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Wettability of silicone-hydrogel contact lenses in the presence of tear-film components.

INTRODUCTION: Modern application of soft contact lenses demands safe and comfortable wear over extended time periods up to one month. Lenses that exhibit and sustain complete water wetting allow thick tear-film deposition, minimize film rupture, and permit smooth tear recovery upon lid closure. Water contact angles determined using an air bubble captive on a lens best gauge the in-vivo wetting state. To achieve highly water wetting lenses demands that contact-angle hysteresis be eliminated and that the advancing and receding angles both approach zero. Since lens wear exposes the anterior surface to tear proteins, lens wettability should be measured in the presence of tear-film components. METHODS: A captive-bubble technique is applied to measure the advancing and receding contact angles of two commercial silicone-hydrogel lenses: PureVision (PV) and Focus Night & Day (CF) and a standard HEMA (hydroxethyl-methacrylate) hydrogel lens: Acuvue (AV). In the captive-bubble method, an air bubble immersed in aqueous solution is brought into contact with the contact lens. The contact angle through water during bubble expansion yields the receding angle. Bubble contraction gives the water advancing angle. Contact-angle hysteresis is the difference between the advancing and receding angles. RESULTS: In isotonic solution, all three lenses display considerable contact-angle hysteresis with advancing angles of almost 90 degrees. When lysozyme and/or mucin were added to the aqueous solution, hysteresis was eliminated, and equivalent and high water wetting was achieved for the three lenses. Only the advancing angle in isotonic solution provided discriminating evidence for differences in surface chemistry. Covalent attachment of polyethyleneglygol (PEG) to the PV lens surface achieved complete water wetting independent of the presence of tear protein in the solution. CONCLUSIONS: The captive-bubble technique provides contact angles that are relevant to on-eye lens wear. Both advancing and receding contact angles are important to lens wettability performance. When lysozyme and/or mucin are present in the solution, PV, CF, and AV lenses display low advancing and receding contact angles indicative of equivalent wettability performance. This result is due to molecular adsorption of the proteins onto the lens external surface. Covalently attached PEG on the PV lens not only provides complete water wetting but also minimizes or even eliminates protein adsorption.

Absorption↗

The force-velocity relationship in vertebrate muscle fibres at varied tonicity of the extracellular medium.

1. The relationship between active force and velocity of shortening was studied during tetanic contraction of isolated semitendinosus muscle fibres of the frog (0.5-2.0 degrees C). Measurements were carried out with the fibre immersed in isotonic (1.00R) Ringer solution and in solutions that were made hypotonic by reduction of NaCl (osmolality 0.62 and 0.81 of normal Ringer) and hypertonic by addition of sucrose (osmolality 1.22 and 1.44 of normal Ringer).2. The force-velocity relation was hyperbolic at loads lower than 80% of measured isometric force (P(0)) but exhibited a reversed curvature between 0.8P(0) and P(0). The maximum velocity of shortening was determined in two different ways: (i) by extrapolation to zero load from force-velocity data truncated at 0.8P(0) (computer fitting of hyperbola, leastsquares method) and (ii) by recording the time required to take up the slack of the fibre after a quick release during tetanus.3. Isometric force and maximum speed of shortening both changed inversely with the tonicity of the extracellular medium. Immersion of the fibre in 0.81R hypotonic solution caused active tension and shortening velocity to increase by 10 +/- 1% (mean +/- S.E. of mean, n = 14) and 12 +/- 1%, respectively. Conversely, force and shortening velocity decreased by 12 +/- 1% (n = 13) and 22 +/- 2% when normal Ringer was replaced by 1.22R hypertonic solution. These changes doubled when the tonicity was altered from normal Ringer to 0.62R and 1.44R, respectively.4. Changes in fibre cross-sectional area equivalent to those obtained in the 0.81R and 1.22R solutions (+11% and -13%, respectively) were produced by varying the sarcomere length within the range 2.0-2.5 mum in the normal Ringer solution. Maximum velocity of shortening remained very nearly constant under these conditions, indicating that the shortening velocity, like the isometric force, is not critically dependent on changes in myofilament lattice width over the range considered.5. The results support the view that both shortening velocity and active force are modulated by changes of the intracellular ionic strength above and below the level that normally exists in the intact muscle fibre.

Animals↗

Coronary artery narrowing in rats: mechanical alterations of left and right myocardium.

To determine the effects of chronic coronary artery narrowing on myocardial contractile performance, nonocclusive constriction of the left coronary artery near its origin was surgically induced in rats and global cardiac hemodynamics, left and right myocardial mechanics, and the magnitude and distribution of tissue damage and interstitial fibrosis in the left ventricular wall were analyzed 1 mo later. Reductions in coronary artery luminal diameter of 55% resulted in left ventricular failure as characterized by decreases in systemic arterial pressures, systolic ventricular pressure, rise and decay in first derivative of left ventricular pressure (+/- dP/dt), and an increase in left ventricular end-diastolic pressure. Right side dysfunction was also present as documented by an elevation in right ventricular end-diastolic pressure and a reduction in -dP/dt. In vitro measurements of papillary muscle mechanics revealed a biventricular reduction in isometric developed tension and peak rates of tension rise and decay. Moreover, the kinetic parameters of isometric contraction duration, time to peak tension and time to one-half relaxation, were significantly shorter in left muscles from coronary artery-narrowed animals. Isotonically, peak muscle shortening was reduced in the left muscle, whereas time to peak shortening was prolonged in the right myocardium. In addition, the velocities of muscle shortening and relengthening were decreased in both ventricles. Foci of replacement fibrosis and diffuse interstitial fibrosis were found in the epimyocardium, midmyocardium, and endomyocardium, demonstrating that a significant amount of myocyte loss occurred throughout the left ventricular wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Postpartum changes in the mechanical responses of the circular muscle of rat uterus.

The circular muscle strips were isolated from rat uterus 10-60 h after parturition, and the electrical and mechanical responses were investigated. The muscle strips exhibited a variety of contractile activity ranging from frequent spontaneous contractions generated on an elevated muscle tone to a sustained contracture, when incubated with Mg-free Krebs solution. The muscle tone was lowered, and phasic contractions were abolished when the external Ca was removed. Muscle tone was also lowered by addition of 1.2 mM Mg, 1 mM spermidine, or 1 mM tetracaine. The membrane potential was about -25 mV in a muscle which exhibited a contracture, and the membrane was hyperpolarized by 20-25 mV by the (1.5-4.5 x 10(-5) M) caused a gradual decrease in muscle tone, and the that Ca-influx was increased, for which prostaglandin(s) was membrane was hyperpolarized. In view of the above results, it is hypothesized that Ca-influx was increased, for which prostaglandin(s) was probably responsible, in the circular muscle of postpartum rat uterus, thereby elevating the muscle tone in Mg-free solution.

Animals↗

Etomidate attenuates phenylephrine-induced contraction in isolated rat aorta.

PURPOSE: A previous study has shown that etomidate inhibits the angiotensin II-induced calcium influx in rat aortic smooth muscle cells. The goals of our current in vitro study were to investigate the effect of etomidate on phenylephrine-induced contraction in rat aorta, and to elucidate the associated signalling pathway. METHODS: Endothelium-denuded aortic rings were suspended for isometric tension recording. Concentration-response curves for phenylephrine (10(-9) to 10(-6) M), 5-hydroxytryptamine (10(-7) to 10(-4) M) and potassium chloride (10 to 60 mM) were generated in the presence and absence of etomidate (5 x 10(-6), 3 x 10(-5), 5 x 10(-5) M). For the rings pretreated with verapamil (10(-5) M), the phenylephrine concentration-response curves were generated in the presence and absence of etomidate (5 x 10(-5) M). In the rings exposed to calcium-free isotonic depolarizing solution, the contractile response induced by the addition of calcium was assessed in the presence and absence of etomidate (5 x 10(-5) M). RESULTS: Etomidate (5 x 10(-5) M) produced a significant rightward shift in the concentration-response curves for phenylephrine, 5-hydroxytryptamine and potassium chloride. Etomidate (5 x 10(-5) M) did not alter phenylephrine-induced contraction in the rings pretreated with verapamil. Etomidate (5 x 10(-5) M) significantly attenuated the contractile response induced by the addition of calcium in the calcium-free isotonic depolarizing solution. CONCLUSION: The results suggest that etomidate, which exceeds the clinically relevant concentration, attenuates the phenylephrine-induced contraction by having an inhibitory effect on the calcium influx by blocking the L-type calcium channels in the rat aortic vascular smooth muscle.

Anesthetics, Intravenous↗

Photoaffinity labelling of dopamine receptors in molluscan smooth muscle.

Relaxation of catch contraction of the anterior byssus retractor muscle of the sea mussel Mytilus edulis L. by dopamine is mediated through a dopamine receptor but not through adrenoceptors (Takayanagi et al 1981). Photoaffinity labelling is a technique widely used in biochemical in vitro studies to test an interaction between a ligand and its binding site. Therefore, we tried photoaffinity labelling of the dopamine receptor in order to study the dopamine receptor in the anterior byssus retractor muscle of M. edulis. Sea mussels, collected from the east coast of Tokyo Bay were stored in aerated seawater (NaCl 456, KCl 11, CaCl2 2H2O 11, MgCl2 6H2O 48 nM and Tris-HCl 25 mM; pH 7 . 8 to 8 . 0) at 10 degrees C and used within a week of collection. Muscle bundles (about 1 mm in diameter) were dissected from the anterior byssus retractor muscle and suspended in a 10 ml organ bath filled with artificial seawater bubbled with air and kept at 24 to 25 degrees C. Responses to drugs were recorded isotonically under a tension of 0 . 2 g. After the muscle had been exposed to acetylcholine (10(-4)M) for 2 min to induce catch contraction and washed with artificial seawater for 5 min, dopamine was applied. Relaxations following a 10 min exposure to various doses of dopamine were estimated. The response to 3 x 10(-7) M dopamine was considered as the maximum response to obtain dose-response curves (Takayanagi et al 1981). To irradiate the muscle, a Toshiba lamp FL-20E (wavelength: 270 to 350 nm) was used as a light source. The muscle, immersed in artificial seawater containing dopamine (10(-4)M), was irradiated (1 cm from the lamp) for 25 min and then washed with artificial seawater for 60 min (Takayanagi et al 1976). After the muscle was irradiated in the presence of dopamine (10(-4)M) for 25 min and washed for 60 min, the dose-response curve of dopamine was shifted in a parallel way towards doses about 8 times higher (Fig. 1). This inhibition of dopamine-induced responses continued for at least 2 h. The dose-response curve for dopamine was unaffected when the muscle was incubated with both dopamine (10(-4)M) and haloperidol (10(-4)M) for 25 min under the irradiation conditions (Fig. 1). However, the inhibitory action of dopamine was unaffected when the muscle was irradiated in the absence of dopamine and washed for 60 min, suggesting that 20 min irradiation did not influence mechanisms for relaxation of this smooth muscle by dopamine. Furthermore, when the muscle was incubated with dopamine (10(-4)M) or haloperidol (10(-4)M) for 25 min and washed with artificial sea water, the dose-response curve for dopamine was not influenced. When promethazine (10(-4)M), an antihistamine drug found to have no antidopaminergic action in this muscle (Yoshida et al 1981), was used instead of haloperidol (10(-4)M), the dose response curve for dopamine was shifted after irradiation (data not shown). These results indicate the possibility that dopamine is photolysed to a reactive compound which reacts irreversibly with the dopamine receptor.

Affinity Labels↗

Stimulation of potassium cycling in mitochondria by long-chain fatty acids.

Nonesterified long-chain fatty acids (myristic, palmitic, oleic and arachidonic), added at low amounts (around 20 nmol/mg protein) to rat liver mitochondria, energized by respiratory substrates and suspended in isotonic solutions of KCl, NaCl, RbCl or CsCl, adjusted to pH 8.0, induce a large-scale swelling followed by a spontaneous contraction. Such swelling does not occur in alkaline solutions of choline chloride or potassium gluconate or sucrose. These changes in the matrix volume reflect a net uptake, followed by net extrusion, of KCl (or another alkali metal chloride) and are characterized by the following features: (1) Lowering of medium pH from 8.0 to 7.2 results in a disappearance of the swelling-contraction reaction. (2) The contraction phase disappears when the respiration is blocked by antimycin A. (3) Quinine, an inhibitor of the K(+)/H(+) antiporter, does not affect swelling but suppresses the contraction phase. (4) The swelling phase is accompanied by a decrease of the transmembrane potential and an increase of respiration, whereas the contraction is followed by an increase of the membrane potential and a decrease of oxygen uptake. (5) Nigericin, a catalyst of the K(+)/H(+) exchange, prevents or partly reverses the swelling and partly restores the depressed membrane potential. These results indicate that long-chain fatty acids activate in liver mitochondria suspended in alkaline saline media the uniporter of monovalent alkali metal cations, the K(+)/H(+) antiporter and the inner membrane anion channel. These effects are presumably related to depletion of mitochondrial Mg(2+), as reported previously [Arch. Biochem. Biophys. 403 (2002) 16], and are responsible for the energy-dissipating K(+) cycling. The uniporter and the K(+)/H(+) antiporter are in different ways activated by membrane stretching and/or unfolding, resulting in swelling followed by contraction.

Animals↗

Acid-induced laryngospasm in a canine model.

A canine model was used to investigate the efferent laryngeal responses to stimulation by topically applied acid and pepsin. Five adult mongrel dogs were studied. Electromyographic recordings from the thyroarytenoid muscle were measured with hooked-wire electrodes as an acid solution (normal saline/hydrochloric acid at pH 6.0, 5.0, 4.0, 3.0, 2.5, 2.0, 1.5, and 1.0) was sequentially instilled into the larynx. Laryngospasm (tonic, sustained contraction of the thyroarytenoid muscle) occurred in all animals at pH 2.5 to 2.0 or less. Control substances such as neutral pH isotonic saline, hypotonic saline, hypertonic saline, water, and pepsin alone failed to produce laryngospasm. Next, solutions containing both acid (in the same pH range) and pepsin were tested. The laryngeal responses were similar to those of acid alone. The superior laryngeal nerves were sectioned bilaterally and the above experiments repeated. None of the test solutions produced laryngospasm; however, when capsaicin (1%) was instilled into the subglottis, laryngospasm occurred. Thus, chemoreceptors in the subglottis (supplied by the recurrent laryngeal nerves) appear to be responsive to capsaicin stimulation but not to acid stimulation. The data suggest that pH-sensitive chemoreceptors in the canine larynx cause laryngospasm (when the pH of the test solution is 2.5 or less) and that these acid receptors are supplied by the superior laryngeal nerves.

Animals↗

Induction of a myogenic response in tonic airway smooth muscle by tetraethylammonium.

In multi-unit tracheal smooth muscle (TSM), quick stretches applied at a velocity of 5 times the measured maximum velocity of isotonic shortening of the muscle, of a magnitude 3 times the measured extension of the series-elastic component when the muscle contracts maximally, and at optimal muscle length (L-o) were unable to elicit any myogenic response (MR). Experimental conditions such as hypoxia (P-O2 smaller than 60 mmHg) and acidosis (pH equals 6.8) or the presence of Ba2+ (2 mM), acetylcholine (10-6 M), or high (K+)-o (59 mM) were also unable to elicit the MR. However, tetraethylammonium chloride (TEA, 0.4-67 mM) produces 1) spontaneous phasic contractions and 2) a MR to quick stretch. The ionic basis for these changes was then investigated by studying the Ca and Mg dependence of the response to TEA. The dose-response relationship to TEA was shifted to the left by decreasing external Mg2+ from 2.5 to 0.5 mM. The ability of TSM to produce a MR was absolutely dependent on external Ca, but the threshold concentration required shifted from 2.5 times 10-5 M at normal external Mg (2.5 mM) to 5 times 10-4 M at the reduced external Mg (0.5 mM). The effects of TEA on spontaneity and the MR were abolished by D-600. These results suggest that 1) TEA functionally converts multiunit smooth muscle into a single unit one and leads to the development of a MR and 2) the MR results from a depolarization-activated mobilization of Ca and is inhibited by ionic conditions known to increase membrane permeability.

Acetylcholine↗

A double-blind, controlled study of botulinum toxin A in chronic myofascial pain.

BACKGROUND: Recent studies have reported a potential analgesic effect of botulinum toxin A (BTXA) in musculoskeletal pain. The present double-blind, randomized, placebo-controlled, parallel clinical trial studied the effect of BTXA on pain from muscle trigger points and on EMG activity at rest and during voluntary contraction. METHODS: Thirty patients with trigger points in the infraspinatus muscles received either 50 units/0.25 mL of BTXA or 0.25 mL of isotonic saline. Baseline measures were determined during a run-in period of 1 week. Outcome measures including local and referred spontaneous pain, pain detection and tolerance thresholds to mechanical pressure, and shoulder movement were assessed at 3 and 28 days after injection. The interference pattern of the EMG during maximal voluntary effort of infraspinatus muscle was recorded and a standardized search for spontaneous electrical motor endplate activity at the trigger points was performed before and 28 days after BTXA or saline injection. RESULTS: BTXA reduced motor endplate activity and the interference pattern of EMG significantly but had no effect on either pain (spontaneous or referred) or pain thresholds compared with isotonic saline. CONCLUSIONS: The results do not support a specific antinociceptive and analgesic effect of botulinum toxin A.

Analgesics↗

Effects of nitric oxide donors on vascular smooth muscles depend on a type of vascular smooth-muscle preactivation.

The abilities of such therapeutic nitrovasodilators as sodium nitroprusside (SNP) and glyceryl trinitrate (GTN) to dilate vascular smooth muscles (VSM) and affect intracellular calcium concentration level ([Ca2+]i) in a rat tail artery were tested under different types of preactivation. To shed light on mechanisms underlying possible differences in the action of these two nitric oxide (NO) donors, simultaneous measurements of [Ca2+]i and contractile force were done. All vascular rings were precontracted either using a high-K+-Krebs solution or phenylephrine (PE). It was shown that the effect of both NO donors strongly depended on a type of VSM preactivation. The EC50 for GTN under K+ stimulation of VSM comprised (2.48 +/- 1.6) x 10(-5) M, whereas the mean EC50 under PE stimulation was (3.05 +/- 2.3) x 10(-4) M (p < 0.05, n = 9). The EC50 for SNP under K+ stimulation of VSM comprised (1.09 +/- 0.47) x 10(-7) M, whereas the EC(50) under PE stimulation was (8.01 +/- 2.4) x 10(-6) M (p < 0.05, n = 9). GTN demonstrated a significant discrepancy in the magnitude of changes in [Ca2+]i and related VSM relaxant responses, indicating the ability of GTN to relax VSM in the absence of a proportional decrease in [Ca2+]i. The main peculiarity of SNP action under K+ stimulation as compared to PE stimulation was the transient decrease in [Ca2+]i while relaxation was sustained. Therefore, both NO donors demonstrated their ability to produce vasorelaxation as a result of an alteration in myofilament calcium sensitivity. These data clearly indicate that the sensitivity of VSM to NO donors is higher under K+ depolarization than that seen under PE stimulation, indicating that Ca2+ entry through voltage-operated calcium channels is more sensitive to NO as compared to calcium mobilization by means of Ca2+ entry through receptor- operated calcium channels or intracellular Ca2+ release, or both.

Animals↗

A "give" in tension and sarcomere dynamics in cardiac muscle relaxation.

Isometric relaxation in cardiac sarcomeres is characterised by an early, very slow phase of tension fall which is terminated by a 'give' in tension. A 'give' which occurs during relaxation in cardiac muscle can not be attributed to decrease in myofilament overlap. After the 'give' asynchronous motion occurs between sarcomeres, but the duration and extent of their displacement is limited. Intriguingly, the effect of isotonic displacements on the early fall in the velocity of sarcomere shortening indicates that an internal resistance increases near the peak of contraction. The complex shape of the sarcomere's complete force-velocity relation, with lengthening motions in particular, was consistent with an idealized model of cross-bridge cycling. The sarcomere's resistance to stretch is high at low velocity, but it diminishes to reveal yielding at larger velocities. Relative to tension, the resistance to yielding does not decrease during relaxation, and it may actually increase. The decay of isometric tension after a controlled stretch also slows during relaxation. Consequently, cycling slows in those cross-bridges which form (or persist but produce less force) later in contraction. Changes in cross-bridge properties may restrict sarcomere shortening, prolong activation, but promote a disequilibrium which favors rapid relaxation in cardiac muscle.

Animals↗

Sex differences in myocardial contractility in the rat.

We examined the intrinsic contractile performance of papillary muscles removed from the left ventricle of male and female Wistar rats. Muscles were studied isometrically and isotonically, stimulated at 0.1 Hz, perfused with Tyrode's solution having an external calcium concentration = 2.4 and maintained at 30 degrees C. In addition, we examined muscle response to changes in external calcium, added norepinephrine or verapamil and alterations in contraction frequency. No significant change in peak isometric development tension was observed between male and female preparations. However, muscles from male rats showed a significantly greater isometric time-to-peak tension and time to 1/2 relaxation with a depression of both the maximum rate of tension rise and maximum rate of tension decay. Isotonically, although peak shortening showed no difference between male and female preparations, the maximum velocities of shortening and relaxation were significantly depressed in muscles from male rats. Muscles from male animals also displayed significant prolongation of the time-to-peak shortening and time-to-peak velocity of shortening. These differences in papillary muscle performance were found over a wide range of muscle lengths, stimulus frequencies and bath concentrations of calcium, norepinephrine and verapamil. Thus differences in the intrinsic contractile performance between papillary muscle from male and female rats have been characterized.

Animals↗

Inhibitory action of hypertonic urea solution on the potassium contracture of the heart ventricular muscle.

Effects of hypertonic urea solution on potassium contracture were investigated in a bullfrot ventricular strip. In a medium of three times hypertonic urea, the contracture induced by 100 mM potassium solution was markedly inhibited whereas the twitch contraction was augmented in the hypertonic urea solution. The extent, as well as the time course, of the membrane depolarization produced by high potassium solution was essentially identical in both isotonic and hypertonic conditions. Endogeneous catecholamine does not seem to participate in this inhibition since the treatment with propranolol did not modify the results. Thus, the possibility of the well-known catecholamine-induced inhibition of potassium contracture can be excluded. The myocardial contractility was never suppressed, or even augmented, at this stage of urea perfusion although a prolonged hypertonic urea perfusion gradually suppressed the contractility. It was suggested that hypertonic urea exerts its negative inotropic action on the potassium contracture independently of its positive inotropism on the twitch contraction by accelerating the uptake of the activator calcium ion to some undefined intracellular sites.

Action Potentials↗

Ultrastructural correlates of inner ear sensory cell shortening.

Ultrastructural analysis was performed on isolated outer hair cells of the inner ear, to further investigate the mechanisms involved in cell shortening. Hair cells were fixed either in their presumed normal, 'relaxed', state or after application of solutions containing high concentrations of potassium to induce shortening, or 'contraction'. Ultrastructural analysis showed that shortened outer hair cells had a more undulated, or wavy, cell membrane as compared to normal cells. Outer hair cell shortening was not accompanied by the formation of vacuoles in the cytoplasm or appreciable swelling of the subsurface cisternae. The results further support the idea that a contractile apparatus associated with the lateral wall could be responsible for outer hair cell motility, and that the mechanism resembles that involved in smooth muscle contraction.

Animals↗

Effect of experimental muscle pain on motor unit firing rate and conduction velocity.

The aim of this human study was to investigate the relationship between experimentally induced muscle pain intensity (i.e., amount of nociceptive activity) and motor unit (MU) firing decrease and MU conduction velocity (CV). In 12 healthy subjects, nociceptive afferents were stimulated in the right tibialis anterior muscle by three intramuscular injections of hypertonic saline (0.2, 0.5, and 0.9 ml) separated by 140 s. The subjects performed six isometric contractions (20 s long) at 10% of the maximal voluntary contraction during the experimental muscle pain. The same set of six contractions was performed without any infusion before the painful condition on the right leg. The procedure was repeated for the left leg with infusion of isotonic (nonpainful) saline. Intramuscular and surface electromyographic (EMG) signals were collected to assess MU firing rate and CV. The firing rate of the active MUs [range: 7.4-14.8 pulses/s (pps)] did not change significantly in the three control conditions (without infusion for the right and left leg and with infusion of isotonic saline in the left leg). There was, on the contrary, a significant decrease (on average, mean +/- SE, 1.03 +/- 0.21 pps) of the firing rates during the painful condition. Moreover, MU firing rates were inversely significantly correlated with the subjective scores of pain intensity. Single MU CV was 3.88 +/- 0.03 m/s (mean +/- SE, over all the MUs) with no statistical difference among any condition, i.e., the injection of hypertonic saline did not alter the muscle fiber membrane properties of the observed MUs. Progressively increased muscle pain intensity causes a gradual decrease of MU firing rates. This decrease is not associated with a change in MU membrane properties, indirectly assessed by CV. This study demonstrates a central inhibitory motor control mechanism with an efficacy correlated to the nociceptive activity.

Action Potentials↗