The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
Nuhan Purali - One of the best experts on this subject based on the ideXlab platform.
-
Antidromic potential spread modulates the Receptor responses in the Stretch Receptor neurons of the crayfish
Pflügers Archiv - European Journal of Physiology, 2011Co-Authors: Nuhan PuraliAbstract:The effects of antidromic potential spread were investigated in the Stretch Receptor neurons of the crayfish. Current and potential responses to conductance changes were recorded in the dynamic clamp condition and compared to those obtained by using some conventional clamp methods and a compartmental neuron model. An analogue circuit was used for dynamic calculation of the injected Receptor current as a function of the membrane potential and the given conductance change. Alternatively, Receptor current responses to a mechanical stimulus were recorded and compared when the cell was voltage clamped to a previously recorded impulse wave form and the resting potential, respectively. Under dynamic clamp, the Receptor current had an oscillating waveform which contrasts with the conventional recordings. Frequency, amplitude and sign of the oscillations were dependent on the applied conductance level, reversal potential and electrotonic attenuation. Mean current amplitude and frequency of the evoked impulse responses were smaller under dynamic clamp, especially for large conductance increases. However, firing frequency was larger if plotted against the mean current response. Recorded responses were similar to those calculated in the model. It was not possible to evoke any adaptation in the slowly adapting neuron by using the dynamic clamp. Evoked potential change served as a self limiting response, preventing the depolarization block. However, impulse duration was significantly shorter in the rapidly adapting neuron when the dynamic clamp was used. It was concluded that, in the Stretch Receptor neurons during a conductance increase, antidromic potential spread modulates the Receptor responses and contributes to adaptation.
-
structure and function relationship in the abdominal Stretch Receptor organs of the crayfish
The Journal of Comparative Neurology, 2005Co-Authors: Nuhan PuraliAbstract:The structure/function relationship in the rapidly and slowly adapting Stretch Receptor organs of the crayfish (Astacus leptodactylus) was investigated using confocal microscopy and neuronal modeling methods. Both Receptor muscles were single muscle fibers with structural properties closely related to the function of the Receptors. Dendrites of the rapidly adapting neuron terminated in a common pile of nerve endings going in all directions. Dendrites of the slowly adapting neuron terminated in a characteristic T shape in multiple regions of the Receptor muscle. The slowly adapting main dendrite, which was on average 2.1 times longer and 21% thinner than the rapidly adapting main dendrite, induced larger voltage attenuation. The somal surface area of the slowly adapting neuron was on average 51% larger than that of the rapidly adapting neuron. Variation in the neuronal geometry was greatest among the slowly adapting neurons. A computational model of a neuron pair demonstrated that the rapidly and the slowly adapting neurons attenuated the dendritic Receptor potential like low-pass filters with cut-off frequencies at 100 and 20 Hz, respectively. Recurrent dendrites were observed mostly in the slowly adapting neurons. Voltage signals were calculated to be propagated 23% faster in the rapidly adapting axon, which is 51% thicker than the slowly adapting axon. The present findings support the idea that the morphology of the rapidly and the slowly adapting neurons evolved to optimally sense the dynamic and the static features of the mechanical stimulus, respectively. J. Comp. Neurol. 488:369–383, 2005. © 2005 Wiley-Liss, Inc.
-
Action Potential and Sodium Current in the Slowly and Rapidly Adapting Stretch Receptor Neurons of the Crayfish (Astacus astacus)
Journal of neurophysiology, 1998Co-Authors: Nuhan Purali, B. RydqvistAbstract:Purali, Nuhan and Bo Rydqvist. Action potential and sodium current in the slowly and rapidly adapting Stretch Receptor neurons of the crayfish (Astacus astacus). J. Neurophysiol. 80: 2121–2132, 199...
-
transducer properties of the rapidly adapting Stretch Receptor neurone in the crayfish pacifastacus leniusculus
The Journal of Physiology, 1993Co-Authors: B. Rydqvist, Nuhan PuraliAbstract:1. The transducer properties of the rapidly adapting Stretch Receptor neurone of the crayfish (Pacifastacus leniusculus) were studied using a two-microelectrode voltage clamp technique. 2. The impulse response to ramp-and-hold extensions of the Receptor muscle typically consisted of a high frequency burst followed by cessation of impulses within a relatively short time depending on the amplitude of extension. The type of adaptation was consistent with earlier studies. The stimulus-response relationship for the impulse frequency was non-linear and had a slope in a log-log plot of 2.9. 3. When impulse generation was blocked by tetrodotoxin (TTX), (block of Na+ channels) the Receptor potential was extension dependent and similar to that found in the slowly adapting Receptor. For small extensions there was an initial peak followed by a fall to a steady potential level. For large extensions the potential response during the ramp phase consisted of a peak followed by a constant potential level lasting to the end of the ramp. When the extension changed to the hold phase the potential fell towards a steady state. The relation between extension and amplitude of Receptor potential was non-linear and saturated at -40 to -30 mV (extensions > 15% of zero length, lo). 4. When potassium channels were blocked by TEA (50 mM) and 4-aminopyridine (4-AP, 5 mM) (and Na+ channels blocked by TTX) the shape of the generator potential become less complex with an increased amplitude for large extensions. 5. When the Receptor neurone was voltage clamped at the resting potential, extension of the Receptor muscle produced an inwardly directed Receptor current, the Stretch-induced current (SIC). The response consisted of a fast transient phase which decayed towards a steady state. The SIC peak amplitude was dependent on extension in a sigmoidal fashion and saturated at 190 nA (extensions > 25% of lo). The slope of the steepest part of the stimulus-response relation (between 10 and 20% extension) was 4.7 +/- 0.25 (mean +/- S.E.M.) in a log-log plot. 6. The peak amplitude of the SIC increased with increasing extension speed (ramp steepness), the relation between the slope of the ramp and current amplitude being a first order (hyperbolic) function. The amplitude of the Receptor current was voltage dependent and had a reversal potential of +16.2 +/- 1.8 mV (mean +/- S.E.M., 32 cells). From the reversal potential the permeability ratio, PNa/PK, of the transducer permeability system was calculated to be 1.5. The I-V curve of SIC was non-linear.(ABSTRACT TRUNCATED AT 400 WORDS)
-
block of potassium outward currents in the crayfish Stretch Receptor neurons by 4 aminopyridine tetraethylammonium chloride and some other chemical substances
Acta Physiologica Scandinavica, 1992Co-Authors: Nuhan Purali, B. RydqvistAbstract:The effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA) on the outward potassium currents in the rapidly and slowly adapting Stretch Receptor neurons (SRNs) of the crayfish (Pacifastacus leniusculus) were studied using a two micro-electrode voltage-clamp technique. The leakage current was not affected by either 4-AP or TEA. External 4-AP blocked the peak outward current in a dose-dependent manner (1:1 stoichiometry) with an apparent dissociation constant (Kd) of 2.3 +/- 0.2 mM (mean +/- SEM) in the slowly and 1.4 +/- 0.2 mM in the rapidly adapting SRN, the block being voltage dependent. External application of TEA resulted in a block of the steady state current enhancing the transient characteristics of the current response. The block appeared to deviate from a 1:1 stoichiometry and the apparent Kd for TEA was 9.6 +/- 3.4 mM with a cooperativity factor n = 0.43 +/- 0.03 in the slowly adapting SRN and 34.5 +/- 9.2 mM and 0.37 +/- 0.03 respectively in the rapidly adapting SRN. Low Ca2+, apamin and charybdotoxin, which are known to block Ca(2+)-dependent K-currents, had no effects on the outward current as was also the case with catechol. It is concluded that the different effects of TEA and 4-AP on the outward current in the two types of SRNs can be explained by the presence of at least two, probably heteromultimeric, channel populations having similar sensitivity to 4-AP but different sensitivity to TEA. One channel has a high affinity (Kd = 0.8-1.6 mM) for TEA and the other a low affinity (Kd = 173-213 mM) for TEA. The low-affinity channel seems to dominate in the slowly adapting SRN while both channels are equally common in the rapidly adapting SRN. Further, the present results do not support the existence of a macroscopic Ca(2+)-dependent K+ current in the SRNs.
B. Rydqvist - One of the best experts on this subject based on the ideXlab platform.
-
mechanotransduction and the crayfish Stretch Receptor
Physiology & Behavior, 2007Co-Authors: B. Rydqvist, Jiahui Lin, Peter Sand, C SwerupAbstract:Mechanotransduction or mechanosensitivity is found in almost every cell in all organisms from bacteria to vertebrates. Mechanosensitivity covers a wide spectrum of functions from osmosensing, cell attachment, classical sensory mechanisms like tactile senses in the skin, detection of sound in hair cells of the hearing apparatus, proprioceptive functions like recording of muscle length and tension in the muscle spindle and tendon organ, respectively, and pressure detection in the circulation etc. Since most development regarding the molecular aspects of the mechanosensitive channel has been made in nonsensory systems it is important to focus on mechanosensitivity of sensory organs where the functional importance is undisputed. The Stretch Receptor organ of the crustaceans is a suitable preparation for such studies. The Receptor organ is experimentally accessible to mechanical manipulation and electrophysiological recordings from the sensory neuron using intracellular microelectrode or patch clamp techniques. It is also relatively easy to inject substances into the neuron, which also makes the neuron accessible to measurements with fluorescent techniques. The aim of the present paper is to give an up to date summary of observations made on the transducer properties of the crayfish Stretch Receptor (Astacus astacus and Pacifastacus leniusculus) including some recent unpublished findings. Finally some aspects on future line of research will be presented.
-
the mechanotransduction of the crayfish Stretch Receptor neurone can be differentially activated or inactivated by local anaesthetics
Acta Physiologica Scandinavica, 1999Co-Authors: Jiahui Lin, B. RydqvistAbstract:The effect of the local anaesthetics lidocaine, its meta-isomer, LL33, bupivacaine, tetracaine and procaine on the transducer properties of the Stretch Receptor neurone of the crayfish Pacifastacus leniusculus was investigated using a two microelectrode voltage clamp. Lidocaine increased the Receptor current whereas LL33, bupivacaine and tetracaine reduced the Receptor current in a reversible dose-dependent way. Procaine did not affect the Receptor responses. The onset of the effect was generally slow in the order of minutes. Lidocaine increased the conductance of the mechanotransducer 50 +/- 7% (mean +/- SD, n = 4) and changed the reversal potential -8 +/- 1 mV (mean +/- SEM, n = 8), which indicates a major K+ conductance increase through the mechanosensitive channels. The other local anaesthetics increase the K+ conductance of the mechanotransducer without increasing the total conductance, which suggests that only P(Na)/P(K) is changed. These substances seem to have a Ca2+ dependent effect on the gating properties of the mechanosensitive channels in addition to their effect on the permeability through the channels as compared with lidocaine. All local anaesthetics investigated decreased the leak conductance of the Receptor neurone. The effects of local anaesthetics on the mechanosensitive channels whether activating or blocking is correlated to the oil:water distribution coefficients and their relative hydrophobicity/hydrophilicity ratio. The results are consistent with the hypothesis that the local anaesthetic effect is mediated by changes in the lipid phase of the membrane.
-
Action Potential and Sodium Current in the Slowly and Rapidly Adapting Stretch Receptor Neurons of the Crayfish (Astacus astacus)
Journal of neurophysiology, 1998Co-Authors: Nuhan Purali, B. RydqvistAbstract:Purali, Nuhan and Bo Rydqvist. Action potential and sodium current in the slowly and rapidly adapting Stretch Receptor neurons of the crayfish (Astacus astacus). J. Neurophysiol. 80: 2121–2132, 199...
-
a mathematical model of the crustacean Stretch Receptor neuron biomechanics of the Receptor muscle mechanosensitive ion channels and macrotransducer properties
Journal of Neurophysiology, 1996Co-Authors: C Swerup, B. RydqvistAbstract:1. A mathematical model of the primary transduction process in a mechanoReceptor, the slowly adapting Stretch Receptor organ of the crayfish, has been developed taking into account the viscoelastic properties of the accessory structures of the Receptor, i.e., the Receptor muscle, the biophysical properties of the mechanosensitive channels (MSCs) and the passive electrical properties of the neuronal membrane (leak conductance and capacitative properties). The work is part of an effort to identify and characterize the mechanical and ionic mechanisms in a complex mechanoReceptor. The parameters of the model are based mainly on results of our own experiments and to some extent on results from other studies. The performance of the model has been compared with the performance of the slowly adapting Receptor. 2. The model resulted in nonlinear differential equations that were solved by an iterative, fourth order Range-Kutta method. For the calculations of potential, the cell was treated as an idealized spherical body. The extension of the Receptor muscle was 0-30%, which is within the physiological limits for this Receptor. 3. The mechanical properties of the Receptor muscle were modeled by a simple Voigt element (a spring in parallel with a dashpot) in series with a nonlinear spring. This element can describe resonably well the tension development in the Receptor muscle at least for large extensions (> 12%). However, for small extensions (< 12%), the muscle seems to be more stiff than for large extensions. 4. The Receptor current at different extensions of the Receptor was computed using typical viscoelastic parameters for a Receptor muscle together with a transformation of muscle tension to tension in the neuronal dendrites and finally the properties of the mechanosensitive channels. The model fit was satisfactory in the high extension range whereas in the low extension range the deviation from the experimental results could be explained partly by insufficient modeling of the nonlinear viscoelastic properties. The voltage dependence of the Receptor current was also well predicted by the model. 5. If the parameters of the viscoelastic model were adjusted for each extension so that each tension response closely resembled the experimental values, the fit of the current responses was improved but still deviated from the experimental currents. One factor that might explain the difference is the possibility that the MSCs in the Stretch Receptor neuron might have intrinsic adaptive properties. Introducing an exponential adaptive behavior of individual MSCs increased the ability of the model to predict the Receptor current. 6. The Receptor potential was calculated by modeling the neuronal membrane by a lumped leak conductance and capacitance The calculated Receptor potential was higher than the experimental Receptor potential. However, the fit of the Receptor potential was improved substantially by introducing an adaptation of the MSCs as outlined in the preceding paragraph. the remaining discrepancy might be explained by insufficient blocking of K+ channels in the experiment. 7. The model can predict a wide range of experimental data from the slowly adapting Stretch Receptor neuron including the mechanical response of the Receptor muscle, the Receptor current and its voltage dependence, and the Receptor potential. It also describes accurately the passive electrical properties of the neuronal membrane.
-
transducer properties of the rapidly adapting Stretch Receptor neurone in the crayfish pacifastacus leniusculus
The Journal of Physiology, 1993Co-Authors: B. Rydqvist, Nuhan PuraliAbstract:1. The transducer properties of the rapidly adapting Stretch Receptor neurone of the crayfish (Pacifastacus leniusculus) were studied using a two-microelectrode voltage clamp technique. 2. The impulse response to ramp-and-hold extensions of the Receptor muscle typically consisted of a high frequency burst followed by cessation of impulses within a relatively short time depending on the amplitude of extension. The type of adaptation was consistent with earlier studies. The stimulus-response relationship for the impulse frequency was non-linear and had a slope in a log-log plot of 2.9. 3. When impulse generation was blocked by tetrodotoxin (TTX), (block of Na+ channels) the Receptor potential was extension dependent and similar to that found in the slowly adapting Receptor. For small extensions there was an initial peak followed by a fall to a steady potential level. For large extensions the potential response during the ramp phase consisted of a peak followed by a constant potential level lasting to the end of the ramp. When the extension changed to the hold phase the potential fell towards a steady state. The relation between extension and amplitude of Receptor potential was non-linear and saturated at -40 to -30 mV (extensions > 15% of zero length, lo). 4. When potassium channels were blocked by TEA (50 mM) and 4-aminopyridine (4-AP, 5 mM) (and Na+ channels blocked by TTX) the shape of the generator potential become less complex with an increased amplitude for large extensions. 5. When the Receptor neurone was voltage clamped at the resting potential, extension of the Receptor muscle produced an inwardly directed Receptor current, the Stretch-induced current (SIC). The response consisted of a fast transient phase which decayed towards a steady state. The SIC peak amplitude was dependent on extension in a sigmoidal fashion and saturated at 190 nA (extensions > 25% of lo). The slope of the steepest part of the stimulus-response relation (between 10 and 20% extension) was 4.7 +/- 0.25 (mean +/- S.E.M.) in a log-log plot. 6. The peak amplitude of the SIC increased with increasing extension speed (ramp steepness), the relation between the slope of the ramp and current amplitude being a first order (hyperbolic) function. The amplitude of the Receptor current was voltage dependent and had a reversal potential of +16.2 +/- 1.8 mV (mean +/- S.E.M., 32 cells). From the reversal potential the permeability ratio, PNa/PK, of the transducer permeability system was calculated to be 1.5. The I-V curve of SIC was non-linear.(ABSTRACT TRUNCATED AT 400 WORDS)
Shigeji Matsumoto - One of the best experts on this subject based on the ideXlab platform.
-
flecainide inhibits the stimulatory effect of veratridine on the response of airway mechanoReceptors to maintained inflations in rats
Life Sciences, 2010Co-Authors: Shigeji Matsumoto, Chikako Saiki, Masayuki Takahashi, Kohsuke Iwasaki, Ryoji Ide, Mamoru TakedaAbstract:Abstract Aims The purpose of the present study was to investigate (a) whether maintained inflations result in the inhibition of slowly adapting pulmonary Stretch Receptor (SAR) discharge to elicit an abrupt change in Receptor activity and (b) whether pretreatment with veratridine, a Na+ channel opener, and/or flecainide, a Na+ channel blocker, alters the responses of SAR properties to maintained inflations. Main methods We measured the properties of SAR activity during maintained inflations at different pressures in 31 anesthetized, artificially ventilated rats with unilateral vagotomy. Key findings During maintained inflations (approximately 5, 10 and 15 cmH2O) for about 5 s, the procedures did not produce the induction of inhibition of either 16 low-threshold SARs (firing during both inflation and deflation) or 15 high-threshold SARs (firing during inflation only). In these preparations, the excitatory responses of SARs to maintained inflations at three different pressures were markedly enhanced after administration of veratridine (50 μg/kg), but under such conditions, the inhibition of SAR discharges was not observed. In the same SAR preparations, after flecainide treatment (9 mg/kg) sufficient for the blockade of veratridine (50 μg/kg)-induced SAR stimulation, maintained inflations at higher pressures (10 and 15 cmH2O) greatly inhibited SAR discharges. Under these conditions, the inhibition of SAR discharges was not observed during maintained inflations at 5 cmH2O. Significance These results suggest that neither low-threshold SARs nor high-threshold SARs in the rat lung are deactivated during maintained inflations at higher pressures.
-
effect of ouabain on the afterhyperpolarization of slowly adapting pulmonary Stretch Receptors in the rat lung
Brain Research, 2006Co-Authors: Shigeji Matsumoto, Chikako Saiki, Shinki Yoshida, Mamoru Takeda, Yumi KumagaiAbstract:Abstract In anesthetized, artificially ventilated rats with one vagus nerve section, the purposes of the present study were to investigate whether release from phasic consecutive hyperinflations (inflation volume = 3 tidal volumes) results in the afterhyperpolarization (AHP) of the slowly adapting pulmonary Stretch Receptor (SAR) activity and whether the effect of ouabain, a Na+–K+ ATPase inhibitor, alters AHP of the SAR activity seen after release from maintained inflations. Release from 10 consecutive phasic hyperinflations did not cause any significant inhibition of SAR activity. Release from maintained inflations (for approximately 10 and 15 cmH2O) for 5 s produced the induction of disappearance of SAR activity, corresponding with the AHP. Intravenous administration of ouabain (20 and 40 μg/kg) had no significant effects on the responses of SAR activity and SAR adaptation index (AI) to maintained inflations, but ouabain treatment with at 40 μg/kg resulted in a significant increase in the SAR activity after stopping the respirator and significantly attenuated the AHP of the SAR activity. In the immunohistochemical study, we found Na+–K+ ATPase α3-subunit-isoforms-like immunoreactivity in SAR terminals, forming leaflike extensions in the intrapulmonary bronchioles at different diameters, and those terminals were buried in the smooth muscle. In the same sections, the α1 subunit immunoreactivity of SAR terminals was not found. These results suggest that the mechanism of generating the AHP of SARs is mainly mediated by the activation of Na+–K+ ATPase α3 subunit isoform.
-
effects of potassium channel and na ca2 exchange blockers on the responses of slowly adapting pulmonary Stretch Receptors to hyperinflation in flecainide treated rats
British Journal of Pharmacology, 2001Co-Authors: Shigeji Matsumoto, Chikako Saiki, Mizuho Ikeda, Toshimi Nishikawa, Shinki Yoshida, Takeshi Tanimoto, Mamoru TakedaAbstract:The effects of K+ channel blockers, such as 4-aminopyridine (4-AP) and tetraethylammonium (TEA), and a reverse-mode Na+ – Ca2+ exchange blocker, 2-[2-[4-(4-nitrobenzyloxyl) phenyl] ethyl] isothiourea methanesulphonate (KB-R7943), on the responses of slowly adapting pulmonary Stretch Receptor activity to hyperinflation (inflation volume=3 tidal volumes) were investigated in anaesthetized, artificially ventilated, unilaterally vagotomized rats after pretreatment with a Na+ channel blocker flecainide. The administration of flecainide (9 mg kg−1) at a dose greater than that which abolished 50 μg kg−1 veratridine-induced SAR stimulation also inhibited hyperinflation-induced stimulation of SARs. In flecainide-treated animals, administration of 4-AP (0.7 and 2 mg kg−1) stimulated SAR activity during normal inflation and also caused a partial blockade of hyperinflation-induced SAR inhibition. The discharges of SARs during normal inflation in flecainide-treated animals were not significantly altered by administration of either TEA (2 and 7 mg kg−1) or KB-R7943 (1 and 3 mg kg−1), but both K+ channel and Na+-Ca2+ exchange blockers partially attenuated hyperinflation-induced SAR inhibition. These results suggest that hyperinflation-induced SAR inhibition in the presence of flecainide (9 mg kg−1) involves the activation of several K+ conductance pathways. British Journal of Pharmacology (2001) 134, 682–690; doi:10.1038/sj.bjp.0704277
-
inhibitory mechanism of slowly adapting pulmonary Stretch Receptors after release from hyperinflation in anesthetized rabbits
Life Sciences, 2000Co-Authors: Shigeji Matsumoto, Mizuho Ikeda, Toshimi Nishikawa, Shinki Yoshida, Takeshi Tanimoto, Chikako SaikiAbstract:Abstract In anesthetized, artificially ventilated rabbits with vagus nerve section, release from 10 consecutive hyperinflations (inflation volume = 3 tidal volume) caused an inhibition of the slowly adapting pulmonary Stretch Receptor (SAR) activity for 16–22 sec. Intravenous administration of tetraethylammonium (TEA, 10 and 20 mg/kg), a K+ channel blocker, did not significantly alter either basal SAR discharge or tracheal pressure (PT). Although TEA treatment at 10.0 mg/kg had no significant effect on the magnitude and duration of inhibited SAR activity seen after release from hyperinflation, the increasing dose of this K+ channel blocker up to 20 mg/kg inhibited these effects of the Receptor activity but this inhibition was small. The Na+-K+ ATPase inhibitor ouabain (5 and 10 μg/kg) that had no significant effect on SAR activity and PT in the control abolished or attenuated the inhibitory action of SARs in a dose-dependent manner. Furthermore, the changes in dynamic lung compliance (Cdyn) and PT in response to post-hyperinflation were not significantly influenced by pretreatment with either TEA or ouabain. These results suggest that the inhibitory action of Receptors seen during post-hyperinflation corresponded with the induction of slow afterhyperpolarization (sAHP), and that the mechanism of generating the sAHP of SARs is mainly mediated by the activation of Na+-K+ pump activity.
Chikako Saiki - One of the best experts on this subject based on the ideXlab platform.
-
flecainide inhibits the stimulatory effect of veratridine on the response of airway mechanoReceptors to maintained inflations in rats
Life Sciences, 2010Co-Authors: Shigeji Matsumoto, Chikako Saiki, Masayuki Takahashi, Kohsuke Iwasaki, Ryoji Ide, Mamoru TakedaAbstract:Abstract Aims The purpose of the present study was to investigate (a) whether maintained inflations result in the inhibition of slowly adapting pulmonary Stretch Receptor (SAR) discharge to elicit an abrupt change in Receptor activity and (b) whether pretreatment with veratridine, a Na+ channel opener, and/or flecainide, a Na+ channel blocker, alters the responses of SAR properties to maintained inflations. Main methods We measured the properties of SAR activity during maintained inflations at different pressures in 31 anesthetized, artificially ventilated rats with unilateral vagotomy. Key findings During maintained inflations (approximately 5, 10 and 15 cmH2O) for about 5 s, the procedures did not produce the induction of inhibition of either 16 low-threshold SARs (firing during both inflation and deflation) or 15 high-threshold SARs (firing during inflation only). In these preparations, the excitatory responses of SARs to maintained inflations at three different pressures were markedly enhanced after administration of veratridine (50 μg/kg), but under such conditions, the inhibition of SAR discharges was not observed. In the same SAR preparations, after flecainide treatment (9 mg/kg) sufficient for the blockade of veratridine (50 μg/kg)-induced SAR stimulation, maintained inflations at higher pressures (10 and 15 cmH2O) greatly inhibited SAR discharges. Under these conditions, the inhibition of SAR discharges was not observed during maintained inflations at 5 cmH2O. Significance These results suggest that neither low-threshold SARs nor high-threshold SARs in the rat lung are deactivated during maintained inflations at higher pressures.
-
effect of ouabain on the afterhyperpolarization of slowly adapting pulmonary Stretch Receptors in the rat lung
Brain Research, 2006Co-Authors: Shigeji Matsumoto, Chikako Saiki, Shinki Yoshida, Mamoru Takeda, Yumi KumagaiAbstract:Abstract In anesthetized, artificially ventilated rats with one vagus nerve section, the purposes of the present study were to investigate whether release from phasic consecutive hyperinflations (inflation volume = 3 tidal volumes) results in the afterhyperpolarization (AHP) of the slowly adapting pulmonary Stretch Receptor (SAR) activity and whether the effect of ouabain, a Na+–K+ ATPase inhibitor, alters AHP of the SAR activity seen after release from maintained inflations. Release from 10 consecutive phasic hyperinflations did not cause any significant inhibition of SAR activity. Release from maintained inflations (for approximately 10 and 15 cmH2O) for 5 s produced the induction of disappearance of SAR activity, corresponding with the AHP. Intravenous administration of ouabain (20 and 40 μg/kg) had no significant effects on the responses of SAR activity and SAR adaptation index (AI) to maintained inflations, but ouabain treatment with at 40 μg/kg resulted in a significant increase in the SAR activity after stopping the respirator and significantly attenuated the AHP of the SAR activity. In the immunohistochemical study, we found Na+–K+ ATPase α3-subunit-isoforms-like immunoreactivity in SAR terminals, forming leaflike extensions in the intrapulmonary bronchioles at different diameters, and those terminals were buried in the smooth muscle. In the same sections, the α1 subunit immunoreactivity of SAR terminals was not found. These results suggest that the mechanism of generating the AHP of SARs is mainly mediated by the activation of Na+–K+ ATPase α3 subunit isoform.
-
effects of potassium channel and na ca2 exchange blockers on the responses of slowly adapting pulmonary Stretch Receptors to hyperinflation in flecainide treated rats
British Journal of Pharmacology, 2001Co-Authors: Shigeji Matsumoto, Chikako Saiki, Mizuho Ikeda, Toshimi Nishikawa, Shinki Yoshida, Takeshi Tanimoto, Mamoru TakedaAbstract:The effects of K+ channel blockers, such as 4-aminopyridine (4-AP) and tetraethylammonium (TEA), and a reverse-mode Na+ – Ca2+ exchange blocker, 2-[2-[4-(4-nitrobenzyloxyl) phenyl] ethyl] isothiourea methanesulphonate (KB-R7943), on the responses of slowly adapting pulmonary Stretch Receptor activity to hyperinflation (inflation volume=3 tidal volumes) were investigated in anaesthetized, artificially ventilated, unilaterally vagotomized rats after pretreatment with a Na+ channel blocker flecainide. The administration of flecainide (9 mg kg−1) at a dose greater than that which abolished 50 μg kg−1 veratridine-induced SAR stimulation also inhibited hyperinflation-induced stimulation of SARs. In flecainide-treated animals, administration of 4-AP (0.7 and 2 mg kg−1) stimulated SAR activity during normal inflation and also caused a partial blockade of hyperinflation-induced SAR inhibition. The discharges of SARs during normal inflation in flecainide-treated animals were not significantly altered by administration of either TEA (2 and 7 mg kg−1) or KB-R7943 (1 and 3 mg kg−1), but both K+ channel and Na+-Ca2+ exchange blockers partially attenuated hyperinflation-induced SAR inhibition. These results suggest that hyperinflation-induced SAR inhibition in the presence of flecainide (9 mg kg−1) involves the activation of several K+ conductance pathways. British Journal of Pharmacology (2001) 134, 682–690; doi:10.1038/sj.bjp.0704277
-
inhibitory mechanism of slowly adapting pulmonary Stretch Receptors after release from hyperinflation in anesthetized rabbits
Life Sciences, 2000Co-Authors: Shigeji Matsumoto, Mizuho Ikeda, Toshimi Nishikawa, Shinki Yoshida, Takeshi Tanimoto, Chikako SaikiAbstract:Abstract In anesthetized, artificially ventilated rabbits with vagus nerve section, release from 10 consecutive hyperinflations (inflation volume = 3 tidal volume) caused an inhibition of the slowly adapting pulmonary Stretch Receptor (SAR) activity for 16–22 sec. Intravenous administration of tetraethylammonium (TEA, 10 and 20 mg/kg), a K+ channel blocker, did not significantly alter either basal SAR discharge or tracheal pressure (PT). Although TEA treatment at 10.0 mg/kg had no significant effect on the magnitude and duration of inhibited SAR activity seen after release from hyperinflation, the increasing dose of this K+ channel blocker up to 20 mg/kg inhibited these effects of the Receptor activity but this inhibition was small. The Na+-K+ ATPase inhibitor ouabain (5 and 10 μg/kg) that had no significant effect on SAR activity and PT in the control abolished or attenuated the inhibitory action of SARs in a dose-dependent manner. Furthermore, the changes in dynamic lung compliance (Cdyn) and PT in response to post-hyperinflation were not significantly influenced by pretreatment with either TEA or ouabain. These results suggest that the inhibitory action of Receptors seen during post-hyperinflation corresponded with the induction of slow afterhyperpolarization (sAHP), and that the mechanism of generating the sAHP of SARs is mainly mediated by the activation of Na+-K+ pump activity.
Robert F. Rogers - One of the best experts on this subject based on the ideXlab platform.
-
Slowly adapting pulmonary Stretch Receptor spike patterns carry lung distension information
Neuroscience Letters, 2010Co-Authors: Yan Chen, Vitaly Marchenko, Robert F. RogersAbstract:Slowly adapting pulmonary Stretch Receptors (SARs) provide the respiratory and cardiovascular control systems with information regarding the rate and depth of breathing. Previous information theoretical analysis demonstrated that SAR spike count provides a reliable representation of lung distension. This study examines whether SAR spike patterns may also provide information about lung distension. To investigate this, artificial spike trains were generated with the same number of spikes (but randomized intervals) as those recorded from SARs in response to three different lung inflation volumes in urethane-anesthetized rabbits. Three different spike train classification methods were applied to estimate which stimulus evoked them, and the accuracy with which artificial spike trains were classified was compared to that of real SAR spike trains using the same methods. Because real SAR spike trains were classified with higher accuracies than artificial ones containing the same number of spikes, we conclude that SAR spike patterns, in addition to spike counts, contain information concerning the amplitude of lung distension.
-
information theoretic analysis of pulmonary Stretch Receptor spike trains
Journal of Neurophysiology, 2001Co-Authors: Robert F. Rogers, Jacob D Runyan, Ganesh A Vaidyanathan, James S SchwaberAbstract:Primary afferent neurons transduce physical, continuous stimuli into discrete spike trains. Investigators have long been interested in interpreting the meaning of the number or pattern of action po...
