◽  
Cell Recording ◽  
Receptor Neurons ◽  
Induced Currents

1. Odor-evoked currents were recorded in Xenopus laevis olfactory receptor neurons (ORNs) by the use of conventional, as well as nystatin and gramicidin-perforated, whole cell recording. The odor-evoked current ran down quickly in conventional, but not in perforated, whole cell recording. All three types of recording gave similar values for the amplitude, latency, time-to-peak, recovery time, and reversal potential of the odor-evoked current. 2. A secondary Cl current comprised a significant part of the odor-evoked current (55-65%). ECl measured by gramicidin perforation, which does not alter [Cl-]i, was -2.3 +/- 5.0 (SE) mV, indicating that these neurons maintain a high [Cl-]i and that the secondary Cl current plays an excitatory role in olfactory transduction.

Pharmacology of a Slowly Inactivating Outward Current in Hippocampal CA3 Pyramidal Neurons

2006 ◽  
Vol 96 (3) ◽  
pp. 1116-1123 ◽  
Author(s):  
Riccardo Bianchi ◽  
Shih-Chieh Chuang ◽  
Robert K. S. Wong
Keyword(s):  
Time Course ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Reversal Potential ◽  
Outward Current ◽  
Pyramidal Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Transient Outward Current ◽  
Activation Threshold

The pharmacology of a slowly inactivating outward current was examined using whole cell patch-clamp recordings in CA3 pyramidal cells of guinea pig hippocampal slices. The current had a low activation threshold (about −60 mV) and inactivated slowly (time constant of 3.4 ± 0.5 s at −50 mV) and completely at membrane voltages depolarized to −50 mV. The slowly inactivating outward current was mainly mediated by K+ with a reversal potential close to the equilibrium potential for K+. The slowly inactivating outward current had distinct pharmacological properties: its time course was not affected by extracellular Cs+ (1 mM) or 4-AP (1–5 mM)—broad spectrum inhibitors of K+ currents and of inactivating K+ currents, respectively. The presence of extracellular Mn2+ (0.5–1 mM), which suppresses several Ca2+-dependent K+ currents, also did not affect the slowly inactivating outward current. The current was partially suppressed by TEA (50 mM) and was blocked by intracellular Cs+ (134 mM). In addition, intracellular QX-314 (5 mM), a local anesthetic derivative, inhibited this current. The slowly inactivating outward current with its low activation threshold should be operational at the resting potential. Our results suggest that the transient outward current activated at subthreshold membrane potentials in hippocampal pyramidal cells consists of at least three components. In addition to the well-described A- and D-currents, the slowest decaying component reflects the time course of a distinct current, suppressible by QX-314.

Isoproterenol activates a chloride current, not the transient outward current, in rabbit ventricular myocytes

1989 ◽  
Vol 257 (6) ◽  
pp. C1177-C1181 ◽  
Author(s):  
R. D. Harvey ◽  
J. R. Hume
Keyword(s):  
Ventricular Myocytes ◽  
Reversal Potential ◽  
Outward Current ◽  
Chloride Current ◽  
Equilibrium Potential ◽  
K Channel ◽  
Transient Outward Current ◽  
Induced Current ◽  
Adrenergic Stimulation ◽  
Rabbit Ventricular Myocytes

The effects of beta-adrenergic stimulation on the Ca2(+)-insensitive transient outward current (Ito) in rabbit ventricular myocytes were examined. Exposure to isoproterenol (ISO; 1 microM) activated a time-dependent current at positive membrane potentials. To determine whether this ISO-induced current was associated with Ito, sensitivity to the K+ channel antagonist, 3,4-diaminopyridine (DAP; 200 microM) was compared before and after exposure to ISO. The DAP-sensitive current was not enhanced by ISO, suggesting that the ISO-induced current was not a component of Ito. Ito and the ISO-induced current could also be dissociated by changing the membrane holding potential. Positive holding potentials, which produced significant inactivation of Ito, had little effect on the ISO-induced membrane current. Furthermore, the ISO-induced current could be observed when K+ was replaced by Cs+. The reversal potential of the ISO-induced current agreed with the predicted Cl- equilibrium potential, and exposure to Cl(-)-free extracellular solutions eliminated the response to ISO. Therefore, we conclude that ISO does not directly activate Ito in rabbit ventricular myocytes, but instead, activates a time-independent chloride current (ICl) similar to that recently described in guinea pig ventricular myocytes and shown to be regulated by adenylate cyclase (R. D. Harvey and J. R. Hume. Science Wash. DC 244: 983-985, 1989).

scholarly journals Electrogenic Na+/Ca2+ Exchange

2000 ◽  
Vol 115 (6) ◽  
pp. 759-768 ◽  
Author(s):  
Jonathan P. Danaceau ◽  
Mary T. Lucero
Keyword(s):  
Olfactory Receptor ◽  
Monovalent Cation ◽  
Olfactory Receptor Neurons ◽  
Induced Response ◽  
Current Response ◽  
Induced Current ◽  
Inward Current ◽  
Cation Current ◽  
Receptor Neurons ◽  
Lolliguncula Brevis

Olfactory receptor neurons (ORNs) from the squid, Lolliguncula brevis, respond to the odors l-glutamate or dopamine with increases in internal Ca2+ concentrations ([Ca2+]i). To directly asses the effects of increasing [Ca2+]i in perforated-patched squid ORNs, we applied 10 mM caffeine to release Ca2+ from internal stores. We observed an inward current response to caffeine. Monovalent cation replacement of Na+ from the external bath solution completely and selectively inhibited the caffeine-induced response, and ruled out the possibility of a Ca2+-dependent nonselective cation current. The strict dependence on internal Ca2+ and external Na+ indicated that the inward current was due to an electrogenic Na+/Ca2+ exchanger. Block of the caffeine-induced current by an inhibitor of Na+/Ca2+ exchange (50–100 μM 2′,4′-dichlorobenzamil) and reversibility of the exchanger current, further confirmed its presence. We tested whether Na+/Ca2+ exchange contributed to odor responses by applying the aquatic odor l-glutamate in the presence and absence of 2′,4′-dichlorobenzamil. We found that electrogenic Na+/Ca2+ exchange was responsible for ∼26% of the total current associated with glutamate-induced odor responses. Although Na+/Ca2+ exchangers are known to be present in ORNs from numerous species, this is the first work to demonstrate amplifying contributions of the exchanger current to odor transduction.

Intracellular-messenger-mediated cation channels in cultured olfactory receptor neurons

1993 ◽  
Vol 178 (1) ◽  
pp. 125-147 ◽  
Author(s):  
M. Stengl
Keyword(s):  
Olfactory Receptor ◽  
Olfactory Receptor Neurons ◽  
Resting Potential ◽  
Cation Channels ◽  
Inward Rectification ◽  
Kinase C ◽  
Inward Currents ◽  
Receptor Neurons ◽  
Species Specific ◽  
Gamma S

After 2–3 weeks in culture, pupal olfactory receptor neurons from the antennae of male Manduca sexta respond to their species-specific sex pheromone by opening cation channels. These pheromone-dependent cation channels are the only channels previously found in cultured olfactory neurons that promote inward currents at membrane potentials more negative than the resting potential. The pheromone-dependent currents depend on external Ca2+ concentration. They are inwardly rectified with 10(−7) mol l-1 external Ca2+ and linear with 6 mmol l-1 external Ca2+. This paper shows that perfusion of cultured olfactory receptor neurons with GTP gamma S, ATP, inositol 1,4,5-trisphosphate or 10(−6) mol l-1 Ca2+ elicits cation currents resembling the pheromone-dependent cation currents in expressing inward rectification with 10(−7) mol l-1 external Ca2+ and being linear at external Ca2+ concentrations of 2 mumol l-1 or more. Stimulation with protein kinase C also elicits cation currents that share properties with the pheromone-dependent cation currents. All agent-induced cation currents appear to depend either directly or indirectly on Ca2+ concentration.

Dopamine Modulates Inwardly Rectifying Hyperpolarization-Activated Current (I h) in Cultured Rat Olfactory Receptor Neurons

1999 ◽  
Vol 81 (1) ◽  
pp. 149-158 ◽  
Author(s):  
Gricelly Vargas ◽  
Mary T. Lucero
Keyword(s):  
Olfactory Receptor ◽  
Voltage Dependence ◽  
Olfactory Receptor Neurons ◽  
Activation Curve ◽  
Receptor Neurons ◽  
Hyperpolarization Activated Current ◽  
Inwardly Rectifying ◽  
Adenylyl Cyclase Inhibitor ◽  
Hyperpolarizing Shift ◽  
Selective Dopamine

Vargas, Gricelly and Mary T. Lucero. Dopamine modulates inwardly rectifying hyperpolarization-activated current ( I h) in cultured rat olfactory receptor neurons. J. Neurophysiol. 81: 149–158, 1999. The presence of dopamine receptors in olfactory receptor neurons (ORNs) suggests that odor sensitivity may be modulated by neurotransmitters at the level of primary sensory neurons. Using standard patch-clamp techniques on rat ORNs, we found that 1 μM dopamine, 500 μM SQ 22536 (SQ, an adenylyl cyclase inhibitor), 20 and 50 μM quinpirole (a selective dopamine D2 receptor agonist), and 1 mM adenosine 3′,5′-cyclic monophosphate (cAMP) modulate the hyperpolarization-activated current I h. On hyperpolarizing from a holding potential of −58 mV, a small Cs+-sensitive inwardly rectifying current ( I h) was observed. Increases in extracellular K+ increased I h amplitude without shifting its voltage dependence of activation, whereas increases in temperature produced an increase in I h amplitude and a hyperpolarizing shift in the activation curve. Application of 1 μM dopamine reversibly shifted I h activation to more negative potentials and decreased I h current amplitudes. These effects were blocked by concomitant application of dopamine with sulpiride, a selective dopamine D2 receptor antagonist. The effects of dopamine were mimicked by quinpirole. Quinpirole (20 μM) decreased I h current amplitude, but was without effect on I h voltage dependence of activation. However, 50 μM quinpirole produced both a reduction of I h peak currents and a hyperpolarizing shift in the activation curve for I h. External application of the adenylyl cyclase inhibitor SQ 22536 produced a reversible decrease in peak currents but had no effect on I h voltage dependence of activation, whereas internal application of cAMP shifted I h activation to more depolarized potentials. Because I h modulates cell excitability and spike frequency adaptation, our findings support a role for dopamine in modulating the sensitivity and output of rat ORNs to odorants.

A hyperpolarization-activated cation conductance in lobster olfactory receptor neurons

1994 ◽  
Vol 72 (1) ◽  
pp. 360-365 ◽  
Author(s):  
F. S. Corotto ◽  
W. C. Michel
Keyword(s):  
Olfactory Receptor ◽  
Reversal Potential ◽  
Input Resistance ◽  
Olfactory Receptor Neurons ◽  
Slow Inward Current ◽  
Inward Rectification ◽  
Current Clamp ◽  
Inward Current ◽  
Cation Conductance ◽  
Receptor Neurons

1. The current underlying inward rectification in lobster olfactory receptor neurons was investigated with the use of whole-cell patch-clamp techniques. Inward rectification could most likely result from an inwardly rectifying potassium conductance or a hyperpolarization-activated cation conductance. To distinguish between these possibilities, the current underlying inward rectification was examined with respect to its sensitivity to extracellular Cs+ and Ba2+, time course of activation, and reversal potential. 2. In current clamp, injection of negative current led to a hyperpolarization followed by a partial return (sag) toward the initial holding potential. The rate and magnitude of the sag depended on the magnitude of the hyperpolarizing current with larger currents leading to larger, faster depolarizing sags. In voltage clamp, hyperpolarizing steps elicited a slowly activating, noninactivating inward current clamp. Both the sag and the slow inward current were blocked reversibly by extracellular application of 5 mM CsCl but were unaffected by 2 mM BaCl2. 3. The rate of inward current activation was best approximated by a single exponential function with time constants that were voltage dependent, ranging from 7.8 s at-69 mV to 248 ms at-114 mV. 4. Cells normally exhibited an average input resistance of 0.99 G omega over the range of-69 to-114 mV. With the hyperpolarization-activated inward current blocked by 5 mM CsCl, the average input resistance increased to 2.12 G omega over the same range. 5. Analysis of tail currents revealed that the average predicted reversal potential of the hyperpolarization-activated inward current was 1.7 mV and was not affected significantly by a shift in ECl.(ABSTRACT TRUNCATED AT 400 WORDS)

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