Steady-state characteristics of the proton receptor in the somatic membrane of rat sensory neurons

AbstractSensory adaptation is the gradual decline in response as recorded from sensory neurons to a constant stimulus. Measuring adaptation involves counting the time-varying rate of action potentials generated by the sensory neuron. A typical adaptation curve will involve spontaneous activity prior to the introduction of the stimulus, a peak level of activity soon after the stimulus is presented, and a gradual fall to a new steady-state value. In this study, the steady-state activity is shown to be equal to the geometric mean of the spontaneous and peak activities. This remarkably simple equation holds across different sensory modalities and in different animal species. It is obeyed in both modern measurements of neural adaptation as well as the original recordings of Lord Adrian in his seminal work on the discovery of the all-or-nothing principle of nerves. It is likely a universal relationship governing the peripheral response of sensory neurons.

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Steady-State Properties of Coding of Odor Intensity in Olfactory Sensory Neurons

Lecture Notes in Computer Science - Advances in Brain, Vision, and Artificial Intelligence ◽

10.1007/978-3-540-75555-5_34 ◽

2007 ◽

pp. 360-367

Author(s):

Ondřej Pokora ◽

Petr Lansky

Keyword(s):

Steady State ◽

Sensory Neurons ◽

Odor Intensity ◽

Olfactory Sensory Neurons

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Augmented Sodium Currents Contribute to the Enhanced Excitability of Small Diameter Capsaicin-Sensitive Sensory Neurons Isolated From Nf1+/− Mice

Journal of Neurophysiology ◽

10.1152/jn.01010.2009 ◽

2010 ◽

Vol 103 (4) ◽

pp. 2085-2094 ◽

Cited By ~ 15

Author(s):

Yue Wang ◽

J.-H. Duan ◽

C. M. Hingtgen ◽

G. D. Nicol

Keyword(s):

Steady State ◽

Sensory Neurons ◽

Small Diameter ◽

Delayed Rectifier ◽

Heterozygous Mutation ◽

Wild Type ◽

Enhanced Production ◽

Steady State Inactivation ◽

Nf1 Gene ◽

Current Densities

Neurofibromin, the product of the Nf1 gene, is a guanosine triphosphatase activating protein (GAP) for p21ras (Ras) that accelerates conversion of active Ras-GTP to inactive Ras-GDP. Sensory neurons with reduced levels of neurofibromin likely have augmented Ras-GTP activity. We reported previously that sensory neurons isolated from a mouse model with a heterozygous mutation of the Nf1 gene ( Nf1+/−) exhibited greater excitability compared with wild-type mice. To determine the mechanism giving rise to the augmented excitability, differences in specific membrane currents were examined. Consistent with the enhanced excitability of Nf1+/− neurons, peak current densities of both tetrodotoxin-resistant sodium current (TTX-R INa) and TTX-sensitive (TTX-S) INa were significantly larger in Nf1+/− than in wild-type neurons. Although the voltages for half-maximal activation ( V0.5) were not different, there was a significant depolarizing shift in the V0.5 for steady-state inactivation of both TTX-R and TTX-S INa in Nf1+/− neurons. In addition, levels of persistent INa were significantly larger in Nf1+/− neurons. Neither delayed rectifier nor A-type potassium currents were altered in Nf1+/− neurons. These results demonstrate that enhanced production of action potentials in Nf1+/− neurons results, in part, from larger current densities and a depolarized voltage dependence of steady-state inactivation for INa that potentially leads to a greater availability of sodium channels at voltages near the firing threshold for the action potential.

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Comparative analysis of ionic currents in the somatic membrane of embryonic and newborn rat sensory neurons

Neuroscience ◽

10.1016/0306-4522(94)90040-x ◽

1994 ◽

Vol 58 (2) ◽

pp. 341-346 ◽

Cited By ~ 11

Author(s):

S.A. Fedulova ◽

P.G. Kostyuk ◽

N.S. Veselovsky

Keyword(s):

Comparative Analysis ◽

Sensory Neurons ◽

Ionic Currents ◽

Somatic Membrane ◽

Newborn Rat

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Prostaglandins Suppress an Outward Potassium Current in Embryonic Rat Sensory Neurons

Journal of Neurophysiology ◽

10.1152/jn.1997.77.1.167 ◽

1997 ◽

Vol 77 (1) ◽

pp. 167-176 ◽

Cited By ~ 100

Author(s):

G. D. Nicol ◽

M. R. Vasko ◽

A. R. Evans

Keyword(s):

Steady State ◽

Sensory Neurons ◽

Potassium Current ◽

Current Treatment ◽

Resting Membrane Potential ◽

Prostaglandin E ◽

Patch Clamp Recording ◽

Cellular Mechanisms ◽

Steady State Inactivation ◽

Outward Potassium Current

Nicol, G. D., M. R. Vasko, and A. R. Evans. Prostaglandins suppress an outward potassium current in embryonic rat sensory neurons. J. Neurophysiol. 77: 167–176, 1997. The cellular mechanisms giving rise to the enhanced excitability induced by prostaglandin E2 (PGE2) and carba prostacyclin (CPGI2) in embryonic rat sensory neurons were investigated using the whole cell patch-clamp recording technique. Exposing sensory neurons to 1 μM PGE2 produced a twofold increase in the number of action potentials elicited by a ramp of depolarizing current, but this eicosanoid had no effect on the resting membrane potential or the amplitude of the slow afterhyperpolarization. Characterization of the outward potassium currents in the embryonic sensory neurons indicated that the composition of the total current was variable among these neurons. A steady-state inactivation protocol was used to determine the extent of residual noninactivating current. A conditioning prepulse to +20 mV demonstrated that some of these neurons exhibited only a sustained potassium current with little steady-state inactivation whereas others exhibited some combination of a sustained as well as a rapidly inactivating I A-type current. Treatment with 1 μM PGE2 or 1 μM CPGI2, but not 1 μM prostaglandin F2α (PGF2α) produced a time-dependent suppression of the total potassium current. After a 20-min exposure, PGE2 and CPGI2 inhibited the maximal current obtained at +60 mV by 48 and 40%, respectively. The prostaglandin-induced suppression of the potassium current was not associated with a shift in the voltage dependence for activation. Subtraction of the currents remaining after PGE2 or CPGI2 treatment from their respective control recordings revealed that the prostaglandin-sensitive current had characteristics that were consistent with a sustained-type of potassium current. This idea is supported by the following observation. The steady-state inactivation protocol revealed that for prepulse voltages activating both rapidly inactivating and sustained currents, the relaxation of the current was accelerated after treatment with PGE2 or CPGI2 suggesting the removal of a slower component. This effect was not observed in neurons exhibiting only the sustained type current. These results suggest that pro-inflammatory prostaglandins enhance the excitability of rat sensory neurons, in part, through the suppression of an outward potassium current that may modulate the firing threshold for generation of the action potential.

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Modulation of a steady-state Ca2+-activated, K+ current in tail sensory neurons of Aplysia: role of serotonin and cAMP

Journal of Neurophysiology ◽

10.1152/jn.1989.61.1.32 ◽

1989 ◽

Vol 61 (1) ◽

pp. 32-44 ◽

Cited By ~ 32

Author(s):

J. P. Walsh ◽

J. H. Byrne

Keyword(s):

Steady State ◽

Sensory Neurons ◽

Outward Current ◽

Tetraethylammonium Chloride ◽

Cyclic Monophosphate ◽

Intracellular Injection ◽

Apparent Decrease ◽

K Current ◽

Ca2 Channels

1. The modulation of membrane currents by serotonin (5-HT) was studied in isolated clusters of tail sensory neurons. Serotonin was applied by micropressure ejection onto the somata of sensory neurons voltage-clamped at fixed holding potentials. The range of holding potentials tested in this study was selected to produce a steady-state Ca2+-activated K+ current (IK,Ca). Serotonin induced an inward shift in the holding current associated with a decrease in slope conductance. 2. Intracellular injection of adenosine 3',5'-cyclic monophosphate (cAMP) mimicked the response to 5-HT and induced an inward current associated with a decrease in slope conductance. The responses to 5-HT and cAMP had similar voltage dependencies and both responses were due to an apparent decrease in K+ current. Responses to cAMP were markedly reduced when generated at the peak of a response to 5-HT. The nonsummation of the maximal current responses indicated that 5-HT and cAMP utilize a common, saturable mechanism. 3. In contrast to the consistent decrease in steady-state K+ conductance elicited by cAMP, injection of guanosine 3',5'-cyclic monophosphate (cGMP) produced variable responses. In most cells, cGMP induced outward shifts in holding current that were associated with an increase in slope conductance. 4. Several lines of evidence indicated that IK,Ca contributed to the holding current at the level of membrane potentials that were examined. Inward shifts in holding current associated with a decrease in slope conductance were produced in the presence of agents that block Ca2+ channels, such as Co2+, Cd2+ or Ni2+ and by replacement of extracellular Ca2+ with Ba2+. Reducing the concentration of cytoplasmic Ca2+ through intracellular injection of EGTA had similar effects. Furthermore, inward shifts in holding current were produced by 5 mM tetraethylammonium chloride (TEA), which is known to block IK,Ca in neurons of Aplysia. This concentration of TEA also attenuated the outward current produced in response to direct intracellular injection of Ca2+. 5. Serotonin appears to modulate the IK,Ca that contributes to the steady-state holding current. The same manipulations that block the steady-state IK,Ca (see above) also attenuated the response to 5-HT. Furthermore, K+ currents activated by intracellular injection of Ca2+ were attenuated by 5-HT. 6. These results indicate that the changes in holding current produced by 5-HT are mediated, at least in part, by cAMP. In addition, it appears that 5-HT modulates a steady-state calcium-activated K+ current in addition to the previously described S-current (40, 58) and delayed K+ current (8, 9).(ABSTRACT TRUNCATED AT 250 WORDS)

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