Inputs to trigeminal brain stem neurones from facial, oral, tooth pulp and pharyngolaryngeal tissues: I. Responses to innocuous and noxious stimuli

Responses evoked in anaesthetized or decerebrate cats by stimulation of afferents supplying the face, mouth, pharynx, larynx, tooth pulp and jaw muscles were recorded from single neurones located in the trigeminal (V) main sensory nucleus, V nucleus oralis, and adjacent regions. Many cells (both V-thalamic relay and non-relay with localized V mechanoreceptive cutaneous fields could be activated by stimulation of a number of these afferents. A particularly prominent short-latency (often monosynaptic) input was noted from the canine tooth pulp, stimulation of which is generally considered to elicit only responses of pain in man. Control experiments showed that pulp-evoked responses were not the result of stimulus spread to tissues outside the pulp. The interaction of these various inputs to neurones at this level of the V brain stem complex typically resulted in a prolonged period of inhibition that was sometimes preceded by a short-lasting facilitatory phase. This inhibitory effect was also apparent in neurones located outside the complex, although a late facilitatory phase was frequently also noted. Our findings indicate a significant nociceptive input to V main sensory-oralis neurones, a proportion of which relay directly to the ventrobasal thalamus. The interactions described may be involved in perceptual and reflex aspects of responses to noxious and innocuous V stimuli.     

Anatomical regeneration and behavioral recovery following crush injury of the trigeminal root in lamprey

In normal larval lamprey, bilateral application of horseradish peroxidase (HRP) to the dorsal part of the anterior oral hood labeled subpopulations of trigeminal components on both sides of the brain; peripherally projecting motoneurons, medullary dorsal cells (sensory), and spinal dorsal cells (sensory), as well as centrally projecting afferents in the trigeminal descending tracts. Following unilateral crush injury of the right trigeminal root, HRP labeling of sensory and motor trigeminal components on the right side gradually increased with increasing recovery time, between 2 weeks and 12 weeks postcrush (PC). Axons of trigeminal motoneurons appeared to exhibit robust regeneration, whereas restoration of projections in the descending trigeminal tract ipsilateral to the injury was incomplete. Control experiments indicated that motor and sensory axons from the intact side of the oral hood did not sprout across the midline to the denervated side. Several results suggested that regenerated trigeminal sensory fibers made synapses with brain neurons that have direct or indirect inputs to reticulospinal (RS) neurons. Following a unilateral crush injury of the right trigeminal root, escape behavior in response to stimulation of the right side of the oral hood gradually returned to normal. Muscle recordings at various recovery times confirmed that anatomical regeneration of trigeminal sensory axons was functional. In addition, at 8 or 12 weeks PC, brief stimulation of the oral hood ipsilateral or contralateral to the crush injury elicited synaptic responses in RS neurons on either side of the brain, similar to that in normal animals. In the lamprey, compensatory mechanisms probably allow recovery of behavioral function despite incomplete regeneration of trigeminal sensory axons within the central nervous system.     

Temporal summation of C-fiber afferent inputs: competition between facilitatory and inhibitory effects on C-fiber reflex in the rat

Long-lasting facilitations of spinal nociceptive reflexes resulting from temporal summation of nociceptive inputs have been described on many occasions in spinal, nonanesthetized rats. Because noxious inputs also trigger powerful descending inhibitory controls, we investigated this phenomenon in intact, halothane-anesthetized rats and compared our results with those obtained in other preparations. The effects of temporal summation of nociceptive inputs were found to be very much dependent on the type of preparation. Electromyographic responses elicited by single square-wave electrical shocks (2 ms, 0.16 Hz) applied within the territory of the sural nerve were recorded in the rat from the ipsilateral biceps femoris. The excitability of the C-fiber reflex recorded at 1.5 times the threshold (T) was tested after 20 s of electrical conditioning stimuli (2 ms, 1 Hz) within the sural nerve territory. During the conditioning procedure, the C-fiber reflex was facilitated (wind-up) in a stimulus-dependent fashion in intact, anesthetized animals during the application of the first seven conditioning stimuli; thereafter, the magnitude of the responses reached a plateau and then decreased. Such a wind-up phenomenon was seen only when the frequency of stimulation was 0.5 Hz or higher. In spinal, unanesthetized rats, the wind-up phenomenon occurred as a monotonic accelerating function that was obvious during the whole conditioning period. An intermediate picture was observed in the nonanesthetized rat whose brain was transected at the level of the obex, but the effects of conditioning were profoundly attenuated when such a preparation was anesthetized. In intact, anesthetized animals the reflex was inhibited in a stimulus-dependent manner during the postconditioning period. These effects were not dependent on the frequency of the conditioning stimulus. Such inhibitions were blocked completely by transection at the level of the obex, and in nonanesthetized rats were then replaced by a facilitation. A similar long-lasting facilitation was seen in nonanesthetized, spinal rats. It is concluded that, in intact rats, an inhibitory mechanism counteracts the long-lasting increase of excitability of the flexor reflex seen in spinal animals after high-intensity, repetitive stimulation of C-fibers. It is suggested that supraspinally mediated inhibitions also participate in long term changes in spinal cord excitability after noxious stimulation.     

Dental innervation: functions and plasticity after peripheral injury

Oral tissues including the periodontal ligament, gingiva, and tooth pulp have a relatively dense sensory innervation and a rich vascular supply. Teeth and supporting tissues are susceptible to tissue injury and inflammation, partly due to lack of collateral blood and nerve supply and to their low compliance. This review focuses on dental nerve functions and adaptive changes in the trigeminal ganglion and tooth pulp after peripheral injuries. An overview of the peptidergic innervation of oral tissues is presented, followed by a discussion of plasticity in neuropeptide expression in trigeminal peripheral neurons after local insults to teeth and peripheral nerve injuries. The functional implications of these adaptive changes are considered, with special reference to nerve regeneration, inflammation, and hemodynamic regulation.     

The descending cortical control of nociceptive signals: the neurochemical mechanisms and pharmacological control

The purpose of the present study was to determine whether electrical cortical stimulation (as a model of descending inhibitory control) could alter the electrophysiological and behavioral signs of a nociceptive response. The inhibitory cortical influence on the neuronal activity produced by nociceptive stimuli (the tooth pulp, C-fibers of afferent somatic nerves, cardiac afferents) was most marked during electrical stimulation the somatosensory (Sn and St) and fronto-orbital cortices. In chronic experiments, somatosensory cortical stimulation delayed the development of the deafferentation pain syndrome and reduced its intensity. The opioid mu-receptor agonists morphine and fentanyl potentiated the inhibitory action of the cortex on evoked neuronal activity. Pentazocine, a kappa-receptor agonist, was less effective. The opioid receptor blocker naloxone eliminated the effect of both cortical stimulation and opioid analgesics. The serotonin receptor blocker methisergide significantly decreased cortical action. Monoamine reuptake inhibitors (amitriptyline, imipramine, fluoxetine) potentiated the effect of cortical stimulation. Adrenergic, dopaminergic cholinergic, and GABA-ergic substances had a little effect. Among nonopioid analgesics, metamyzol and ketorolak only increased moderately descending cortical control.     

Snake bite accidents in children in Costa Rica: epidemiology and determination of risk factors in the development of abscess and necrosis

In previous studies, we have shown that electrically or chemically evoked activation of the ventrolateral orbital cortex (VLO) depresses the rat tail-flick (TF) reflex, and this antinociceptive effect is mediated by the periaqueductal gray (PAG). The aim of the present study was to examine whether electrical stimulation of the VLO could inhibit the rat jaw-opening reflex (JOR), and to determine whether electrolytic lesions of the PAG could attenuate this VLO-evoked inhibition. Unilateral electrical stimulation of the VLO significantly depressed the JOR elicited by tooth pulp or facial skin stimuli, with a mean threshold of 30.5+/-2.3 microA (n=22). Increasing stimulation intensities from 30 to 80 microA resulted in greater reduction of the dEMG amplitude from 22.9+/-5.0% to 69.7+/-3.7% of the baseline value (P<0.01, n=22). The inhibitory effect appeared 50 ms after the beginning of VLO stimulation and lasted about 150 ms, as determined by varying the conditioning-test (C-T) time interval. Unilateral lateral or ventrolateral lesions of the PAG produced only a small attenuation of the VLO-evoked inhibition of the JOR, but bilateral lesions eliminated this inhibition. These findings suggest that the VLO plays an important role in modulation of orofacial nociceptive inputs, and provide further support for the hypothesis that the antinociceptive effect of VLO is mediated by PAG leading to activation of a brainstem descending inhibitory system and depression of nociceptive inputs at the trigeminal level. The role played by VLO in pain modulation is discussed in association with the proposed endogenous analgesic system consisting of medullary cord-Sm-VLO-PAG-medullary cord.     

Tolerance to the antinociceptive effect of morphine in spinally transected rats.

Examined the effect of a spinal transection (ST) on morphine (MOR)-induced tolerance in rats with the tail withdrawal reflex (tail flick; TF), elicited by noxious thermal stimulation. Intact Ss became tolerant to sc MOR injections if they were tested on the TF after each injection. MOR administration alone did not produce tolerance; TF tests alone did, although not always to a significant extent. However, when MOR only, TF tests only, or both were administered prior to ST (acute spinal Ss), all groups were tolerant when tested 1 day after spinalization. When the same treatments were administered to Ss 3 wks after ST (chronic spinal Ss), neither MOR nor TF tests alone produced tolerance. Chronic spinal Ss became tolerant only if they were tested after each injection. Results suggest that tolerance develops at the spinal cord as a result of either chronic opiate exposure or performance of the nociceptive response, but in intact Ss, tolerance is inhibited or suppressed by a supraspinal action of MOR. Results also suggest that such tolerance is mediated by descending input or that ST produced intrinsic changes in the spinal cord that preclude the development of tolerance induced only by opiate or behavioral stimulation. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of local standards on the implementation of national guidelines for asthma: primary care agreement with national asthma guidelines

In vivo electrophysiological assays in anesthetized rats have been used to compare the effects of the 5HT1B/1D receptor agonist, naratriptan, on central trigeminal nociceptive processing from dural and cutaneous inputs with its effects on nociceptive processing in the spinal cord. Naratriptan inhibited responses of single trigeminal neurons, to noxious electrical and mechanical stimulation of the dura and face, dose dependently by a maximum of 67+/-3% and 70+/-18%, respectively, at 3 mg kg(-1) i.v. In contrast, naratriptan did not affect spinal dorsal horn neuronal responses to noxious mechanical stimulation of the hind-paw. These findings suggest that 5HT1B/1D receptors have differential effects on nociceptive processing in the trigeminal versus spinal dorsal horns and provide a potential explanation for the lack of general analgesic effects of brain penetrant 5HT(1B/1D) agonist antimigraine drugs.     

Effects of ketamine on somatosympathetic reflex discharges in cats

Effects of ketamine on somatosympathetic reflex discharges induced from sympathetic trunk with electrical stimulation of superficial peroneal nerve were investigated in 51 cats under anesthesia with urethane and alpha chloralose. These reflex discharges through spinal cord and medulla oblongata consist of two components, A and C reflexes, which are derived from somatic myelinated and unmyelinated afferent fiber respectively. Amplitudes of both A and C reflex potentials were depressed significantly after intravenous injection of ketamine 10 mg.kg-1. The maximum depression was observed 5 min after administration. In decerebrated cats with surgical transection at the midbrain, both A and C reflexes were also depressed after administration of the same dosages, and the maximum level of the depression was more profound than that in brain intact cats. After intrathecal injection of ketamine 1 mg.kg-1 to the lumbar spinal region, a slight depression of C reflex was found, but, dosages of 10 mg.kg-1 significantly depressed both A and C reflexes to the similar levels as those in iv injection to brain intact cats. The maximum depression was observed 30 min after administration. The depressive effects on both reflexes of intravenous ketamine 10 mg.kg-1 were not antagonized by naloxone 0.06 mg.kg-1 in brain intact cats. These results suggest that the suppressive effects of ketamine on somatosympathetic reflexes are caused by direct inhibition of medulla oblongata and spinal cord, whereas supra-midbrain regions may be activated by ketamine, and the effect of ketamine is predominant on medulla oblongata in this situation rather than on the spinal cord.     

Effects of pulsed Nd:YAG laser radiation on action potential conduction in nerve fibres inside teeth in vitro

OBJECTIVE: This study aimed to simulate the effects of lasing dentine on pulpal nerve function. METHODS: Rat spinal nerve roots were threaded through the prepared pulp canal of a 10 mm long tooth root segment which was mounted in a perspex bath. The protruding ends of the nerve were placed on platinum wire electrodes used to elicit and to record compound nerve action potentials (CAPs). Laser energy (average power = 0.3-3.0 W) was applied to the surface of the root segment using a pulsed Nd:YAG dental laser (dLase 300). RESULTS: With the laser probe tip placed in static contact with the tooth surface, the nerve CAP was irreversibly abolished within 60 s of lasing at 1.0-3.0 W power. When the laser tip was moved to and fro over the root surface in a scanning mode, similar levels of radiation produced less marked effects. In the latter mode, CAP attenuation increased with increasing power and duration of lasing. After 60 s lasing at 0.3 W, the CAP size was 95% (+/- 5, S.D.) of the prelasing controls value; with 2.0 W the CAP was reduced to 54% (+/- 33). The CAP recovered to 90% of control levels after lasing at powers up to 1.5 W, but reached only 72% of control values after lasing at 2.0 W power. CONCLUSIONS: Laser radiation applied to dentine caused a dose-dependent block of action potential conduction in nerve fibres in the underlying pulp chamber.     

Three types of reticular neurons involved in the spino-bulbo-spinal reflex of cats

Reticular neuron activity was recorded in 28 chloralosed cats in order to analyze the reflex arc of the spino-bulbo-spinal (SBS) reflex. Three types of reticular neurons, types I (input), II(output) and III (relay), were identified by unit discharges in response to stimulation of the sural nerve. (1) Type I (input) neurons received spinal ascending volleys monosynaptically and responded to stimulation of the sural nerve with spikes of low amplitude and short latency. Unit spikes, however, were not produced by stimulation of the superficial radial nerve and the sensorimotor cortex. These input neurons were located in the dorsocaudal part of the medial bulbar reticular formation. (2) Type II (output) neurons were part of the reticulospinal tract, which sends axons to the spinal cord, since these neurons exhibited antidromic spikes following stimulation of the ventrolateral funiculus of the spinal cord. Unit spikes were evoked by stimulation either to the sural or superficial radial nerves. These neurons were located in the ventrocaudal part of the medial bulbar reticular formation. (3) Type III neurons included relay neurons. Unit spikes were evoked by stimulation of the sural nerve, superficial radial nerve and sensorimotor cortex. However, unit discharges were not obtained by antidromic stimulation to the reticulospinal tract. These neurons were distributed widely in the brain stem, both in the bulb and pons. (4) Latency difference of unit discharges between input and output neurons was 3.5--5 msec, indicating the presence of interneurons (relays) between input and output neurons. Spikes of output neurons with 3.8--4.2 msec latency were observed following stimulation of the region where input neuron activity was found. We may conclude that three kinds of reticular neurons, input, relay and output, were involved in pathways of the SBS reflex.     

Central projection of calcitonin gene-related peptide (CGRP)- and substance P (SP)-immunoreactive trigeminal primary neurons in the rat

Substance P (SP) is implicated in transmission of primary afferent nociceptive signals. In primary neurons, SP is colocalized with calcitonin gene-related peptide (CGRP), which is another neuropeptide marker for small to medium primary neurons. CGRP coreleased with SP augments the postsynaptic effect of SP and thereby modulates the nociceptive transmission. This study demonstrates the distribution of CGRP-like immunoreactivity (-ir) and SP-ir in the lower brainstem of normal rats and after trigeminal rhizotomy or tractotomy at the level of subnucleus interpolaris (Vi). By comparing the results obtained from normal and deafferented rats, we analyzed the central projection of trigeminal primary nociceptors. The CGRP-immunoreactive (-ir) trigeminal primaries projected to the entire rostrocaudal extent of the spinal trigeminal nucleus, the principal nucleus (PrV), the paratrigeminal nucleus (paraV), and the lateral subnucleus of solitary tract nucleus (STN) on the ipsilateral side. The trigeminal primaries projecting to the spinal trigeminal nucleus, paraV and STN also contained SP-ir. The ipsilateral trigeminal primaries were the exclusive source of CGRP-ir terminals in the PrV, the Vi and the dorsomedial nucleus within the subnucleus oralis (Vo). The medullary dorsal horn (MDH) and the lateral edge of Vo received convergent CGRP-ir projection from the ipsilateral trigeminal primaries and other neurons. The glossopharyngeal and vagal primaries are candidates for the source of CGRP-ir projection to the Vo and the MDH, while the dorsal root axons supply the MDH with CGRP-ir terminals. In addition, contralateral primary neurons crossing the midline appear to contain CGRP and to terminate in the MDH.     

Differential expression of galanin immunoreactivities in the primary sensory neurons following partial and complete sciatic nerve injuries

Neuropeptide expression in primary sensory neurons is highly plastic in response to peripheral nerve axotomy. While neuropeptide changes following complete sciatic nerve injury have been extensively studied, much less is known about the effects of partial sciatic nerve injuries on neuropeptide plasticity. Galanin. a possible endogenous analgesic peptide, was up-regulated in primary sensory neurons following complete sciatic nerve injury. We investigated the effects of partial sciatic nerve injuries on galanin expression in primary sensory neurons, and compared this effect with that after complete sciatic nerve injury. Complete transection, partial transection and chronic constriction injury were made, respectively, on the sciatic nerves of three groups of rats at high thigh level. Animals were allowed to survive for four and 14 days before being killed. L4 and L5 dorsal root ganglia, L4 5 spinal cord and lower brainstem were processed for galanin immunocytochemical staining. After all three types of sciatic nerve injuries, galanin-immunoreactive neurons were significantly increased in the ipsilateral dorsal root ganglia, and galanin-immunoreactive axonal fibres were dramatically increased in the superficial laminae of the dorsal horn and the gracile nuclei, compared to the contralateral side. However, in partial injury models, the percentages of galanin-immunoreactive dorsal root ganglion neurons were significantly higher than in complete nerve transection. Size frequency distribution analysis detected that more medium- and large-size galanin-immunoreactive dorsal root ganglion neurons were present after partial nerve transection and constriction injury than after complete nerve transection. Using a combined approach of retrograde tracing of flurorescent dyes and galanin immunostaining, we found that a partial transection increased the proportions of galanin-immunoreactive neurons among both axotomized and non-axotomized neurons. Galanin-immunoreactive axonal fibres were not only detected in the superficial laminae, but also in the deeper laminae of the dorsal horn of partial injury animals. Furthermore, more galanin-immunoreactive axonal fibres were observed in the ipsilateral gracile nuclei of partially injured rats than in completely injured rats. We conclude that partial sciatic nerve injuries induced greater galanin up-regulation in medium- and large-size dorsal root ganglion neurons than complete sciatic nerve injury. Galanin expression in primary sensory neurons seems to be differentially regulated following partial and complete sciatic nerve injuries.     

Differential c-fos expression in the nucleus of the solitary tract and spinal cord following noxious gastric distention in the rat

c-Fos has been used as a marker for activity in the spinal cord following noxious somatic or visceral stimulation. Although the viscera receive dual afferent innervation, distention of hollow organs (i.e. esophagus, stomach, descending colon and rectum) induces significantly more c-Fos in second order neurons in the nucleus of the solitary tract and lumbosacral spinal cord, which receive parasympathetic afferent input (vagus, pelvic nerves), than the thoracolumbar spinal cord, which receives sympathetic afferent input (splanchnic nerves). The purpose of this study was to determine the contribution of sympathetic and parasympathetic afferent input to c-Fos expression in the nucleus of the solitary tract and spinal cord, and the influence of supraspinal pathways on Fos induction in the thoracolumbar spinal cord. Noxious gastric distention to 80 mmHg (gastric distension/80) was produced by repetitive inflation of a chronically implanted gastric balloon. Gastric distension/80 induced c-Fos throughout the nucleus of the solitary tract, with the densest labeling observed within 300 microns of the rostral pole of the area postrema. This area was analysed quantitatively following several manipulations. Gastric distension/80 induced a mean of 724 c-Fos-immunoreactive nuclei per section. Following subdiaphragmatic vagotomy plus distention (vagotomy/80), the induction of c-Fos-immunoreactive nuclei was reduced to 293 per section, while spinal transection at T2 plus distention (spinal transection/80) induced a mean of 581 nuclei per nucleus of the solitary tract section. Gastric distension/80 and vagotomy/80 induced minimal c-Fos in the T8-T10 spinal cord (50 nuclei/section), but spinal transection/80 induced 200 nuclei per section. Repetitive bolus injections of norepinephrine produced transient pressor responses mimicking the pressor response produced by gastric distension/80. This manipulation induced minimal c-Fos in the nucleus of the solitary tract and none in the spinal cord. It is concluded that noxious visceral input via parasympathetic vagal afferents, and to a lesser extent sympathetic afferents and the spinosolitary tract, contribute to gastric distention-induced c-Fos in the nucleus of the solitary tract. The induction of c-Fos in the nucleus of the solitary tract is significantly greater than in the viscerotopic segments of the spinal cord, which is partially under tonic descending inhibition, but is not subject to modulation by vagal gastric afferents. Distention pressures produced by noxious gastric distention are much greater than those produced during feeding, suggesting that c-Fos induction in the nucleus of the solitary tract to noxious distention is not associated with physiological mechanisms of feeding and satiety. The large vagal nerve-mediated induction of c-Fos in the nucleus of the solitary tract following gastric distension suggests that parasympathetic afferents contribute to the processing of noxious visceral stimuli, perhaps by contributing to the affective-emotional component of visceral pain.     

Effect of electrical stimulation of the central amygdaloid nucleus on the nociceptive neuron of the cortex (SI) in the cat

The effect of conditioning stimulation of the central amygdaloid nucleus (ACE) on the response of tooth pulp-driven (TPD) neurons in the first somatosensory cortex (SI) was investigated in cats anesthetized with N2O-O2 (2:1) and 0.5% halothane. The tooth pulp test stimulus was a single 30-450 microA rectangular pulse, and the conditioning stimuli of the ACE were trains of 33 pulses (300 microA) delivered at 330 Hz. The ACE conditioning stimulation markedly suppressed the response of the slow-type neurons with latencies of more than 20 ms without any effect on the discharges of fast-type TPD neurons and spontaneous discharges. This inhibition was 68.9 +/- 24.7% (mean +/- SD) of the control. These findings suggest that there are at least two pathways for the ascending pulpal (nociceptive) information to the SI, and that the ACE modulates the transmission of impulses in one of the pathways.     

Nociceptive c-fos expression in supraspinal areas in avoidance of descending suppression at the spinal relay station

The number and distribution of Fos-like-immunoreactive neurons in different supraspinal brain areas induced by formalin injection into one hindpaw was estimated in rats with transected dorsal half of the spinal cord at the thoracic level in an attempt to avoid most of the descending modulatory actions. The results showed that: (i) after spinal lesion, the peripheral noxious inputs, going up mainly through the ventral spinal cord, elicited a more widespread and densely located Fos-like-immunoreactive neurons in subcortical areas, many of them showed no Fos expression when noxious stimulation was given in rats with intact spinal cord; (ii) at the same time, a small number of subcortical areas, such as the lateral ventroposterior thalamic nucleus and dorsal raphe nucleus, exhibited no significant increase of nociceptive Fos-like immunoreactive neurons after spinal lesion as compared to that with intact spinal cord; and (iii) there appeared a prominent expansion of cortical areas with densely located Fos-like-immunoreactive neurons in spinal-lesioned rats as compared with the limited labelled areas in the control group with intact spinal cord. These results indicate that: (i) in avoiding the spinally descending modulatory mechanisms, more widespread supraspinal and cortical neurons will be recruited and activated in response to the noxious stimulation; and (ii) the descending systems exert differential actions on the spinal targets which project nociceptive signals to different supraspinal regions. The implication of these facts is discussed.     

Differential expression of Fos protein after transection of the rat infraorbital nerve in the trigeminal nucleus caudalis

To determine the effects of nerve injury on Fos expression, temporal and spatial distributions of Fos-positive neurons in the trigeminal nucleus caudalis were examined after tissue injury for isolation of the infraorbital nerve as controls and transection of this nerve as well as noxious chemical stimulation by formalin injection in adult rats. Fos immunoreactivity was markedly elevated in laminae I and II of the only ipsilateral nucleus caudalis 2 h after these surgical procedures and noxious chemical stimulation. The distributions of Fos-positive neurons were restricted rostro-caudally following formalin injection and tissue injury compared to transection of the infraorbital nerve. One day after tissue injury and nerve transection, however, Fos-positive neurons were distributed bilaterally in laminae III and IV extending rostro-caudally and medio-laterally in this nucleus, and this persisted over the 2-week study period. The number of Fos-positive neurons in the side ipsilateral to nerve transection was markedly less than that in the contralateral side whereas positive neurons in the tissue injured rats were distributed symmetrically along the rostro-caudal axis. There was no difference in the contralateral sides between nerve transection and tissue injury groups. The rostro-caudal level showing reduction in Fos expression corresponded roughly to the sites of central termination of the injured nerve in this nucleus, suggesting a role for the primary afferents in the reduction of Fos expression in laminae III and IV neurons of the ipsilateral nucleus caudalis.     

Effects of a classical conditioning paradigm on hind-limb flexor nerve response in immobilized spinal cats.

Maintained 50 adult cats on Flaxedil after spinal transection at T-12 under ether anesthesia. Experimental Ss were classically conditioned by electrical stimulation of the exposed superficial peroneal nerve (CS), paired with cutaneous shock to the ankle of the same limb (UCS). The CR was the gross efferent volley recorded from the exposed deep peroneal nerve. Controls were divided into unpaired CS and UCS, CS-only, and UCS sensitization groups. Results show that the experimental conditions produced increases in amplitude of the gross efferent volley while unpaired CS and UCS, and CS-only control conditions produced no change or a decrease in amplitude. The UCS sensitization group showed that no sensitization was present at the intertrial intervals used in experimental conditions. (27 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Direct evidence of parasympathetic vasodilatation in cat periodontal ligament

Sympathetic regulation of periodontal ligament blood flow (PLBF) is well-attested; however, vasodilator responses mediated by parasympathetic nerve fibers have yet to be conclusively demonstrated in the periodontal ligament (PL). The present study was designed to determine whether parasympathetic vasodilator mechanisms do or do not exist in the cat PL. In our cats, the cervical sympathetic trunks were sectioned bilaterally prior to any stimulation in order to eliminate sympathetic effects on the vascular beds under study. Dynamic changes in PLBF, with mandibular lip blood flow (LBF) recorded for comparison, were investigated in cat mandibular canine teeth using laser Doppler flowmetry. The peripheral cut ends of the facial and glossopharyngeal nerve roots, which have been reported to contain parasympathetic nerve fibers to the oral tissues, were electrically stimulated intracranially. Such stimulation caused blood flow to increase in the ipsilateral PL and lip, without an increase in systemic blood pressure. These vasodilator responses in the PL and lip were sensitive to ganglion blockade (with hexamethonium), indicating vasodilation via activation of parasympathetic vasodilator fibers. In contrast, although intracranial stimulation of the trigeminal nerve root also induced increases in both PLBF and LBF, these were unaffected by hexamethonium, but reduced by tripelennamine, indicating antidromic vasodilatation via the trigeminal sensory nerve. These results suggest that parasympathetic vasodilator mechanisms do exist in feline PL.     

Tooth pulp neurons in the caudal medulla oblongata of the cat

The medulla oblongata caudal to the obex was explored for neurons responsive to tooth pulp (TP) stimulation in cats. Four different subclasses of TP neurons were found. The latter included TP specific (TPS) neurons, trigeminal wide dynamic range (trigeminal WDR) neurons with TP input, trigeminal subnucleus reticularis ventralis (trigeminal SRV) neurons with TP input and convergent reticular formation (convergent RF) neurons with TP input. TPS neurons were located in the dorsal marginal rim of the trigeminal subnucleus caudalis, i.e., in the marginal layer or the outer zone of substantia gelatinosa. WDR neurons with TP input were found in the neck region of medullary dorsal horn which corresponds to the lateral part of subnucleus reticularis dorsalis (SRD). Trigeminal SRV neurons with TP input were located in the lateral part of SRV. Convergent RF neurons with TP input were found in the middle third of the caudal bulbar RF consisting of SRD and SRV. Both TPS neurons and WDR neurons with TP input included trigeminothalamic neurons as evidenced by the antidromic activation from the nucleus ventralis posteromedialis of the contralateral thalamus. A significant proportion of both trigeminal SRV and convergent RF neurons with TP input were antidromically activated by stimulation of the nucleus centralis lateralis of the contralateral thalamus. The former two subclasses may subserve the sensory-discriminative aspect of toothache, while the latter two subclasses, the emotional-motivational aspect.