Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “rapid adaptation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1991

Response properties of the periodontal mechanosensitive neurons in the thalamus of the cat: a comparison between the slowly adapting and rapidly adapting neurons.

Slowly adapting (SA) and rapidly adapting (RA) types of the periodontal mechanosensitive units (PM units) were recorded in the thalamus and their response properties were examined in the cat. Both types of the PM units were located in the medial area (PM area) of the nucleus ventralis posteromedialis (VPM) of the thalamus. The SA units were located in a rostro-medial part of the PM area, while the RA units were distributed in the caudo-lateral part. An incidence of the SA and RA units was 45.5 and 54.5%, respectively. The single-tooth units were found in 23.5% of the SA units and in 14.9% of the RA units, and they responded chiefly to mechanical stimulation of the contralateral canine tooth. The multi-tooth units of the SA type had smaller receptive fields than those of the RA type, because the majority of the RA units had their receptive fields at the bilateral and/or bimaxillary area. In total, the units having the contralateral receptive fields were also dominant in both adaptation types. The latency of the neuronal discharges to electrical stimulation of the receptive field was fairly shorter in the SA units than in the RA units. These findings suggest that the SA units of the thalamus receive periodontal inputs directly from the trigeminal nuclear complex (Vcomp) of the brain stem, while the RA units receive them polysynaptically from the Vcomp via other pathways.

Adaptation, Physiological↗
PubMed1975

Ion conductance changes associated with spike adaptation in the rapidly adapting stretch receptor of the crayfish.

The time course of the repetitive impulse discharges has been investigated for two high intensities of maintained depolarizing currents, 30 nA and 50 nA, for which the receptor adaptation was complete within 70 msec. The changes in sodium and potassium conductance associated with the decline in spike activity have been analyzed at different instances of time by interrupting in successive experiments the various action potentials in the pulse trains either at the early phase by holding the potential at about -60 mV and recording the inward current (upstroke-gNa) or by evaluating the delayed outward current flowing as the result of a depolarizing voltage pulse which at the end of the action potential re-increased the membrane potential by mV (after potentialgK). At the higher current intensity of 50 nA the discharge frequency was increased, while larger reductions in upstroke-gNa and after potential-gK during receptor adaptation became apparent. The progressive decrease in pulse amplitude from 99 mV to 63 or 55 mV is paralleled by a gradual reduction in upstroke-gNa from 97 mmho/cm-2 to 37 or 27.5 mmho/cm-2 and in after potential-gK from 11.5 mmho/cm-2 to about 7 mmho/cm-2. When under a stimulus of 30 nA the sodium conductance decreases to an average value of 37 mmho/cm-2 only a distorted spike can be elicited, while the spike activity was completely suppressed at upstroke-gNa equals 27.5 mmho/cm-2 was essentially the same under both conditions. The results have been interpreted in terms of the model for impulse generation formulated by Michaelis and Chaplain (1973). According to the model both sodium and potassium inactivation reduce the pulse amplitude. However, while Na-inactivation reduces the frequency of impulse discharge, the K-inactivation actually leads to an increase in spike frequency. As the frequency of the short train of pulses recorded under high-intensity current stimulation remained essentially unaltered, it is suggested that the coupling between Na- and K-inactivation actually leads to an increase in spike frequency. As the frequency of the short train of pulses recorded under high-intensity current stimulation remained essentially unaltered, it is suggested that the coupling between Na- and K-inactivation ensures a constancy of the information-carrying parameter, i.e. the average impulse density.

Action Potentials↗
PubMed1978

[Na-K ionic pump and spike adaptation in the slowly and rapidly adapting stretch receptor neuron of the crayfish Orconectes limosus (RAF.)].

A very important cause of the spike adaptation in the slowly adapting stretch receptor neuron (SN1) is the Na-K ionic pump. An increasing inhibition of the ionic pump, produced by gradual reduction of the external K+-concentration or application of rising doses of ouabain, is correlated with an adequate diminution of frequency decay. But even high concentrations of ouabain (10(-3) -- 5 . 10(-3) M) can not completely abolish the spike adaptation. Immediately after the onset of a current step the impulse frequency still declines. In agreement with these findings the gain in the Bode diagram shows a maximum further on. The spike adaptation in the rapidly adapting neuron (SN2) can only in a smaller part be attributed to the action of the ionic pump. Application of ouabain causes in the SN2, contrary to SN1, only a low depolarization of the membrane potential. The decay of impulse frequency is considerably diminished but a long lasting nearly stationary discharge like in the SN1 can never be observed.

Animals↗
PubMed1992

Responses of airway rapidly adapting receptors to bradykinin before and after administration of enalapril in rabbits.

1. The present study was performed in anaesthetized, artificially ventilated, open-chested rabbits to examine whether (a) the rapidly adapting receptors of the airways were stimulated by exogenously administered bradykinin, and (b) if this sensitivity could be enhanced by the angiotensin-converting-enzyme inhibitor, enalapril. 2. Rapidly adapting receptor activity (n = 8) was recorded from the cervical vagus. Bradykinin was injected intravenously (0.25-1.0 microgram/kg) and a dose-response curve relating receptor activity to bradykinin was elicited. In the control state, the threshold dose of bradykinin required for stimulation of rapidly adapting receptors was 0.53 +/- 0.11 microgram/kg. Five minutes after the administration of enalapril maleate (2 mg intravenously), the dose-response curve was shifted to the left significantly (P < 0.01). 3. In seven other rapidly adapting receptors, enalapril (2 mg) increased the resting activity significantly (P < 0.05) over a period of 60 min. This increase was significantly different from the spontaneous variation in neural activity of rapidly adapting receptors (n = 7) recorded over a period of 60 min. 4. Bradykinin either alone (0.25-1.0 microgram/kg) or in the presence of enalapril did not stimulate the slowly adapting receptors (n = 5) of the airways. 5. These results show that (a) exogenous bradykinin stimulates the rapidly adapting receptors, (b) the sensitivity of rapidly adapting receptors to bradykinin is enhanced by enalapril and (c) enalapril increases the resting activity of rapidly adapting receptors. It is suggested that the cough reported after the administration of enalapril may be due to stimulation of rapidly adapting receptors of the airways.

Action Potentials↗
PubMed1986

Transmembrane ion balance in slowly and rapidly adapting lobster stretch receptor neurones.

The transmembrane exchange of Na+, K+, and Cl- in slowly and rapidly adapting lobster stretch receptor neurones was studied using ion-sensitive microelectrodes in combination with conventional electrophysiological techniques. The investigation was founded on the assumption that the transmembrane ion exchange is accomplished by active and passive transports which add up to zero in steady state for each ion involved. The active transports are assumed to include Na+ and K+ transports driven by an electrogenic Na-K pump. To these transports are also added equimolar fluxes of K+ and Cl- leaking from the impaling micro-electrode. The passive transports are assumed to pass through membrane channels in accordance with constant field kinetics. For a quantitative evaluation of the transmembrane ion exchange in resting conditions measurements were made of the resting concentrations of Na+, K+ and Cl-; the voltage dependence of the ungated leak current; and ouabain-induced changes in resting membrane current and intracellular ion concentrations. From the results it follows that both the resting pump current and the leak permeabilities for the ions investigated have values which do not seem to differ between slowly and rapidly adapting receptor neurones. For a quantitative evaluation of the relation between internal Na+ and pump current production, measurements were made of the outward membrane current as a function of internal Na+ and K+ following a shift of these ions by means of prolonged repetitive impulse activation. It was found that the investigated relation is compatible with Garay-Garrahan kinetics (Garay & Garrahan, 1973) in both receptor neurones, but the results imply a larger maximum Na+-extrusion capacity in slowly than in rapidly adapting cells. From recordings of the time course of post-tetanic normalization of both the membrane current and intracellular Na+ concentration, cell volume values could be deduced which were closely similar in slowly and rapidly adapting receptors. A corresponding similarity was also found for the cell area which was derived from membrane capacitance measurements.

Adaptation, Physiological↗
PubMed1991

Potential-dependent potassium currents in the rapidly adapting stretch receptor neuron of the crayfish.

The outward current was analysed in the rapidly adapting stretch receptor neuron of the crayfish Pacifastacus leniusculus with a two-micropipette potential clamp technique and K(+)-selective microelectrodes in an attempt to establish if the properties of this current could explain the difference in adaptive behaviour compared to the slowly adapting receptor. A fast activating outward current carried by K+ was revealed. The time constant of activation(tau n) was dependent on potential and had a mean value of 0.5 ms at potential steps to 0 mV. Activation followed a second-order process according to the Hodgkin-Huxley model. The potential dependence of activation (n infinity) followed by a sigmoid curve n infinity = 1/(1 + exp/[(E - En)/a]) with a half maximal activation potential En = -44 mV and a = -13 mV. When long pulses were applied the outward potassium current decreased with two time constants, one that was potential independent (0.2 s) and one that was potential dependent (2-8 s). The latter could be explained by accumulation of K+ in the extracellular space of the neuron. The potential dependence of inactivation followed a sigmoid function infinity = 1/(1 + exp[(E - Ek)/+a]) with Ek = -36 mV and a = 13 mV. The inactivation properties are different from those of the classical fast transient (IA) current. The transport system for the outward potassium current during depolarizing potential steps in the rapidly adapting stretch receptor is similar to the current found in the slowly adapting receptor neuron. However, the activation is faster and seems to occur at potentials more negative than in the slowly adapting receptor. These differences can contribute to but not entirely explain the difference in adaptive behaviour between the slowly and rapidly adapting receptor.

Action Potentials↗
PubMed1979

The nature of the receptor mediating stimulant effects of histamine on rapidly adapting vagal afferents in the lungs.

1. The effects of histamine H1- and H2-agonists on these airway sensory receptors were also examined. 2. Neither I.V. infusion of metiamide (5 mg/kg, min for 35 min) in seven experiments, nor I.V. bolus injection of burimamide (15 mg/kg) in six other experiments, both substances being H2-antagonists, altered the response of rapidly adapting receptors to aerosols of histamine (from 0.1 or 1.0% solutions). 3. Chlorpheniramine (H1-antagonist), 2--5 mg/kg, I.V., completely abolished responses of rapidly adapting receptors to histamine in seven experiments in which metiamide had been given previously and in seven other preparations in which it had not, but had no effect on responses to prostaglandin F2 alpha. Chlorpheniramine itself caused a brief stimulation of rapidly adapting receptors. 4. The H2-agonist S-[3-(N,N-dimethylamino) propyl] isothiourea (Dimaprit), given as aerosol (1% solution for 2 min) or I.V. (2 mg/kg), was without effect on activity of four airway rapidly adapting receptors. These receptors were stimulated, however, by the H1-agonist 2,(2 pyridylethylamine) dihydrochloride (PEA), administered both as aerosol (from a 10% solution) and I.V. (0.4--2 mg/kg). These stimulant effects were abolished by chlorpheniramine. 5. The results indicate that stimulation of airway rapidly adapting receptors by histamine is mediated by histamine H1-receptors.

Animals↗
PubMed1976

[Properties of the mechanoreceptors of the nipple of the guinea pig mammary gland. (Rapidly adapting mechanoreceptor units)].

Two types of rapidly adapting mechanosensitive units have been found in skin of the teat of guinea--pig mammary gland (RA1 and RA2). They wee not both spontaneously active. RA1 and RA2 have no position response. The relation between average frequency of discharge and displacement velocity at a constant displacement amplitude was linear for RA1. With constant velocity displacements, frequency versus displacement curves assume a horizontal orientation of relatively low discharge frequencies and are then displaced upward as velocity increases for RA1. The number and frequency of afferent impulses of RA1 decreased during repeated ramp mechanical stimulation. Vibratory tuning points were in the range of 10--25 Hz for RA1. 20% of mechanosensitive units were RA2, which have a high velocity threshold and rarely produce more than 2--3 impulses to high velocity. The fatigue of RA2 is not prominent. RA1 were classed as the velocity detectors and RA2 as "transient" detectors.

Action Potentials↗
PubMed1977

Mechanisms by which histamine stimulates rapidly adapting receptors in dog lungs.

The stimulant effect of histamine on intrapulmonary rapidly adapting receptors was studied in anesthetized, paralyzed, artificially ventilated dogs, to determine whether it was dependent on contraction of airway smooth muscle. Single- or few-afferent fiber recordings were made from small strands dissected from the otherwise intact vagus nerve. Aerosols of histamine increased both receptor discharge and tracheal pressure (Pt). In 27 experiments, isoproterenol prevented the increase in Pt but not in receptor activity induced by histamine. In another 32 experiments, acetylcholine (ACh) increased Pt to a greater extent than did histamine, whereas histamine increased receptor discharge more than ACh. When given as aerosol directly to the vicinity of the sensory receptor via a fiber bronchoscope, histamine stimulated 12 receptors, whereas ACh and buffer solution did not. Isoproterenol reduced slightly the stimulant effect of locally applied histamine on 8 receptors. We conclude that smooth muscle contraction is not essential for stimulant effects of histamine on rapidly adapting receptors in dog lungs, and that histamine acts directly on the receptors to increase their activity.

Acetylcholine↗
PubMedDate not supplied

Effect of carbon dioxide on the activity of slowly and rapidly adapting pulmonary stretch receptors in cats.

Single fiber activity from slowly and rapidly adapting pulmonary stretch receptors (PSR) was recorded from the left cervical vagus of anesthetized, open-chested and artificially ventilated cats. Reducing the end-tidal CO2 to low values did not affect the frequency of occurrence of higher threshold (HT) PSR. Occlusion of the left pulmonary artery (LPA) had no significant effect on the resting discharge of both HT and low threshold (LT) PSR. Cyclic ventilation with 8% CO2 in O2 reduced the activity of LT and HT receptors by similar amounts, irrespective of their anatomical location. After LPA occlusion, CO2 ventilation reduced markedly the activity of both type of PSR but to the greatest extent that of the HT receptors, the majority of which were located in the intrapulmonary airways. The CO2 depressant effect may not be due solely to changes in H+ concentration at the receptor level, since acetazolamide did not totally abolish the effect even though it significantly reduced it. Sustained inflation with 8% CO2 in O2 significantly reduced the activity of HT receptors in both the dynamic and static phases of inflation, but had no effect on the activity of LT receptors. Direct localization showed that the receptors which were more accessible to CO2 (all HT and one LT) were located in the lung parenchyma. In the case of rapidly adapting receptors, sustained inflations with CO2 gave inconsistent results. The results show clearly that, as in other mammalian species, the PSR activity in cats is also reduced by hypercapnia. The present study stresses the importance of localizing the PSR and making the observations separately on the two types of PSR, for there may be qualitative and quantitative differences.

Acetazolamide↗
PubMed1990

Stimulation of rapidly adapting receptors in canine lungs by a single breath of cigarette smoke.

Inhalation of smoke generated from high-nicotine cigarettes frequently evoked an immediate augmented inspiration in conscious dogs (J. Appl. Physiol. 54: 562-570, 1983); this reflex response was believed to result from a stimulation of rapidly adapting receptors in the lungs. To test this hypothesis, we recorded the vagal afferent activity arising from the rapidly adapting receptors in the lungs and delivered 120 ml of high- and low-nicotine cigarette smoke separately in a single ventilatory cycle in 20 anesthetized open-chest and artificially ventilated dogs. These receptors were stimulated on the first breath of delivery of smoke generated by high-nicotine cigarettes; activity increased from a base line of 0.9 +/- 0.2 to a peak of 9.9 +/- 1.2 (SE) impulses/breath (n = 58). After three to six breaths when the receptors' discharge returned toward base-line activity, a delayed increase of activity emerged (peak activity = 3.4 +/- 0.6 impulses/breath, n = 58) in 32 of the 58 receptors studied and lasted for three to seven breaths. By contrast, only a mild stimulatory effect of low-nicotine cigarette smoke was found, either immediately or after a delay, in 15 of the 54 receptors studied. We conclude that rapidly adapting receptors are stimulated by a single breath of cigarette smoke and that nicotine is the primary stimulant agent.

Adaptation, Physiological↗
PubMed1991

Mechanisms of cigarette smoke-induced stimulation of rapidly adapting receptors in canine lungs.

The stimulation of rapidly adapting receptors (RARs) in the lungs evoked by cigarette smoke consists of an initial and either a type I or a type II delayed response (Kou and Lee, J. Appl. Physiol. 68: 1203, 1990). In the type I response, receptor activity increased during expirations and exhibited a prominent cardiac modulation, whereas in the type II response, receptor discharge reached its peak during inspiration at peak transpulmonary pressure. To investigate the mechanisms of this stimulation, we recorded the vagal afferent activity arising from 39 RARs and delivered a single breath (120 ml) of cigarette smoke in 15 anesthetized, open-chest and artificially ventilated dogs. Studies were repeated after a pretreatment with aerosolized hexamethonium (3-8 breaths, 10%), aerosolized isoproterenol (12-15 breaths, 2%), or after the cardiac impact on the lung had been minimized by elevating the apex of the heart. The initial response of RARs was totally abolished by hexamethonium but was not affected by isoproterenol. The increase of total lung resistance induced by cigarette smoke and the concomitant type II delayed response of RARs were both abolished by isoproterenol. The type I delayed response of RARs was eliminated or largely attenuated after the apex of the heart had been elevated. Based upon these results, we conclude that a direct effect of nicotine on these receptors may be responsible for the immediate stimulation while the systemic effects of absorbed nicotine may play a part in evoking the delayed stimulation.

Adaptation, Physiological↗
PubMed1989

Excitation of both slowly and rapidly adapting pulmonary stretch receptors attenuates tachypnea induced by ammonia.

To elucidate the mechanism of attenuating the ammonia-induced tachypnea, the present study examined the discharge patterns and rates of slowly adapting pulmonary stretch receptors (SARs) and rapidly adapting pulmonary stretch receptors (RARs) in relation to the change in respiration produced by ammonia inhalation in anesthetized, spontaneously breathing rabbits. Extracellular action potentials of these two receptors were recorded at the peripheral cut-end of the left vagus nerve. A prolongation of expiration following ammonia inhalation occurred during the discharge of receptors increased continuously, particularly when the level of the discharge rate during expiration reached to approximately 20-fold, and under such circumstances the respiratory response was regularly associated with gasps. On the other hand, RARs increased their activity during only inspiration; this increased activity correlated with augmentation of inspiration. Furthermore, the prolongating effect of expiration due to ammonia inhalation was not observed after surgical denervation of the remaining right vagus nerve. These results suggest that vigorous stimulation of the SAR activity induced by ammonia inhalation can elicit a prolongation of expiration possibly resulting from augmentation of the Hering-Breuer inflation reflex and that augmentation of the increased RAR activity after ammonia inhalation counteracts the Hering-Breuer inflation reflex to shorten inspiration. Therefore, it is conceivable that strong stimulation of the SAR activity after ammonia inhalation counteracts the ammonia-induced tachypnea.

Action Potentials↗
PubMed1989

Effects of 5-hydroxytryptamine on rapidly adapting pulmonary stretch receptor activity in the rabbit.

In anesthetized rabbits, intravenous administration of 5-hydroxytryptamine (5-HT, 10, 20, 40 and 80 micrograms/kg) led to an increase of rapidly adapting pulmonary stretch receptor activity. The magnitude of the increase was dose-dependent. The excitatory responses to any doses of 5-HT were not inhibited by prior treatment with isoprenaline (100-150 micrograms). The results indicate that the stimulation of rapidly adapting pulmonary stretch receptors by 5-HT is not caused by contraction of the airway smooth muscle.

Animals↗
PubMed1991

Intracellular measurements from a rapidly adapting sensory neuron.

1. The femoral tactile spine of the cockroach contains a single sensory neuron with its cell body in the lumen of the spine. Step movements of the spine produce rapidly adapting bursts of action potentials that decay to 0 in 1 s. Previous work has shown that a large part of this adaptation occurs during action potential encoding. 2. Intracellular recordings from the tactile spine neuron were obtained by lowering a microelectrode through the spine lumen and penetrating the cell body. Injection of Lucifer yellow followed by fluorescence microscopy confirmed the morphology of the soma, with a diameter of 30 microns, and showed an axon of 9 microns leaving the spine and proceeding proximally along the femur. 3. Membrane-potential records were digitized and examined at high resolution during bursts of action potentials produced by depolarizing current pulses. No significant changes in action potential shape were detected during adaptation. However, the rate of depolarization between action potentials slowed dramatically during the burst. This slowing could be reduced and the burst substantially prolonged by chloramine-T (CT), an agent that reduces sodium channel inactivation in several preparations. 4. A 100 Hz sinusoidal current was superimposed on depolarizing current pulses to test for changes in membrane conductance during a burst of action potentials. No such changes were detected, indicating that rapid adaptation is not due to changes in membrane permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1976

[Functional characteristics of rapidly adapting mechanoreceptor units of the rat mammary gland nipple].

Two types of rapidly adapting mechanosensitive units were found in the teat of the rat mammary gland (RAI and RAII). Neither was spontaneously active. 10% of the units were RAII and had the functional characteristics of "transient" receptors. The relation between the average frequency of discharge and the velocity of displacement at a constant displacement amplitude was linear for RAI. The latency of the first spike decreased when indentation velocity increased. The number and frequency of afferent impulses decreased at a repeated mechanical stimulation. Vibratory tuning points were in the range 10--25 Hz for RAI. RAI units were not directionally sensitive to the teat displacement.

Action Potentials↗
PubMed1989

Vibration sensitivity of slowly and rapidly adapting cutaneous mechanoreceptors in the human foot and leg.

The activities of 30 rapidly adapting cutaneous receptors (FA) and 23 slowly adapting cutaneous receptors (SA) were recorded from the lateral peroneal nerve using the microneurographic method. Their sensitivity to mechanical vibrations with constant amplitude applied at various frequencies to the center of the receptive field was studied. These two populations of cutaneous receptors were found to be very sensitive to this stimulus: they could be driven in a one to one manner up to between 100 and 200 Hz. The difference lay in the response observed when the vibration frequency was increased to above this critical value: the FA receptors sharply stopped firing, whereas the SA receptors became progressively unlinked from the stimulus. The effects of vibration on the physiological messages were also studied. The results showed that the messages coding the properties of tactile stimuli were either completely or partly masked by the receptor response to vibration. These vibration-induced modifications of cutaneous sensory messages might be at least partly responsible for the sensorimotor alterations observed when subjects are exposed to vibration.

Electrophysiology↗
PubMed1989

Action of histamine on the rapidly adapting airway receptors in the dog.

The effects of histamine on the activity of rapidly adapting receptors (RAR) of the airways were investigated in anesthetized dogs. With bolus injections given into the right atrium, the threshold dose of histamine required for the excitation of RAR (n = 7) was 0.82 microgram/kg (+1.33/-0.51, geometric mean). With increasing doses of histamine, a dose-response relationship was seen in the activity of RAR. Obstruction of the lymphatic drainage from the lungs reduced the threshold dose to histamine (i.e., shifted the dose-response curve to the left significantly). This change in the dose-response relationship was not accompanied by a corresponding change in the relationship of histamine dose to airway pressures recorded before and after lymphatic obstruction. Against a background of pulmonary venous congestion produced by partial obstruction of the mitral valve, subthreshold doses of histamine stimulated the RAR (n = 4). The excitatory effect of histamine on RAR was found to be abolished by the administration of the H1 receptor antagonist diphenhydramine but not by the H2 receptor antagonist cimetidine. Intravenous infusion of histamine (0.4 microgram.kg-1.min-1) for a period of 10 min increased the RAR activity (n = 6) significantly without producing detectable changes in airway mechanics. The results indicate that contraction of the smooth muscle of the airways may not be a prerequisite for the excitation of RAR, especially at low doses. It is suggested that some of the effects of histamine on RAR are mediated by a local expansion of the extravascular fluid caused by an increase in the permeability of the bronchial vasculature.

Action Potentials↗