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J W Hu

Publications and source records attributed to J W Hu.

At least 19 recordsLinked to original sources

Development of inflammation after application of mustard oil or glutamate to the rat temporomandibular joint.

Application of the small-fibre excitant and inflammatory irritant mustard oil or the excitatory amino-acid receptor agonist glutamate to the rat temporomandibular joint (TMJ) region evokes similar changes in jaw-muscle activity, suggesting that peripheral application of glutamate may be nociceptive. Application of mustard oil to the TMJ region is also inflammatory, but, it is not clear if application of glutamate is equally inflammatory. In this study the extent of plasma-protein extravasation and oedema induced by mustard oil application to the TMJ region was compared with that induced by glutamate. Application of mustard oil resulted in plasma-protein extravasation into the TMJ tissues and oedema of the TMJ region. In contrast, glutamate did not cause plasma-protein extravasation or oedema.

Analysis of Variance

Effects of pre-emptive local anaesthesia on tooth pulp deafferentation-induced neuroplastic changes in cat trigeminal brainstem neurones.

Previous work has shown increased excitability of brainstem neurones in the trigeminal (V) subnucleus oralis following the deafferentation produced by tooth-pulp removal. The present study was designed to determine if the changes in oralis neuronal properties seen in cats 1-2 wk after the deafferentation could be blocked by local anaesthesia of the Vth nerve proximal to the sites of pulp injury just before the actual deafferentation. The response properties of neurones recorded in V subnucleus oralis were determined in anaesthetized cats. One or two weeks before neuronal recording, the pulps of the posterior mandibular teeth were removed under local mandibular anaesthesia in one group of cats (group A) and without local anaesthesia in a second group (group B); a third group (group C) had no pulp removal but received local anaesthesia. Consistent with the earlier data, there was a significantly increased incidence of neurones having an enlarged mechanoreceptive field, spontaneous activity and habituating tap sensitivity in group B compared to group C, but no significant differences were found between the two deafferented groups (A and B). As local anaesthesia did not prevent the development of pulp deafferentation-induced changes in the oralis neurones, it is unlikely that an afferent barrage of impulses induced by the deafferentation procedure was responsible for the neuroplastic changes that subsequently developed in the V subnucleus oralis.

Anesthetics, Local

C-fiber depletion alters response properties of neurons in trigeminal nucleus principalis.

The effects of C-fiber depletion induced by neonatal capsaicin treatment on the functional properties of vibrissa-sensitive low-threshold mechanoreceptive (LTM) neurons in the rat trigeminal nucleus principalis were examined in adult rats. Neonatal rats were injected either with capsaicin or its vehicle within 48 h of birth. The depletion of unmyelinated afferents was confirmed by the significant decrease in plasma extravasation of Evan's blue dye induced in the hindlimb skin of capsaicin-treated rats by cutaneous application of mustard oil and by the significant decrease of unmyelinated fibers in both the sciatic and infraorbital nerves. The mechanoreceptive field (RF) and response properties of 31 vibrissa-sensitive neurons in capsaicin-treated rats were compared with those of 32 vibrissa-sensitive neurons in control (untreated or vehicle-treated) rats. The use of electronically controlled mechanical stimuli allowed quantitative analysis of response properties of vibrissa-sensitive neurons; these included the number of center- and surround-RF vibrissae within the RF (i.e., those vibrissae which when stimulated elicited >/=1 and <1 action potential per stimulus, respectively), the response magnitude and latency, and the selectivity of responses to stimulation of vibrissae in different directions with emphasis on combining both the response magnitude and direction of vibrissal deflection in a vector analysis. Neonatal capsaicin treatment was associated with significant increases in the total number of vibrissae, in the number of center-RF vibrissae per neuronal RF, and in the percentage of vibrissa-sensitive neurons that also responded to stimulation of other types of orofacial tissues. Compared with control rats, capsaicin-treated rats showed significant increases in the response magnitude to stimulation of surround-RF vibrissae as well as in response latency variability to stimulation of both center- and surround-RF vibrissae. C-fiber depletion also significantly altered the directional selectivity of responses to stimulation of vibrissae. For neurons with multiple center-RF vibrissae, the proportion of center-RF vibrissae with net vector responses oriented toward the same quadrant was significantly less in capsaicin-treated compared with control rats. These changes in the functional properties of principalis vibrissa-sensitive neurons associated with marked depletion of C-fiber afferents are consistent with similarly induced alterations in LTM neurons studied at other levels of the rodent somatosensory system, and indeed may contribute to alterations previously described in the somatosensory cortex of adult rodents. Furthermore, these results provide additional support to the view that C fibers may have an important role in shaping the functional properties of LTM neurons in central somatosensory pathways.

Animals

Activation of peripheral GABAA receptors inhibits temporomandibular joint-evoked jaw muscle activity.

We have previously shown that injection of mustard oil or glutamate into rat temporomandibular joint (TMJ) tissues, an experimental model of acute TMJ injury, can reflexly induce a prolonged increase in the activity of both digastric (jaw-opener) and masseter (jaw-closer) muscles. In this study, GABA was applied to the TMJ region by itself or in combination with glutamate, and the magnitude of evoked jaw muscle electromyographic (EMG) activity was measured. Application of GABA alone to the TMJ region did not evoke significant jaw muscle EMG activity when compared with normal saline controls. In contrast, co-application of GABA and glutamate into the TMJ region decreased the magnitude of glutamate-evoked EMG activity. This GABA-mediated inhibition of glutamate-evoked EMG activity followed an inverse dose-response relationship with an estimated median inhibitory dose (ID50) of 0.17 +/- 0.05 (SE) micromol and 0.031 +/- 0.006 micromol for the digastric and masseter muscles, respectively. Co-administration of the GABAA receptor antagonist bicuculline (0.05 micromol) but not the GABAB receptor antagonist phaclofen (0.05 or 0. 15 micromol) reversed the suppressive actions of GABA, indicating that this action of GABA may be mediated by peripheral GABAA receptors located within the TMJ region. Our results suggest that activation of peripheral GABAA receptors located within the TMJ region could act to decrease the transmission of nociceptive information.

Animals

Morphine application to peripheral tissues modulates nociceptive jaw reflex.

This study assessed the effect of peripherally applied opioids on the electromyographic activity reflexly evoked in digastric and masseter muscles by injection of the small-fiber excitant and inflammatory irritant mustard oil (MO) into the temporomandibular joint. In 39 anaesthetized rats, local pretreatment of joint tissues with morphine (15 nmol) significantly depressed the jaw muscle responses compared with saline, and the depression was antagonized by simultaneous local injection of the opiate antagonist naloxone (2.7 nmol); systemic morphine pretreatment (15 nmol, i.v.) did not influence the muscle responses. The naloxone-reversible depression of the MO-evoked muscle responses by local, but not systemic morphine, supports the presence of peripheral opioid receptors that may have a role in modulating nociceptive responses.

Animals

Evidence that excitatory amino acid receptors within the temporomandibular joint region are involved in the reflex activation of the jaw muscles.

We have previously shown that injection of the inflammatory irritant and small-fiber excitant mustard oil (MO) into the temporomandibular joint (TMJ) region can reflexively induce a prolonged increase in the activity of both digastric and masseter muscles in rats. It is possible that peripheral excitatory amino acid (EAA) receptors play a role in this effect, because MO-evoked increases in jaw muscle activity are attenuated by preapplication of the noncompetitive NMDA receptor antagonist MK-801 into the TMJ region. In the present study the EAA receptor agonists glutamate, NMDA, kainate, and AMPA were applied locally to the TMJ region. Jaw muscle responses similar to those evoked by MO application to the TMJ region were achieved with glutamate, NMDA, AMPA, and kainate. Repeated application of glutamate, NMDA, or AMPA at intervals of 30 min evoked responses in the ipsilateral jaw muscles that were of comparable magnitude. Co-application of the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate (0.5 micromol) significantly reduced the magnitude of the glutamate- and NMDA-evoked ipsilateral jaw muscle responses without affecting responses evoked by AMPA. In contrast, co-application of the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (1 nmol) significantly reduced the magnitude of the glutamate- and AMPA-evoked ipsilateral jaw muscle responses without affecting responses evoked by NMDA. This evidence suggests that both NMDA and non-NMDA EAA receptor types are located within the TMJ region and may contribute to jaw muscle activity that can be reflexively evoked from the TMJ region.

2-Amino-5-phosphonovalerate

Involvement of NK-1 and NK-2 tachykinin receptor mechanisms in jaw muscle activity reflexly evoked by inflammatory irritant application to the rat temporomandibular joint.

An electromyographic (EMG) study was carried out in 51 anesthetized rats to assess if neurokinin, NK-1 and NK-2, receptor mechanisms and tachykinins were involved in the increased jaw muscle activity which can be reflexly evoked by injection of the small-fiber excitant and inflammatory irritant mustard oil (MO) into the temporomandibular joint (TMJ) region. A baseline level of EMG activity was recorded bilaterally for 20 min from digastric (DIG) and masseter (MASS) muscles and then each animal was treated with NK-1 or NK-2 antagonist or vehicle. In one series of experiments either the NK-1 antagonist CP-99,994 (20 microg approximately 54 nmol), the NK-2 antagonist MEN-10,376 (10 microg approximately 9 nmol or 20 microg approximately 18 nmol) or vehicle (control) was administrated into the lateral ventricle (i.c.v.); in another series the NK-1 antagonist (4 mg/kg approximately 3-4 micromol/rat) or vehicle (control) was given intravenously (i.v.). After 10 min, MO (20 microl, 20%) was applied to one TMJ (first injection) and 45 min later, MO was applied to the opposite TMJ (second injection). Pretreatment with neurokinin antagonists had little effect on the incidence of the MO-evoked EMG responses but did significantly reduce the EMG magnitude and duration. In the animals pretreated with NK-1 antagonist only the responses to the second MO injection was significantly affected whereas NK-2 pretreatment reduced the EMG responses to both MO injections to the TMJ. The systematic depression of the MO-evoked EMG responses by the NK-2 antagonist suggests that neurokinin A may be involved in the EMG responses. Since the NK-1 antagonist produced no systematic changes in responses elicited by the first MO injection, substance P does not seem to be associated directly with the initiation or maintenance of the EMG responses but may be involved if a 'central sensitization' has been induced by the first MO injection to the TMJ.

Animals

Differential effects of morphine on corneal-responsive neurons in rostral versus caudal regions of spinal trigeminal nucleus in the rat.

The initial processing of corneal sensory input in the rat occurs in two distinct regions of the spinal trigeminal nucleus, at the subnucleus interpolaris/caudalis transition (Vi/Vc) and in laminae I-II at the subnucleus caudalis/spinal cord transition (Vc/C1). Extracellular recording was used to compare the effects of morphine on the evoked activity of corneal-responsive neurons located in these two regions. Neurons also were characterized by cutaneous receptive field properties and parabrachial area (PBA) projection status. Electrical corneal stimulation-evoked activity of most (10/13) neurons at the Vi/Vc transition region was increased [146 +/- 16% (mean +/- SE) of control, P < 0.025] after systemic morphine and reduced after naloxone. None of the Vi/Vc corneal units were inhibited by morphine. By contrast, all corneal neurons recorded at the Vc/C1 transition region displayed a naloxone-reversible decrease (55 +/- 10% of control, P < 0.001) in evoked activity after morphine. None of 13 Vi/Vc corneal units and 7 of 8 Vc/C1 corneal units tested projected to the PBA. To determine if the Vc/C1 transition acted as a relay for the effect of intravenous morphine on corneal stimulation-evoked activity of Vi/Vc units, morphine was applied topically to the dorsal brain stem surface overlying the Vc/C1 transition. Local microinjection of morphine at the Vc/C1 transition increased the evoked activity of 4 Vi/Vc neurons, inhibited that of 2 neurons, and did not affect the remaining 12 corneal neurons tested. In conclusion, the distinctive effects of morphine on Vi/Vc and Vc/C1 neurons support the hypothesis that these two neuronal groups contribute to different aspects of corneal sensory processing such as pain sensation, autonomic reflex responses, and recruitment of descending controls.

Administration, Topical

NMDA receptor mechanisms contribute to neuroplasticity induced in caudalis nociceptive neurons by tooth pulp stimulation.

We recently demonstrated that application of mustard oil (MO), a small-fiber excitant and inflammatory irritant, to the rat maxillary molar tooth pulp induces significant and prolonged increases in jaw muscle electromyographic (EMG) activity that are suggestive of central neuroplasticity. Because small-fiber afferents, including pulp afferents, access nociceptive neurons in trigeminal (V) subnucleus caudalis, this study examined whether pulpal application of MO induces neuroplastic changes in caudalis nociceptive neurons (wide dynamic range and nociceptive specific) and whether central N-methyl--aspartate (NMDA) receptor mechanisms are involved in these MO-induced neuroplastic changes. After pretreatment with vehicle (saline, 10 microliter i.t.) to the surface of the medulla, the pulpal application of MO to the maxillary molar tooth pulp produced a significant increase in neuronal spontaneous activity, a significant expansion of the pinch and/or tactile mechanoreceptive field (RF), a significant decrease in mechanical threshold, and significant increases in neuronal responses to graded pinch stimuli. Compared with vehicle-treated rats, pretreatment with the NMDA receptor antagonist MK-801 (10 microgram/10 microliter i.t.) followed by MO application to the pulp in another group of rats significantly reduced or abolished these MO-induced neuroplastic changes in nociceptive neurons. In another group of rats pretreated with saline (intrathecally), mineral oil application to the pulp did not show any significant changes in spontaneous activity or RF properties over the 40-min observation period. The pulpal application of MO in other rats (pretreated with saline, intrathecally) did not produce any significant neuroplastic changes in caudalis low-threshold mechanoreceptive neurons. These results indicate that the MO-induced activation of molar pulpal afferents can produce profound NMDA receptor-related neuroplastic changes in caudalis nociceptive neurons. Such neuroplastic changes may contribute to the hyperalgesia and spread of pain that can be associated with pulpal inflammation.

Animals

Encoding of corneal input in two distinct regions of the spinal trigeminal nucleus in the rat: cutaneous receptive field properties, responses to thermal and chemical stimulation, modulation by diffuse noxious inhibitory controls, and projections to the parabrachial area.

To determine whether corneal input is processed similarly at rostral and caudal levels of the spinal trigeminal nucleus, the response properties of second-order neurons at the transition between trigeminal subnucleus interpolaris and subnucleus caudalis (Vi/Vc) and at the transition between subnucleus caudalis and the cervical spinal cord (Vc/C1) were compared. Extracellular single units were recorded in 68 Sprague-Dawley rats under chloralose or urethan/chloralose anesthesia. Neurons that responded to electrical stimulation of the cornea at the Vi/Vc transition region (n = 61) and at laminae I/II of the Vc/C1 transition region (n = 33) were classified regarding 1) corneal mechanical threshold; 2) cutaneous mechanoreceptive field, if present; 3) electrical input characteristics (A and/or C fiber); 4) response to thermal stimulation; 5) response to the small-fiber excitant, mustard oil (MO), applied to the cornea; 6) diffuse noxious inhibitory controls (DNIC); and 7) projection status to the contralateral parabrachial area (PBA). On the basis of cutaneous receptive field properties, neurons were classified as low-threshold mechanoreceptive (LTM), wide dynamic range (WDR), nociceptive specific (NS), or deep nociceptive (D). All neurons recorded at the Vc/C1 transition region were either WDR (n = 19) or NS (n = 14). In contrast, 54% of the Vi/Vc neurons had no cutaneous receptive field. Of those Vi/Vc neurons that had a cutaneous receptive field, 57% were LTM, 25% were WDR, and 18% were D. All Vc/ C1 neurons responded to noxious thermal and MO stimulation. Only 22 of 47 and 13 of 19 Vi/Vc corneal units responded to thermal or MO stimulation, respectively. At the Vc/C1 transition region, 12 of 17 neurons demonstrated DNIC, whereas at the Vi/Vc transition region, DNIC was present in only 4 of 26 neurons. Of 15 Vc/C1 corneal units, 12 could be antidromically activated from the contralateral PBA (average latency 6.29 ms, range 1.8-26 ms). None of 22 Vi/Vc corneal units tested could be antidromically activated from the PBA. These findings suggest that neurons in laminae I/II at the Vc/C1 transition and at the Vi/Vc transition process corneal input differently. Neurons in laminae I/II at the Vc/C1 transition process corneal afferent input consistent with that from other orofacial regions. Corneal-responsive neurons at the Vi/Vc transition region may be important in motor reflexes or in recruitment of descending antinociceptive controls.

Anesthetics

NMDA receptor involvement in neuroplastic changes induced by neonatal capsaicin treatment in trigeminal nociceptive neurons.

NMDA receptor involvement in neuroplastic changes induced by neonatal capsaicin treatment in trigeminal nociceptive neurons. J. Neurophysiol. 78: 2799-2803, 1997. This study examines whether 1) the neonatal loss of C-fiber afferents results in neuroplastic changes in the mechanoreceptive field (RF) properties and spontaneous activity of nociceptive neurons in trigeminal subnucleus caudalis (medullary dorsal horn) of adult rats, and that 2) N-methyl--aspartic acid (NMDA) receptor mechanisms are involved in these neuroplastic changes. Compared with vehicle-treated (i.e., control, CON) rats, capsaicin-treated (CAP) rats showed a marked increase in neuronal spontaneous activity and RF size per se, but these neuroplastic changes could be significantly reduced by MK-801 (1 mg/kg, iv), a noncompetitive NMDA receptor antagonist; RF size and spontaneous activity remained unchanged in CON rats after MK-801 administration and in CAP rats after vehicle (saline, iv). Administration of 7-chlorokynurenic acid intrathecally (5 microgram/10 microliter), an antagonist of strychnine-insensitive glycine bindin sites on the NMDA receptor, also significantly reduced neuronal RF size and spontaneous activity in CAP rats, but not in CON rats. These data provide evidence that C-fiber afferents play a role in shaping the properties of nociceptive neurons and that the neuroplastic changes involve NMDA receptor mechanisms.

Animals

Neurogenic inflammation and tooth pulp innervation pattern in sympathectomized rats.

This study investigated possible collateral C-fiber innervation between the pulps of rat molars by assessing neurogenic inflammation (NI) induced by the C-fiber excitant mustard oil (MO). MO was applied to the pulp of the left mandibular first molar in two groups of rats: group 1, guanethidine sympathectomized rats (to dismiss sympathetic activation by MO); and group 2, unsympathectomized rats. A third group of unsympathectomized rats (group 3) had saline applied to the pulp of the left mandibular molar and served as a MO control. The NI-related plasma extravasation was examined in these teeth and in the remaining left mandibular teeth by a spectrophotometric analysis of extravasated plasma protein bound to Evans' Blue (EB) dye. The collateral innervation pattern was inferred from the NI pattern. EB concentrations were measured in the left mandibular teeth and the corresponding contralateral teeth, and expressed as a ratio. Statistical analysis of the data revealed significant differences in EB ratios in the first, second, and third molars between groups 1 and 3. This result suggests collateral C-fiber innervation exists within the pulps of molar teeth in the same dental quadrant. No difference in EB ratios was noted in the first and second molars between groups 1 and 2. Therefore, sympathetic efferents have no apparent effect on the degree of MO-induced NI.

Animals

Neuroplastic effects of neonatal capsaicin on neurons in adult rat trigeminal nucleus principalis and subnucleus oralis.

1. The effects of C-fiber depletion induced by neonatal capsaicin treatment on the functional properties of low-threshold mechanoreceptive (LTM) neurons in the rat trigeminal (V) subnucleus oralis and nucleus principalis were examined. Neonatal rats were injected with capsaicin within 48 h of birth. The mechanoreceptive field (RF) and response properties of 184 oralis LTM neurons and 185 principalis LTM neurons were studied in adult capsaicin-treated rats. These properties were compared with those of 200 oralis LTM neurons and 253 principalis LTM neurons from untreated or vehicle-treated (control) adult rats. 2. The effectiveness of neonatal capsaicin in depleting C fibers was tested by determining the plasma extravasation of Evans blue dye that was induced in the hindlimb skin by the cutaneous application of the C-fiber excitant and inflammatory irritant mustard oil. The amount of extravasation in capsaicin-treated rats was significantly less than that of control rats. 3. Neonatal capsaicin treatment was associated with significant increases in neuronal RF size and in the percentage of neurons with convergent inputs from more than one type of peripheral tissue (e.g., nonsinus hair, vibrissae, glabrous skin/mucosa, subcutaneous structures such as joint or muscle, periodontal ligament) in both subnucleus oralis and nucleus principalis. In subnucleus oralis, neonatal capsaicin treatment produced a significant increase in the percentage of neurons with a RF involving both V1 and V2 divisions, and a significant decrease in the percentage of neurons with a RF restricted to the V1 division. Analogous changes were not observed in nucleus principalis, although for principalis vibrissa-sensitive neurons, neonatal capsaicin treatment was associated with significant increases in the total number of vibrissae per neuronal RF and in the maximal length of the vibrissal row (i.e., the number of vibrissae in the longest row of vibrissae, stimulation of which was effective in activating a given neuron). 4. Neonatal capsaicin treatment did not significantly affect other oralis or principalis neuronal properties, including the percentage of neurons exhibiting spontaneous activity or abnormal response properties (such as habituating tap sensitivity, discontinuous RF, or mixed adaptation properties within the RF). 5. The changes in the functional properties of oralis and principalis LTM neurons induced by neonatal capsaicin treatment are consistent with those previously reported at other levels of the rodent CNS. They provide additional support to the view that C fibers may have an important role in shaping the functional properties of central LTM somatosensory neurons.

Animals

Inflammatory lesions of the tooth pulp induce changes in brainstem neurons of the rat trigeminal subnucleus oralis.

Neuroplastic changes are known to occur in the CNS in response to injury of peripheral nerves. Previous investigation has demonstrated neuroplasticity in second-order neurons of the subnucleus oralis (SO) of the trigeminal (V) nuclear complex in association with aseptic injury to the tooth pulp. A question arises, therefore, as to whether similar changes occur in response to injury associated with inflammation induced by tooth pulp infection. The effects of tooth pulp infection on the mechanoreceptive fields (RFs) of SO neurons were examined in rats. Infection was established by exposure and removal of the coronal pulp of the mandibular first molar, which was left open to the oral environment for 7 (n = 5) or 28 (n = 6) days. Neurons in SO were then electrophysiologically characterized in chloralose/urethane-anesthetized rats. The RF and the response properties of 118 low-threshold mechanoreceptive (LTM) neurons from seven-day-old rats and 149 LTM neurons from 28-day-old rats were compared with those of 204 LTM neurons tested in 11 untreated (control) rats. Significant differences were noted in RF size and location when control, seven-day-old, and 28-day-old groups were compared. Radiographic examination revealed inconsistencies among examiners in the interpretation of periapical lesions < 2 mm in diameter and general agreement in the identification of periapical lesions > 2 mm in diameter. Histological examination of teeth with pulp exposure revealed superficial necrosis and inflammation without periapical extension in the seven-day-old animals and total pulp necrosis with periapical inflammation, abscess formation, and alveolar bone resorption in the 28-day-old animals. The results indicate that neuroplastic changes in LTM oralis neurons can develop subsequent to tooth pulp infection and that there may be a correlation between the incidence of these changes and the extension of the attending inflammation from the pulp to the dental supporting tissues.

Age Factors

Opioid involvement in electromyographic (EMG) responses induced by injection of inflammatory irritant into deep neck tissues.

Previously, we have demonstrated (Hu et al., 1993) that injection of the small-fiber excitant and inflammatory irritant mustard oil (MO) into deep paraspinal tissues surrounding C1-C2 vertebrae can evoke a sustained and reversible increase of electromyographic (EMG) activity of neck and jaw muscles, and can also produce an acute inflammatory response. This increased EMG activity lasts up to 20 min; within 30 min following MO injection, the activity returns to preinjection levels. The aim of our present study was to determine whether an opioid suppressive mechanism may be involved in limiting the increased EMG activity, despite the presence of an ongoing inflammatory response. Three doses (0.6 mg/kg, 1.2 mg/kg, and 2.5 mg/kg) of the opioid antagonist naloxone, along with vehicle (saline), were administered intravenously to determine whether naloxone is capable of inducing a significant recurrence ("rekindling" effect) of EMG activity. A dose-dependent process in the naloxone-induced rekindling effect was demonstrated for the area under the curve of rectified and integrated EMG activity. At the highest dose (2.5 mg/kg), the relative area of naloxone-evoked EMG activity increases reached 83% of the original MO-induced EMG activity level. These results suggest that a central opioid suppressive mechanism is activated by the MO-induced small-afferent barrage, and that this may limit the duration and magnitude of the evoked EMG changes.

Afferent Pathways

Distribution of Fos-like immunoreactivity in the caudal brainstem of the rat following noxious chemical stimulation of the temporomandibular joint.

Central expression of the protooncogene c-fos was used to examine areas receiving noxious sensory input from the rat temporomandibular joint (TMJ). Fos-like immunoreactivity (Fos-LI) in the caudal brainstem was visualized 2 hours after unilateral injection of the small-fiber-specific excitant/inflammatory irritant mustard oil into the TMJ region. Control animals received injection of either mustard oil into the subcutaneous fascia overlying the masseter muscle or mineral oil vehicle into the TMJ region. In all groups, Fos-LI was consistently observed ipsilaterally in the spinal trigeminal nucleus and cervical dorsal horn and, bilaterally, in the nucleus of the solitary tract and the ventrolateral medulla. The expression of Fos-LI ipsilaterally in the paratrigeminal nucleus was variable. Within the trigeminal sensory complex, Fos-LI was restricted to subnucleus caudalis and the caudal portions of subnucleus interpolaris near the level of the obex. Approximately 12% of Fos-LI cells in subnucleus caudalis and in the cervical dorsal horn were found in laminae III-VI. Compared to TMJ mustard oil injection, mineral oil injection produced less Fos-LI at all rostrocaudal levels, whereas subcutaneous mustard oil injection produced less Fos-LI in caudal subnucleus caudalis but similar amounts in the cervical dorsal horn. Neither of these injections yielded significant ipsilateral responses in subnucleus caudalis, indicating that Fos-LI in this region following TMJ mustard oil injection could be ascribed solely to small-fiber stimulation in the deep TMJ region. The wide rostrocaudal distribution of Fos-LI within the caudal brainstem reflects the distribution of TMJ-responsive nociceptive neurons that may underlie the spread and referral of pain from the TMJ region.

Animals

Effects of inflammatory irritant application to the rat temporomandibular joint on jaw and neck muscle activity.

An electromyographic (EMG) study was carried out in 40 anaesthetized rats to determine if the activity of jaw and neck muscles could be influenced by injection of the small-fibre excitant and inflammatory irritant mustard oil into the region of the temporomandibular joint (TMJ). Injection of a vehicle (mineral oil, 20 microliters) did not produce any significant change in EMG activity. In contrast, injection of mustard oil (20 microliters, 20%) evoked increases in EMG activity in the jaw muscles but not in the neck muscles. The increased EMG activity evoked by mustard oil was reflected in 1 or 2 phases of increased activity. The early EMG increase occurred soon after the mustard oil injection (mean latency +/- SD: 3.5 +/- 2.3 sec), peaked within 1 min, and then subsided (mean duration: 7.5 +/- 5.2 min). The later EMG increase occurred at 14.6 +/- 10.0 min after the mustard oil injection and lasted 14.3 +/- 12.3 min. These excitatory effects of mustard oil on the EMG activity of jaw muscles appear to have a reflex basis since they could be abolished by pre-administration of local anaesthetic into the TMJ region. These results document that TMJ injection of mustard oil results in a sustained and reversible activation of jaw muscles that may be related to the reported clinical occurrence of increased muscle activity associated with trauma to the TMJ.

Animals

Central projections of identified trigeminal primary afferents after molar pulp deafferentation in adult rats.

It is known that removal of the tooth pulp from mandibular molar teeth in adult rats alters the mechanoreceptive field properties of many low-threshold mechanoreceptive neurons in the trigeminal brainstem nuclear complex. The present study investigates one possible way that such deafferentation-induced receptive field changes could occur: altered central projections of uninjured trigeminal low-threshold mechanoreceptive primary afferent fibers. Intra-axonal injection of horseradish peroxidase (n = 22) or neurobiotin (n = 44) into characterized fibers was performed ipsilateral to, and 10-32 days after, removal of the coronal pulp from the left mandibular molars in adult rats. Collaterals were reconstructed, quantified, and compared by means of multivariate analyses of variance to equivalent fibers stained in normal adult rats. Stained mechanosensitive fibers from experimental animals were rapidly conducting and responded to light mechanical stimulation of one vibrissa, one tooth, oral mucosa, facial hairy skin, or guard hairs. Their central projections were indistinguishable from those of control axons in all four trigeminal subnuclei. The numbers of collaterals, areas subtended by collateral arbors, numbers of boutons per collateral, and arbor circularity did not differ from those of control afferents. Collateral somatotopy was also unaffected. These data suggest that following pulpotomy, the central collaterals of uninjured trigeminal afferents display normal morphologies and maintain normal somatotopy. Changes in the morphology of low-threshold primary afferents cannot account for the changes that occur in the receptive field properties of trigeminal brainstem neurons after pulp deafferentation.

Afferent Pathways