Abstract:SUMMARY1. In chloralose-anaesthetized cats, the impulse activity of single afferent units conducting at less than 30 m sol and having receptive fields in the triceps surae muscle or the calcaneal tendon, was recorded from thin filaments of the dorsal roots L7 and SI. The receptive fields of the units were tested with a variety of graded natural stimuli (local pressure, stretch, contractions, temperature changes). In addition, the algesic agent bradykinin was injected into the receptive fields, but the sensitiv… Show more
“…These values were about the half those of the cutaneous thin fiber receptors measured by our group with the same instruments in vivo and in vitro (Suzuki et al 2002;Takahashi et al 2003). The existence of thin-fiber receptors with low and high mechanical threshold in the muscle has been reported (Mense and Meyer 1985). However, the distribution of the mechanical thresholds was continuous in the present study and no natural segregation into subgroups was observed.…”
Section: Thin-fiber Receptor Recording In Muscle-nerve Preparation Incontrasting
Taguchi, Toru, Jun Sato, and Kazue Mizumura. Augmented mechanical response of muscle thin-fiber sensory receptors recorded from rat muscle-nerve preparations in vitro after eccentric contraction. J Neurophysiol 94: 2822Neurophysiol 94: -2831Neurophysiol 94: , 2005 doi:10.1152/jn.00470.2005. Unaccustomed strenuous exercise, especially that from eccentric muscular work, often causes muscle tenderness, which is a kind of mechanical hyperalgesia. We developed an animal model of delayed-onset muscle soreness (DOMS) from eccentric muscular contraction (ECC) in rats and demonstrated the existence of muscle tenderness by means of behavioral pain tests and c-Fos protein expression in the spinal dorsal horn. The purpose of the present study was to examine whether the sensitivities of muscle thin-fiber sensory receptors to mechanical, chemical, and thermal stimuli were altered after repetitive ECC in a rat model of DOMS. ECC was caused in the animals by electrical stimulation of the common peroneal nerve innervating the extensor digitorum longus muscle (EDL) while the muscle was being stretched. Activities of single thin-fiber receptors (sensitive to pressure but insensitive to stretch, with conduction velocity slower than 2.0 m/s) were recorded from muscle (EDL)-nerve preparations in vitro 2 days after ECC when mechanical hyperalgesia was at its peak. The mechanical threshold of thin-fiber receptors was found to be very much lower in the ECC preparations than in the nontreated control (CTR) [median 65.4 mN (interquartile range [IQR]; 46.6 -122.0 mN) in the CTR preparation vs. 38.2 mN (IQR; 26.8 -55.8 mN) in the ECC, P Ͻ 0.001]. In addition, the total number of evoked discharges during a ramp mechanical stimulus, taken as an index of the magnitude of the mechanical response, nearly doubled in the ECC preparations compared with the CTR [24.7 spikes (IQR; 14.2-37.1 spikes) in the CTR preparation vs. 54.2 spikes (IQR; 24.3-89.0 spikes) in the ECC, P Ͻ 0.001]. In contrast, the numbers of discharges induced by chemical (pH 5.5, lactic acid, adenosine triphosphate, and bradykinin) and thermal (cold and heat) stimuli were not different between the two preparations. These results suggest that augmentation of the mechanical response in muscle thin-fiber sensory receptors might be related to the muscle tenderness in DOMS after ECC.
“…These values were about the half those of the cutaneous thin fiber receptors measured by our group with the same instruments in vivo and in vitro (Suzuki et al 2002;Takahashi et al 2003). The existence of thin-fiber receptors with low and high mechanical threshold in the muscle has been reported (Mense and Meyer 1985). However, the distribution of the mechanical thresholds was continuous in the present study and no natural segregation into subgroups was observed.…”
Section: Thin-fiber Receptor Recording In Muscle-nerve Preparation Incontrasting
Taguchi, Toru, Jun Sato, and Kazue Mizumura. Augmented mechanical response of muscle thin-fiber sensory receptors recorded from rat muscle-nerve preparations in vitro after eccentric contraction. J Neurophysiol 94: 2822Neurophysiol 94: -2831Neurophysiol 94: , 2005 doi:10.1152/jn.00470.2005. Unaccustomed strenuous exercise, especially that from eccentric muscular work, often causes muscle tenderness, which is a kind of mechanical hyperalgesia. We developed an animal model of delayed-onset muscle soreness (DOMS) from eccentric muscular contraction (ECC) in rats and demonstrated the existence of muscle tenderness by means of behavioral pain tests and c-Fos protein expression in the spinal dorsal horn. The purpose of the present study was to examine whether the sensitivities of muscle thin-fiber sensory receptors to mechanical, chemical, and thermal stimuli were altered after repetitive ECC in a rat model of DOMS. ECC was caused in the animals by electrical stimulation of the common peroneal nerve innervating the extensor digitorum longus muscle (EDL) while the muscle was being stretched. Activities of single thin-fiber receptors (sensitive to pressure but insensitive to stretch, with conduction velocity slower than 2.0 m/s) were recorded from muscle (EDL)-nerve preparations in vitro 2 days after ECC when mechanical hyperalgesia was at its peak. The mechanical threshold of thin-fiber receptors was found to be very much lower in the ECC preparations than in the nontreated control (CTR) [median 65.4 mN (interquartile range [IQR]; 46.6 -122.0 mN) in the CTR preparation vs. 38.2 mN (IQR; 26.8 -55.8 mN) in the ECC, P Ͻ 0.001]. In addition, the total number of evoked discharges during a ramp mechanical stimulus, taken as an index of the magnitude of the mechanical response, nearly doubled in the ECC preparations compared with the CTR [24.7 spikes (IQR; 14.2-37.1 spikes) in the CTR preparation vs. 54.2 spikes (IQR; 24.3-89.0 spikes) in the ECC, P Ͻ 0.001]. In contrast, the numbers of discharges induced by chemical (pH 5.5, lactic acid, adenosine triphosphate, and bradykinin) and thermal (cold and heat) stimuli were not different between the two preparations. These results suggest that augmentation of the mechanical response in muscle thin-fiber sensory receptors might be related to the muscle tenderness in DOMS after ECC.
“…Small-diameter afferents from muscle, tendons (Mense and Meyer, 1985) and joints (Schiable and Schmidt, 1983) have been studied in the cat and consist of a mixture of low-and high-threshold units, with the majority of C-fibers falling into the latter category. C-fibers terminate in the superficial dorsal horn (Light and Perl, 1979) where many intemeurons are excited directly or indirectly by the arrival ofa volley in C-afferents (Fitzgerald and Wall, 1980;Woolf and Fitzgerald, 1983).…”
Changes in the excitability of the hamstring flexor withdrawal reflex produced by conditioning stimuli applied to C-afferent fibers of different origins have been examined in the decerebrate spinal rat. In the absence of conditioning stimuli, the flexor reflex elicited by a standard suprathreshold mechanical stimulus to the toes is stable when tested repeatedly for hours. Three categories of conditioning stimuli have been used in an attempt to modify the excitability of the flexor reflex; electrical stimulation of a cutaneous (sural) nerve or a muscle (gastrocnemiussoleus) nerve at C-fiber strength, the application of mustard oil, a chemical irritant that activates chemosensitive C-afferents, to the skin or injected intramuscularly and intraarticularly; and the indirect activation of high-threshold muscle afferents by fused tetanic contractions of the tibia1 muscles. Conditioning stimuli of an intensity sufficient to activate C-afferent fibers result in a heterosynaptic facilitation of the flexor motoneuronal response to the standard test input, which lasts from 3 min to more than 3 hr, depending on the stimulus and the C-afferents activated. Pretreatment of the sciatic nerve with the C-fiber neurotoxin capsaicin abolishes all the postconditioning facilitations, which is an indication that it is likely that it is C-afferents that are primarily responsible for the facilitatory effects of the conditioning stimuli, although some A delta afferents may contribute. Capsaicin pretreatment does not modify the reflex response to the test stimulus. The most prolonged increase in the excitability of the flexor reflex resulted from intraarticular injections of 5 11 mustard oil. Using the subsequent injection of lignocaine intraarticulary, it was found that the prolonged facilitation of the reflex is triggered by the afferent input generated by the conditioning stimulus and does not require an ongoing input for its maintenance. These results indicate that there is a spectrum of central changes in the stimulus response relations of the spinal cord resulting from the activation of C-fibers of different origins. The prolonged duration of some of these changes means that the peripheral activation of C-afferents will modify the functional response of the spinal cord to other inputs applied long after the conditioning input, and this may be responsible for some of the sensory and motor alterations found after peripheral tissue injury.Unmyelinated C-fibers constitute the majority of afferents in the dorsal roots of all mammalian species (Willis and Coggeshall, 1978). In the rat, only cutaneous C-fibers have been studied, and most of these are activated exclusively by intense me-
“…A major proportion of small diameter group III and IV muscle afferents are sensitive to noxious mechanical and chemical stimuli (Mense and Meyer 1985;Mense and Stahnke 1983). According to the pain adaptation model (Lund et al 1991), the activity of thin nociceptive muscle afferents facilitates inhibitory pathways when the muscle acts as an agonist and facilitates excitatory pathways during antagonist activity.…”
. Effect of experimental muscle pain on motor unit firing rate and conduction velocity. J Neurophysiol 91: 1250 -1259, 2004. First published November 12, 2003 10.1152/jn.00620.2003. 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 Ϯ SE, 1.03 Ϯ 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 Ϯ 0.03 m/s (mean Ϯ 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.
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