Unilateral application of an inflammatory irritant to the rat temporomandibular joint region produces bilateral modulation of the jaw-opening reflex

The aim of this study was to determine the effect of unilateral acute inflammation of craniofacial deep tissues on the ipsilateral and contralateral jaw-opening reflex (JOR). The effects of mustard oil (MO), injected into the temporomandibular joint region, were tested on the JOR recorded in the digastric muscle and evoked by low-intensity electrical stimulation of the ipsilateral and contralateral inferior alveolar nerve in anesthetized rats. The MO injection induced a long-lasting suppression of the amplitude of both ipsilaterally and contralaterally evoked JOR, although the latency and duration of the JOR were unaffected. The suppressive effect was more prominent for the contralaterally evoked JOR, and observed even when background activity in the digastric muscle was increased by the MO injection. The results indicate that changes in the JOR amplitude following MO injection do not simply reflect alterations in motoneuronal excitability, and suggest that inflammation of deep craniofacial tissues modulates low-threshold sensory transmission to the motoneurons.     

Suppressive effect of vagal afferents on the activity of the trigeminal spinal neurons related to the jaw-opening reflex in rats: involvement of the endogenous opioid system

The purpose of the present study is to test the hypothesis that via the endogenous pain control system, vagal afferent input modulates the activity of the trigeminal spinal nucleus oralis (TSNO) related to the tooth pulp (TP)-evoked jaw-opening reflex (JOR). Extracellular single-unit recordings were made from 36 TSNO units responding to TP electrical stimulation with a constant temporal relationship to a digastric electromyogram (dEMG) signal in 26 pentobarbital-anesthetized rats. The activity of 36 TSNO neurons and the amplitude of the dEMG increased proportionally during 1.0–3.5 times the threshold for JOR. Some of these neurons (4 out of 5) were also excited by chemical stimulation (bradykinin, 1–2 μl, 1 mM) of TP. In 31 out of 36 TSNO neurons (86%), their activities during tooth pulp stimulation were suppressed by conditioning stimulation of the right vagus nerve. The suppressive effect of vagal afferent stimulation occurred at conditioning-test intervals of 20–150 ms after the onset of the stimulation, and its maximal suppressive effect occurred at approximately 50 ms. The mean time course of this suppressive effect paralleled that of the dEMG. After administration of naloxone (0.5 and 1.0 mg/kg, i.v.), an opiate receptor blocker, the suppressive effect on the activity of TSNO neurons (6 out of 8) was significantly attenuated at the conditioning-test interval of 50 ms compared to the control (p < 0.01). These results suggested that vagal afferent input inhibits nociceptive transmission in the TSNO related to TP-evoked JOR and this inhibitory effect may occur via the endogenous opioid system in rats.     

Study of the neural basis of striatal modulation of the jaw-opening reflex

Previous experimental data from this laboratory demonstrated the participation of the striatum and dopaminergic pathways in central nociceptive processing. The objective of this study was to examine the possible pathways and neural structures associated with the analgesic action of the striatum. The experiments were carried out in rats anesthetized with urethane. The jaw-opening reflex (JOR) was evoked by electrical stimulation of the tooth pulp of lower incisors and recorded in the anterior belly of the digastric muscles. Intrastriatal microinjection of apomorphine, a nonspecific dopamine agonist, reduced or abolished the JOR amplitude. Electrolytic or kainic acid lesions, unilateral to the apomorphine-injected striatum, of the globus pallidus, substantia nigra pars reticulata, subthalamic nucleus and bilateral lesion the rostroventromedial medulla (RVM), blocked the inhibition of the JOR by striatal stimulation. These findings suggest that the main output nuclei of the striatum and the RVM may be critical elements in the neural pathways mediating the inhibition of the reflex response, evoked in jaw muscles by noxious stimulation of dental pulp.     

Intracellular responses of raphe magnus neurons during the jaw-opening reflex evoked by tooth pulp stimulation

Neurons in the nucleus raphe magnus (RM) may play an important role in the modulation of nociception. To determine how RM neurons are activated during a nociceptive reflex, the intracellular responses of raphe neurons were studied during the jaw-opening reflex (JOR) elicited by tooth pulp shock in lightly anesthetized cats. Tooth pulp stimulation produces reflex EMG activation of the digastric muscle at a latency of 7-11 ms, resulting in jaw opening. Tooth pulp shock that elicits the JOR also produces an EPSP in a subset of raphe neurons. This EPSP consists of an early small depolarization that occurs at a latency of 10-15 ms followed by a larger depolarization at a latency of 20-60 ms. In all cases the latency to EPSP is longer than the latency to digastric EMG onset. Electrical stimulation of the 4 paws elicits oligosynaptic EPSPs in the same cells at a latency of 16-20 ms. Electrical train stimulation of the midbrain periaqueductal gray region (PAG) suppresses the JOR. Single shock stimulation at the same PAG sites that suppress the JOR evokes monosynaptic EPSPs in the large majority of raphe neurons recorded. In all cases, the threshold for EPSP is below the threshold for suppression of the JOR. The EPSP amplitude is a direct function of PAG stimulus intensity and there is temporal summation of EPSPs evoked by paired PAG shocks. At condition-test intervals of 40-90 ms, train stimulation of PAG suppresses the tooth pulp-evoked EPSP in raphe neurons. The threshold for EPSP suppression occurs at a PAG stimulation intensity below that required for suppression of the JOR. The present findings provide evidence that RM neurons may play an important role in the modulation of the tooth pulp-evoked JOR, but only after the initial withdrawal reflex has occurred.     

Inhibition of the tooth pulp-evoked jaw opening reflex by stimulation of raphe nuclei in the rat

Effects of conditioning electrical stimuli applied to nucleus raphe dorsalis (NRD), nucleus raphe medialis (NRMed), and nucleus raphe magnus (NRMag) on the jaw opening reflex (JOR) were compared using Wistar rats. Activity of the digastric musle after tooth-pulp stimulation was used as an index of the magnitude of the JOR which was considered a noxious response. The JOR was suppressed to about 30 to 40% of the control after a single-pulse stimulation of the NRD, NRMed, or NRMag. None of these raphe-induced suppressions was reversed by naloxone, a specific opiate antagonist, suggesting that these effects are not related to the endogenous opiate system. By contrast, 50-Hz electrical pulse trains of 0.1-ms duration for 1 min applied to the NRD and NRMed suppressed the reflex to about 30% of the control, an effect sustained for 10 to 20 min, whereas this stimulation of the NRMag suppressed the reflex to about 20% of the control and the suppressive effects were maintained for more than 30 min. In these cases, NRMed- and NRd-induced suppression was partially antagonized and the NRMag-induced suppression was almost completely antagonized by naloxone, suggesting that this long-term suppression, especially that induced by NRMag, is closely related to endogenous opiates. These results show that raphe-induced suppression may be produced by complex actions of a short-term neural mechanism and a long-term opiate-related mechanism.     

Facilitation of the jaw reflexes by stimulation of the red nucleus in the rat

The effects of the red nucleus (RN) stimulation on the jaw-opening reflex (JOR) and the masseteric monosynaptic reflex (MMR) were studied in anesthetized rats. The JOR was evoked by electrical stimulation of the inferior alveolar nerve. The MMR was evoked by electrical stimulation of the mesencephalic trigeminal nucleus. The JOR and the MMR were recorded as electromyographic responses of the anterior belly of the digastric and the masseter muscles, respectively. The conditioning electrical stimulation of the RN facilitated both the JOR and the MMR bilaterally. The facilitatory effect on the JOR was much larger than that on the MMR. Additionally, microinjection of monosodium glutamate into the RN also elicited facilitation of the JOR and the MMR. The results suggest the RN plays an important role in reflex control of jaw movements.     

Site and action of electroacupuncture-induced effects on the rat jaw-opening reflex

The aims of the present study were to identify the specificity of the pain-relieving effects of electroacupuncture (EA) stimulation by comparing its effects on the jaw-opening reflex evoked by noxious and nonnoxious inputs, and to identify the site of action of EA in the jaw-opening reflex arc. I examined the EA effects on three responses involved in the jaw-opening reflex arc using Wistar albino rats: (i) the jaw-opening reflex to stimulation of the orofacial region, (ii) evoked responses in a secondary neuron site, and (iii) jaw-opening responses to stimulation of the secondary neuron site. EA stimulation almost suppressed the responses involved in the pathway of the jaw-opening reflex evoked by high-threshold afferent fibers, whereas it scarcely affected those in the pathway of the reflex evoked by low-threshold afferent fibers. From a comparison of the degree of suppression of the three responses, I suggest that EA suppression of the jaw-opening reflex was induced chiefly on the activity of the spinal trigeminal nucleus. In conclusion, it can be said that EA stimulation is almost selectively effective on the activity of the secondary neuron site involved in the jaw-opening reflex evoked by noxious input.     

Effect of cervical sympathetic nerve stimulation on nociceptive jaw opening reflex in the cat

In anaesthetized cats the electrical stimulation of the cervical sympathetic nerve induces a considerable increase (150-250%) in the nociceptive jaw opening reflex elicited by tooth pulp stimulation (JOR). The mechanisms potentially responsible for this effect are discussed and the possibility is suggested, that a portion of the response is due to a modulatory action exerted by the sympathetic on the nociceptive input.     

Modulation of the jaw-opening reflex by peripheral electrical stimulation

Modulation of the jaw-opening reflex (JOR) by peripheral electrical stimulation was studied in the rat. The JOR was evoked by electrical stimuli delivered to the tongue, infraorbital nerve, or tooth pulp chamber, and single-pulse conditioning stimuli were delivered to the forelimb, hind limb, or tail. Threshold current for eliciting the JOR was modulated in a biphasic manner with facilitation when the delay between conditioning and test stimuli was short (peaking at 10 to 15 ms) and inhibition at longer intervals (peaking at 40 to 60 ms). Modulation was similar for all peripheral conditioning sites and was not affected by Fentanyl, naloxone, or picrotoxin. Thus, the modulation of the JOR by single-pulse peripheral electrical stimulation is a widespread, nonsegmental phenomenon, and is probably not associated with the endogenous opiate system. Data collected during the course of this study call into question the usefulness of the JOR elicited by electrical stimulation in the rat incisor tooth pulp chamber as a pain model.     

Nerve growth factor injection into semispinal neck muscle evokes sustained facilitation of the jaw-opening reflex in anesthetized mice -- possible implications for tension-type headache

Nociceptive input from neck muscles probably plays a role in the pathophysiology of tension-type headache. In order to elaborate an animal model, the impact of noxious input from neck muscles on orofacial sensorimotor processing was investigated by electrophysiological means in anesthetized mice. Group IV muscle afferents of the semispinal neck muscle were excited by local injection of nerve growth factor (NGF, 0.8 microM, 20 microl). Orofacial sensorimotor processing was monitored by the jaw-opening reflex (JOR) elicited by electric tongue stimulation. After unilateral NGF injection into the right neck muscle (n = 10), JOR integral (+89%) and duration (+9%) increased and latency decreased (-5%) for at least 1 h. Bilateral injection of NGF (n = 10) into neck muscles induced an increase of JOR integral (+111%) and duration (+20%) and a reduction of latency (-9%). This facilitation of the JOR lasted for at least 90 min without any downward drift (n = 5). Electric JOR threshold diminished after NGF injection. After intramuscular injection of isotonic saline into the right semispinal neck muscle (20 microl), the JOR remained unchanged (n = 10). Local NGF injection into neck muscles evoked noxious input to the brainstem that induced a sustained central facilitation of the JOR for more than 1 h. This long-term facilitation of orofacial sensorimotor processing by a singular NGF injection possibly reflects plastic changes of nociceptive synaptic processing that may be involved in the pathophysiology of headache.     

Differentiation of nociceptive- from stress-induced modulatory influences on human reflexes

This paper describes a new protocol that addresses the question of whether, in human experiments, modulatory effects of remote nociceptive conditioning stimuli on reflex responses are mediated by the stress induced by the conditioning stimuli. The protocol has been illustrated by a study into the effect of a remote nociceptive conditioning stimulus on an inhibitory jaw reflex. Electromyograms were recorded from an active masseter muscle and inhibitory reflexes were evoked by applying electrical stimuli to the upper lip. This protocol utilised the application of discrete electrical conditioning stimuli applied to the sural nerve prior to the test stimulus. A preliminary experiment determined that the optimal interval between the conditioning and test stimuli, which produced modulatory effects was 100 ms. In the definitive study, computer software was used to deliver control and conditioned sweeps in a double-blind randomised sequence. This resulted in a "stress-equal" protocol in which the level of stress would be the same for both control and conditioned sweeps. Therefore any observed modulatory effects on the reflexes could not have been wholly secondary to stress. This protocol could be adapted to the study of the modulation of other reflexes or evoked sensations by nociceptive conditioning stimuli.     

Influence of stimulation of the central gray matter on low- and high-threshold startle reflexes

Influences of the periaqueductal gray matter (PAG) stimulation on high-threshold jaw opening reflex (JOR) evoked by tooth pulp stimulation and on two functional types of startle reflexes were studied in chloralose anesthetized cats; the startle reflexes were high-threshold ones evoked by intense peripheral nerve stimulation (spino-bulbo-spinal, SBS, reflex) and low-threshold ones evoked by tactile stimuli (tactile spino-reticulo-spinal, TSRS, reflex). Stimulation of the majority of PAG sites induced considerable inhibition of JOR as well as profound depression of SBS-reflexes and moderate depression of TSRS-reflexes. Some PAG sites were found to exert a facilitatory action on the latter reflex. Effects of PAG stimulation were short-term (hundred ms) and/or long-lasting (minutes). Possible mechanisms of these effects are discussed.     

Striatal modulation of the jaw opening reflex

The effect of striatal electrical and chemical conditioning stimulation (L-glutamate 80-160 nmoles/0.5 microl) on the jaw opening reflex (JOR) was studied in Sprague-Dawley male rats anesthetized with urethane. The JOR was evoked by stimulation of the tooth pulp of lower incisors. This response was suppressed by transection of the dental root, which indicates according with the bibliography, a specific activation of the pulp nerves. Three type of responses were obtained on the evoked JOR by conditioning stimulation of the striatum; being the main one the suppression of the reflex elicited by tooth pulp activation. A second type of response was an increase of the tooth-JOR amplitude. This effect was observed more frequently with glutamate stimulation rather than with electrical activation of the striatum. A third response was observed with chemical stimulation but not by electrical stimulation of the striatum. This was a triphasic response which consisted in an increase followed by an inhibition and a late increase of the tooth-JOR amplitude. A biphasic effect, an increase prior to a decrease of the JOR amplitude, was also recorded with a minor frequency. The distribution of effective sites for electrical and chemical stimulation within the striatum are mainly similar located in the rostral aspect of the nucleus, with the inhibitory sites in the middle of the nucleus and intermingled with the excitatory ones. The complex responses (tri/biphasic) were observed ventrally and caudally in the nucleus. On the basis of the results mentioned above, one could assume that the striatum is related to the modulation of the JOR evoked probably by nociceptive stimulation. However, activation of other type of fibers could not be ruled out.     

Volume expansion suppresses the tooth-pulp evoked jaw-opening reflex related activity of trigeminal neurons in rats

The aim of the present study is to clarify whether physiological stimulation of vagal afferents modulates the activity of the trigeminal spinal nucleus oralis (TSNO) neurons related to the tooth-pulp (TP)-evoked jaw-opening reflex (JOR) in pentobarbital-anesthetized rats. The activity of TSNO neurons and the amplitude of digastric electromyogram (dEMG) increased proportionally during 1.0-3.5 times the threshold for JOR. The amplitude of the dEMG of 14 out of 17 rats was suppressed by physiological stimulation of vagal afferents after intravenous infusion of Ficoll. Out of 23, 18 TSNO unit activities in 14 rats were also suppressed by Ficoll infusion. This suppressive effect of unit and dEMG activities returned to the control level within 25 min. After administration of naloxone (0.5 and 1.0 mg/kg, i.v.) the suppressive effect of Ficoll infusion on the activity of TSNO neurons (5/7) was significantly attenuated compared to the control (p < 0.01). The inhibition TSNO neuronal and dEMG activities by Ficoll infusion was volume-dependent in a range of 5-10% of total blood volume. Furthermore, right vagus nerve ligation greatly inhibited the suppressive effect of Ficoll-induced TSNO activity. These results therefore suggest that low-pressure cardiopulmonary baroreceptors whose afferents travel in the vagus nerve inhibit the pulpal nociceptive transmission.     

Iontophoretic analysis of the pharmacologic mechanisms responsible for initiation and modulation of trigeminal motoneuronal discharge evoked by intra-oral afferent stimulation

This study investigated the effects of iontophoretic application of excitatory amino acid (EAA) and norepinephrine (NE) agonists and antagonists on synaptic transmission to individual jaw-opener motoneurons (digastric) during activation of the jaw-opening reflex (JOR) evoked by stimulation of either fibers within the oral mucosa (OM), or tooth-pulp (TP). During both OM and TP stimulation, kynurenic acid (KYN), a wide-spectrum EAA antagonist, suppressed jaw-opener motoneuron discharge. Application of APV, an NMDA receptor antagonist, also suppressed motoneuron discharge evoked by TP stimulation, but produced minimal effects on motoneuron discharge evoked by OM stimulation. These data suggest a role of EAA in mediating synaptic transmission from last-order interneurons to jaw-opener motoneurons during the jaw-opening reflex evoked by intra-oral stimulation. Iontophoretic application of NE produced dual effects (facilitation or suppression) on motoneuronal discharge evoked by OM or TP stimulation. The effects were not related to the mode of motoneuronal activation. Iontophoretic application of the alpha 1 agonist, phenylephrine, facilitated motoneuronal discharge. In contrast, application of the alpha 2 agonist, clonidine, suppressed motoneuronal discharge during intra-oral stimulation. These effects were antagonized by prior iontophoretic application of the alpha 1 antagonist, prazosin, or the alpha 2 antagonist, yohimbine, respectively. In those cells in which the predominant effect of NE application on synaptic transmission was either facilitation or suppression of motoneuronal discharge, prior iontophoretic application of prazosin or yohimbine, respectively, antagonized the effects of NE application. These data suggest that NE can modulate synaptic transmission to jaw-opener motoneurons evoked by intra-oral stimulation via activation of alpha 1 or alpha 2 adrenoreceptors on trigeminal motoneurons.     

Potentiation of fentanyl suppression of the jaw-opening reflex by transcranial electrical stimulation

Stinus et al. [L. Stinus, M. Auriacombe, J. Tignol, A. Limoge, M. Le Moal, Transcranial electrical stimulation with high frequency intermittent current (Limoge's) potentiates opiate-induced analgesia: blind studies, Pain, 42 (1990) 351–363.] observed that transcranial electrical stimulation (TCES) with high-frequency intermittent current potentiated opiate-induced analgesia using the tail-flick test. In unanesthetized, chronic preparations, electrical stimulation (0.5 Hz) of the lower incisor pulp of rats elicits a short-(6 ms) and a long-latency (12–18 ms) jaw-opening reflex (JOR) without any evidence of aversive behavior [J. Azérad, F. Fuentes, I. Lendais, A. Limoge, B. Pollin, Methods for selective tooth pulp stimulation in acute and chronic preparations in rats, J. Physiol., 406 (1988) 3P.]. Fentanyl increases thresholds of both reflexes and transiently suppresses the long-latency JOR. We then decided to look at the influence of TCES on both drug-induced mean of maximal threshold variation (MMTV) and duration of JOR suppression period. These parameters have been investigated in 43 Wistar rats with or without TCES administered for 3 h before the drug injection and throughout the testing period. TCES alone has no effect. In contrast, it significantly increases the duration of the reflex suppression period (149 ± 5% vs. control, P < 0.001) while fentanyl-increased reflex thresholds remain unchanged. The fentanyl-induced JOR suppression period returns to the control values 2 days later. When a second 3-h TCES session is delivered 2 or 4 days after the first TCES session, a similar increase of this suppression period is observed. Moreover, 2 days after a second TCES session, an increase of the duration of the fentanyl-induced JOR suppression period is systematically observed. In contrast, a 6-h TCES session never induces such effects. These results confirm a potentiating effect of TCES on opioid action and demonstrate the value of repeated TCES sessions.     

Differential Effects of a Distant Noxious Stimulus on Hindlimb Nociceptive Withdrawal Reflexes in the Rat

Recent studies indicate that the nociceptive withdrawal reflexes to individual muscles are evoked by separate reflex pathways. The present study examines whether nociceptive withdrawal reflexes to different muscles are subject to differential supraspinal control in rats. A distant noxious stimulus was used to activate a bulbospinal system which selectively inhibits 'multireceptive' neurons (i.e. neurons receiving excitatory tactile and nociceptive inputs) in the dorsal horn of the spinal cord. Withdrawal reflexes, recorded with electromyographic techniques in single hindlimb muscles, were evoked by standardized noxious pinch. Thirty-seven rats, anaesthetized with halothane and nitrous oxide, were used. Whereas withdrawal reflexes to the extensor digitorum longus and brevis, tibialis anterior and biceps posterior muscles were strongly inhibited, reflexes to interossei muscles were potentiated during noxious pinch of the nose. Reflexes to peronei muscles were not significantly changed. The effects on the reflexes usually had an onset latency of <0.5 s and outlasted the conditioning stimulation by up to 2 s. The monosynaptic la reflex to the deep peroneal nerve, innervating dorsiflexors of the digits and ankle, was not significantly changed during noxious pinch of the nose. Hence, the inhibitory effects on the hindlimb withdrawal reflexes induced by the conditioning stimulation were presumably exerted on reflex interneurons. It is concluded that nociceptive withdrawal reflexes to different hindlimb muscles are differentially controlled by descending pathways activated by a distant noxious stimulus. The results support our previous conclusion that there are separate nociceptive withdrawal reflex pathways to different hindlimb muscles.     

Effect of pinching-evoked pain on jaw-stretch reflexes and exteroceptive suppression periods in healthy subjects.

OBJECTIVE: To investigate the influence of conditioning cutaneous nociceptive inputs by a new "pinch" model on the jaw-stretch reflex and the exteroceptive suppression periods (ES1 and ES2) in jaw muscles. METHODS: The jaw-stretch reflex was evoked with the use of a custom-made muscle stretcher and electrical stimuli were used to evoke an early and late exteroceptive suppression period (ES1 and ES2) in the jaw-closing muscles. Electromyographic (EMG) activity was recorded bilaterally from the masseter and temporalis muscles. These brainstem reflexes were recorded in 19 healthy men (28.8+/-1.1 years) during three different conditions: one painful clip applied to the earlobe; one painful clip applied to the nostril, and four painful clips applied simultaneously to the earlobe, nostril, eyebrow, and lower lip. Pain intensity induced by the application of the clips was scored continuously by the subjects on a 100mm visual analogue scale (VAS). RESULTS: The highest VAS pain scores were evoked by placement of four clips (79+/-0.5mm). There was no significant modulation of the jaw-stretch reflex (ANOVAs: P=0.929), the ES1 (P=0.298) or ES2 (P=0.082) in any of the three painful conditions. CONCLUSIONS: Intense and tonic cutaneous pain could be elicited by this new "pinch" pain model; however, there was no significant modulation on either excitatory or inhibitory brainstem reflex responses. SIGNIFICANCE: The novel observation that high-intensity pinch stimuli applied to the craniofacial region fail to modulate two different brainstem reflexes is in contrast to other experimental pain studies documented facilitation of the jaw-stretch reflexes or inhibition of exteroceptive suppression periods. The clinical implication of the present findings is that only some craniofacial pain conditions could be expected to show perturbation of the brainstem reflex responses.     

Nucleus accumbens facilitates nociception

We have previously demonstrated an opioid link in nucleus accumbens (NAc) that mediates antinociception produced by a novel ascending pain modulation pathway. For example, noxious stimulation induces heterosegmental antinociception that is mediated by both mu- and delta-opioid receptors in NAc. However, spinal intrathecal administration of the mu-receptor agonist [d-Ala², N-Me-Phe⁴,Gly⁵-ol]-enkephalin (DAMGO) also induces heterosegmental antinociception. The aim of the present study in the rat was to identify the intra-NAc opioid receptors that mediate the antinociceptive effects of spinally administered DAMGO and also to determine the effect of NAc efferent activity on nociception. Intra-NAc administration of either the mu-opioid receptor antagonist Cys²,Tyr³, Orn⁵,Pen⁷amide (CTOP) or the delta-opioid receptor antagonist naltrindole blocked the antinociceptive effect of spinally administered DAMGO on the jaw-opening reflex (JOR). Injection of quaternary lidocaine (QX-314) attenuated the JOR, suggesting that the output of NAc is pronociceptive. In support of this, intra-NAc injection of the excitatory amino acid agonist kainate enhanced the JOR. Thus, it is possible to modulate activity in NAc to bidirectionally attenuate or enhance nociception, suggesting a potential role for NAc in setting nociceptive sensitivity.     

Examination of the afferent fiber responsible for the suppression of jaw-opening reflex in heat, cold, and manual acupuncture stimulation in rats

The possible afferent fibers that participate in the inhibition of jaw-opening reflex (JOR) were examined using selective conduction blockade by topically applied capsaicin. Blood pressure, heart rate, and rectal temperature were monitored, and bilateral femoral nerves were denervated in thiamylal anesthetized Wistar rats. The sciatic nerves were exposed bilaterally and two cotton balls, one soaked with 1.5% capsaicin and the other with saline, were directly applied to the nerve trunk on the respective sides. We verified the conduction blockade of the compound action potentials of A δ and C fibers by 1.5% capsaicin. The evoked activity of the digastric electromyography elicited by electrical stimulation of the tongue (1.5 X T, duration 200 /is, interval 2 ms, twin pulse, 0.2 Hz) was monitored. On the saline-treated side, the JOR was gradually inhibited by manual acupuncture stimulation of the ipsilateral hindpaw (80 s), and the effect continued after the cessation of the stimulus. This response was not obtained with the manual acupuncture stimulation on the capsaicin-treated side. Immersion of the hindpaw in hot water (53°C, 40 s) induced a rapid and potent inhibition of the JOR on the saline-treated side, but not on the capsaicin-treated side. Cold water immersion (10°C, 40 s) had no apparent suppressive effect on either side, but it had a rather facilitative effect on the JOR on the saline-treated side. The inhibition of the JOR was elicited by manual acupuncture stimulation of various segmental areas such as the nose, auricle, forepaw, abdomen, hindleg and hindpaw. These results suggest that the capsaicin-sensitive thin afferent fibers (A δ and C afferent fibers) mediated by receptors such as polymodal receptors are activated by manual acupuncture stimulation and that they participate in the peripheral processes that of inhibition of the JOR by diffuse noxious inhibitory controls.