α1 adrenergic receptor activation has a dynamic effect on masticatory muscle afferent fibers.

Temporomandibular Disorder (TMD) patients report amplification of pain in the masticatory muscles after psychological trauma or stressful conditions. The mechanisms underlying this phenomenon are yet to be elucidated. This study combined immunohistochemistry with single cell in vivo electrophysiology recordings of masticatory muscle afferent fibers to investigate the role of α1-adrenergic receptors in muscle nociception. It was found that a subset of trigeminal afferent fibers which innervate the masseter and temporal muscles expressed α1a, α1b and α1d receptors, including a smaller number of putative nociceptors which co-expressed TrpV1 receptors. Local injection of the selective α1 adrenergic receptor agonist phenylephrine into masticatory muscle decreased and increased the mechanical activation threshold of slow and fast conducting afferent fibers, respectively. This effect was reversed by co-administration of the α1 selective antagonist terazosin. To rule out the possibility that local ischemia was responsible for the observed effect of phenylephrine on masticatory muscle afferent fibers, additional experiments were conducted where blood flow to the masticatory muscle was reduced by common carotid artery occlusion. This investigation found that muscle blood flow occlusion increased the mechanical activation threshold of the majority of masticatory muscle afferent fibers unrelated to conduction velocity. These findings suggest that under conditions of increased sympathetic tone, such as those related to stress, noradrenaline may sensitize masticatory muscle nociceptors to increase pain and desensitize muscle proprioceptors to alter muscle tone, through activation of α1 receptors.

Masticatory Muscles and Branches of Mandibular Nerve: Positional Relationships Between Various Muscle Bundles and Their Innervating Branches.

The masticatory muscles, which are composed of four main muscles, are innervated by branches of only one of the cranial nerves, the mandibular nerve. This muscle group has a variety of very complex functions. We have investigated the origins and insertions of the masticatory muscles and the adjacent bundles of the main muscles, and closely examined the positional relationships between the muscle bundles and innervating branches. According to the findings of the nerve branching patterns, the masticatory muscles can be classified into two groups: the inner group consisting of the lateral pterygoid muscle, and the outer group consisting of the other muscles and adjacent muscle bundles. Further, the outer muscle group is sub-divided into the three other main muscles (the masseter, the temporalis, and the medial pterygoid muscle) and the adjacent various transitional muscle bundles. Anat Rec, 302:609-619, 2019. © 2018 Wiley Periodicals, Inc.

Observation of Effects of Different Surgical Treatments on Unilateral Masticatory Muscle Spasm.

BACKGROUND: Unilateral masticatory muscle spasm is a rare disease without a generally accepted and efficacious treatment plan. OBJECTIVE: We sought to compare the effects of different surgical treatments on unilateral masticatory muscle spasm. METHODS: A retrospective analysis of the surgical treatment and effects of 10 cases of unilateral masticatory muscle spasm occurred between February 2010 and September 2016. Three cases underwent complete amputation of the trigeminal motor branch, 3 cases underwent partial amputation of the trigeminal motor branch, and 4 cases received only vascular decompression. All patients were followed up by telephone interview after surgery. RESULTS: In the simple vascular decompression group, 3 cases were cured and 1 was cured after a delay. Of these 3 cases, 1 case became aggravated 2 years after the operation, 1 case became aggravated 5 years after the operation, and 1 case showed no change during the follow-up period. In the partial amputation group, 2 cases were cured and 1 case was alleviated. Of the 2 patients who were cured, 1 suffered recurrence 2 years later, while the other case showed no recurrence during the follow-up period. In the complete amputation group, 1 case was cured with a delay and 2 cases were cured immediately with no recurrence during the follow-up. Mild atrophy of the temporal muscle occurred gradually with no restriction of the mouth opening in 2 cases. CONCLUSIONS: Complete amputation of the trigeminal nerve did achieve better effects than pure microvascular decompression and partial amputation of the trigeminal motor branch, but it may lead to mild temporal muscle atrophy.

High variability of facial muscle innervation by facial nerve branches: A prospective electrostimulation study.

OBJECTIVES/HYPOTHESIS: To examine by intraoperative electric stimulation which peripheral facial nerve (FN) branches are functionally connected to which facial muscle functions. STUDY DESIGN: Single-center prospective clinical study. METHODS: Seven patients whose peripheral FN branching was exposed during parotidectomy under FN monitoring received a systematic electrostimulation of each branch starting with 0.1 mA and stepwise increase to 2 mA with a frequency of 3 Hz. The electrostimulation and the facial and neck movements were video recorded simultaneously and evaluated independently by two investigators. RESULTS: A uniform functional allocation of specific peripheral FN branches to a specific mimic movement was not possible. Stimulation of the whole spectrum of branches of the temporofacial division could lead to eye closure (orbicularis oculi muscle function). Stimulation of the spectrum of nerve branches of the cervicofacial division could lead to reactions in the midface (nasal and zygomatic muscles) as well as around the mouth (orbicularis oris and depressor anguli oris muscle function). Frontal and eye region were exclusively supplied by the temporofacial division. The region of the mouth and the neck was exclusively supplied by the cervicofacial division. Nose and zygomatic region were mainly supplied by the temporofacial division, but some patients had also nerve branches of the cervicofacial division functionally supplying the nasal and zygomatic region. CONCLUSIONS: FN branches distal to temporofacial and cervicofacial division are not necessarily covered by common facial nerve monitoring. Future bionic devices will need a patient-specific evaluation to stimulate the correct peripheral nerve branches to trigger distinct muscle functions. LEVEL OF EVIDENCE: 4 Laryngoscope, 127:1288-1295, 2017.

Microvascular Decompression for Hemimasticatory Spasm: A Case Report and Review of the Literature.

BACKGROUND: Hemimasticatory spasm is a rare clinical entity characterized by involuntary and paroxysmal contractions of the jaw-closing muscles on 1 side of the face. Although its cause is not fully known, vascular compression of the trigeminal nerve has been speculated. CASE DESCRIPTION: Here, we report 1 case of hemimasticatory spasm that was cured by microvascular decompression of the motor branch of the trigeminal nerve; a relevant literature review was also performed. CONCLUSIONS: Hemimasticatory spasm is a rare disease that may be recalcitrant to conservative medical therapy, and vascular decompression of the trigeminal nerve may be required to relieve the spasm.

Analgesic effect of cathodal transcranial current stimulation over right dorsolateral prefrontal cortex in subjects with muscular temporomandibular disorders: study protocol for a randomized controlled trial.

BACKGROUND: Temporomandibular disorders are a group of orofacial pain conditions that are commonly identified in the general population. Like many other chronic pain conditions, they can be associated with anxiety/depression, which can be related to changes in the activity of the dorsolateral prefrontal cortex. Some studies have demonstrated clinical improvement in subjects with chronic pain who are given therapeutic neuromodulation. Transcranial direct current stimulation is a noninvasive brain stimulation technique that allows the modulation of neuronal membranes. This therapy can enhance or inhibit action potential generation in cortical neurons. In some instances, medications acting in the central nervous system may be helpful despite their adverse side effects. It is important to determine if cathodal transcranial direct current stimulation over the dorsolateral prefrontal cortex, an area that modulates emotion and motor cortex excitability, has an analgesic effect on chronic temporomandibular disorders pain. METHOD/DESIGN: The investigators will run a randomized, controlled crossover double blind study with 15 chronic muscular temporomandibular disorder subjects. Each subject will undergo active (1 mA and 2 mA) and sham transcranial direct current stimulation. Inclusion criteria will be determined by the Research Diagnostic Criteria for Temporomandibular Disorders questionnaire, with subjects who have a pain visual analogic scale score of greater than 4/10 and whose pain has been present for the previous 6 months, and with a State-Trait Anxiety Inventory score of more than 42. The influence of transcranial direct current stimulation will be assessed through a visual analogic scale, quantitative sensory testing, quantitative electroencephalogram, and the State-Trait Anxiety Inventory score. DISCUSSION: Some studies have demonstrated a strong association between anxiety/depression and chronic pain, where one may be the cause of the other. This is especially true in chronic temporomandibular disorders, and breaking this cycle may have an effect over the symptoms and associated dysfunction. We believe that by inhibiting activity of the dorsolateral prefrontal cortex though cathodal transcranial direct current stimulation, there may be a change in both anxiety/depression and pain level. Transcranial direct current stimulation may emerge as a new tool to be considered for managing these patients. We envision that the information obtained from this study will provide a better understanding of the management of chronic temporomandibular disorders. TRIAL REGISTRATION: This trial was registered at clinicaltrials.gov on 24 May 2014 (Identifier: NCT02152267 ).

Evolutionary Conservation of the Early Axon Scaffold in the Vertebrate Brain.

The early axon scaffold is the first axonal structure to appear in the rostral brain of vertebrates, paving the way for later, more complex connections. Several early axon scaffold components are conserved between all vertebrates; most notably two main ventral longitudinal tracts, the tract of the postoptic commissure and the medial longitudinal fascicle. While the overall structure is remarkably similar, differences both in the organization and the development of the early tracts are apparent. This review will bring together extensive data from the last 25 years in different vertebrates and for the first time, the timing and anatomy of these early tracts have been directly compared. Representatives of major vertebrate clades, including cat shark, Xenopus, chick, and mouse embryos, will be compared using immunohistochemistry staining based on previous results. There is still confusion over the nomenclature and homology of these tracts which this review will aim to address. The discussion here is relevant both for understanding the evolution of the early axon scaffold and for future studies into the molecular regulation of its formation.

Effects of Neuromuscular Electrical Stimulation on the Masticatory Muscles and Physiologic Sleep Variables in Adults with Cerebral Palsy: A Novel Therapeutic Approach.

Cerebral palsy (CP) is a term employed to define a group of non-progressive neuromotor disorders caused by damage to the immature or developing brain, with consequent limitations regarding movement and posture. CP may impair orapharygeal muscle tone, leading to a compromised chewing function and to sleep disorders (such as obstructive sleep apnea). Thirteen adults with CP underwent bilateral masseter and temporalis neuromuscular electrical stimulation (NMES) therapy. The effects on the masticatory muscles and sleep variables were evaluated using electromyography (EMG) and polysomnography (PSG), respectively, prior and after 2 months of NMES. EMG consisted of 3 tests in different positions: rest, mouth opening and maximum clenching effort (MCE). EMG values in the rest position were 100% higher than values recorded prior to therapy for all muscles analyzed (p < 0.05); mean mouth opening increased from 38.0 ± 8.0 to 44.0 ± 10.0 cm (p = 0.03). A significant difference in MCE was found only for the right masseter. PSG revealed an improved in the AHI from 7.2±7.0/h to 2.3±1.5/h (p < 0.05); total sleep time improved from 185 min to 250 min (p = 0.04) and minimun SaO2 improved from 83.6 ± 3.0 to 86.4 ± 4.0 (p = 0.04). NMES performed over a two-month period led to improvements in the electrical activity of the masticatory muscles at rest, mouth opening, isometric contraction and sleep variables, including the elimination of obstructive sleep apnea events in patients with CP. Trial registration: ReBEC RBR994XFS http://www.ensaiosclinicos.gov.br.

Distribution of transient receptor potential melastatin-8-containing nerve fibers in rat oral and craniofacial structures.

The transient receptor potential melastatin-8 (TRPM8) is a cold and menthol receptor located in the sensory ganglia. Immunohistochemistry for TRPM8 was performed on oral and craniofacial structures of the rat. TRPM8-immunoreactive (-IR) nerve fibers were detected in the oral mucous membrane. In the gingiva, TRPM8-IR nerve fibers were abundant beneath and within crestal and outer epithelia. Such nerve fibers were also common beneath and within taste buds in the incisive papilla. In addition, TRPM8-immunoreactivity was expressed by some taste bud cells in the papilla. Lips, periodontal ligaments and salivary glands as well as masticatory muscles and temporomandibular joints were mostly devoid of TRPM8-IR nerve fibers. A double immunofluorescence study indicated different distribution patterns of nerve fibers containing TRPM8 and calcitonin gene-related peptide in oral and craniofacial tissues. Retrograde tracing method also indicated that TRPM8-IR nerve fibers in the gingiva and incisive papilla originate from small sensory neurons in the trigeminal ganglion. TRPM8 may be associated with cool, cold nociceptive (

Homeostatic dysregulation in membrane properties of masticatory motoneurons compared with oculomotor neurons in a mouse model for amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative motoneuron disease with presently no cure. Motoneuron (MN) hyperexcitability is commonly observed in ALS and is suggested to be a precursor for excitotoxic cell death. However, it is unknown whether hyperexcitability also occurs in MNs that are resistant to degeneration. Second, it is unclear whether all the MNs within homogeneous motor pools would present similar susceptibility to excitability changes since high-threshold MNs innervating fast fatigable muscle fibers selectively degenerate compared with low-threshold MNs innervating fatigue resistant slow muscle fibers. Therefore, we concurrently examined the excitability of ALS-vulnerable trigeminal motoneurons (TMNs) controlling jaw musculature and ALS-resistant oculomotor neurons (OMNs) controlling eye musculature in a well studied SOD1(G93A) ALS mouse model using in vitro patch-clamp electrophysiology at presymptomatic ages P8-P12. Our results show that hyperexcitability is not a global change among all the MNs, although mutant SOD1 is ubiquitously expressed. Instead, complex changes occur in ALS-vulnerable TMNs based on motor unit type and discharge characteristics. Firing threshold decreases among high-threshold TMNs and increases in a subpopulation of low-threshold TMNs. The latter group was identified based on their linear frequency-current responses to triangular ramp current injections. Such complex changes in MN recruitment were absent in ALS-resistant OMNs. We simulated the observed complex changes in TMN excitability using a computer-based jaw closer motor pool model. Model results suggest that hypoexcitability may indeed represent emerging disease symptomology that causes resistance in muscle force initiation. Identifying the cellular and molecular properties of these hypoexcitable cells may guide effective therapeutic strategies in ALS.

Treatment of hemimasticatory spasm with microvascular decompression.

Hemimasticatory spasm is a rare disorder characterized by paroxysmal involuntary contraction of the jaw-closing muscles. As the ideology and pathogenesis of the disease are still unclear, there has been no treatment that could give rise to a good outcome so far. Herein, we tried to use surgical management to cure the disease. Six patients with the disease were included in this study. These patients underwent microvascular decompression of the motor fibers of the trigeminal root. After the operation, all faces of the patients felt relaxed at varied degrees, except for 1 patient. Our study showed that microvascular decompression of the trigeminal nerve could lead to a better outcome. However, a control study with a large sample is needed before this technique is widely used.

The difficult relationship between occlusal interferences and temporomandibular disorder - insights from animal and human experimental studies.

The aetiology of temporomandibular disorder (TMD) is multifactorial, and numerous studies have addressed that occlusion may be of great importance. However, whether occlusion plays a crucial role in the pathogenesis of TMD remains controversial. Study designs utilising animal models have been used to study the effects of artificial occlusal alterations. Experimental traumatic occlusion affects blood flow in the temporomandibular joint and results in changes in the condylar cartilage, and artificial occlusal interference induces masticatory muscle nociceptive responses that are associated with peripheral sensitisation and lead to central sensitisation, which maintains masticatory muscle hyperalgesia. The possibility that occlusal interference results in TMD has been investigated in humans using a double-blind randomised design. Subjects without a history of TMD show fairly good adaptation to interferences. In contrast, subjects with a history of TMD develop a significant increase in clinical signs and self-report stronger symptoms (occlusal discomfort and chewing difficulties) in response to interferences. Meanwhile, psychological factors appear meaningful for symptomatic responses to artificial interferences in subjects with a history of TMD. Thus, individual differences in vulnerability to occlusal interferences do exist. Although there are advantages and disadvantages to using human and animal occlusal interference models, these approaches are indispensable for discovering the role of occlusion in TMD pathogenesis.

Parotid gland atrophy in patients with chronic trigeminal nerve denervation.

BACKGROUND AND PURPOSE: Trigeminal nerve injury or dysfunction is associated with denervation atrophy of muscles innervated by the mandibular branch of the trigeminal nerve. The purpose of our study was to evaluate the association between chronic CN V denervation and parotid gland atrophy. MATERIALS AND METHODS: Twenty-six patients with chronic masticator muscle atrophy were retrospectively identified and evaluated for the presence of ipsilateral parotid gland atrophy. Twenty-six age-matched control subjects with no clinical or imaging evidence of chronic masticator space atrophy were also identified. Segmentation of the parotid gland was performed to calculate a parotid asymmetry index. The Fisher exact test and t test were respectively used to determine the correlation between parotid gland atrophy and ipsilateral masticator muscle atrophy and to evaluate any difference in the size of the involved parotid gland when compared with that in the control subjects. RESULTS: Ipsilateral parotid gland atrophy was seen in 9/26 (42.8%) patients with fatty replacement of the masticator group of muscles, suggesting a correlation between parotid gland atrophy and CN V denervation (P<.001). The parotid asymmetry index was significantly different in patients with CN V denervation (0.59±0.25) compared with control subjects (0.92±0.03) (P<.001). CONCLUSIONS: Ipsilateral parotid gland atrophy can accompany chronic CN V denervation change, and its clinical significance remains to be determined.

Jaw muscle spindle afferents coordinate multiple orofacial motoneurons via common premotor neurons in rats: an electrophysiological and anatomical study.

Jaw muscle spindle afferents (JMSA) in the mesencephalic trigeminal nucleus (Vme) project to the parvocellular reticular nucleus (PCRt) and dorsomedial spinal trigeminal nucleus (dm-Vsp). A number of premotor neurons that project to the trigeminal motor nucleus (Vmo), facial nucleus (VII) and hypoglossal nucleus (XII) are also located in the PCRt and dm-Vsp. In this study, we examined whether these premotor neurons serve as common relay pool for relaying JMSA to multiple orofacial motoneurons. JMSA inputs to the PCRt and dm-Vsp neurons were verified by recording extracellular responses to electrical stimulation of the caudal Vme or masseter nerve, mechanical stimulation of jaw muscles and jaw opening. After recording, biocytin in recording electrode was inotophorized into recording sites. Biocytin-Iabeled fibers traveled to the Vmo, VII, XII, and the nucleus ambiguus (Amb). Labeled boutons were seen in close apposition with Nissl-stained motoneurons in the Vmo, VII, XII and Amb. In addition, an anterograde tracer (biotinylated dextran amine) was iontophorized into the caudal Vme, and a retrograde tracer (Cholera toxin B subunit) was delivered into either the VII or Xll to identify VII and XII premotor neurons that receive JMSA input. Contacts between labeled Vme neuronal boutons and premotor neurons were observed in the PCRt and adjacent dm-Vsp. Confocal microscopic observations confirmed close contacts between Vme boutons and VII and XII premotor neurons. This study provides evidence that JMSA may coordinate activities of multiple orofacial motor nuclei, including Vmo, VII, XII and Amb in the brainstem via a common premotor neuron pool.

Clinical anatomy of the auriculotemporal nerve in the area of the infratemporal fossa.

The auriculotemporal nerve is a sensory branch extending from the posterior section of the mandibular nerve trunk. Its nerve roots form a short trunk, which gives off a number of branches, innervating: the temporomandibular joint, the temporal region, structures of the external ear: auricle, and external acoustic meatus, and the parotid gland. It also conducts excretory fibres to the buccal and labial glands. Anatomical relationships between the auriculotemporal nerve and the muscles of mastication, temporomandibular joint, and surrounding vessels in the area of the infratemporal fossa create favourable conditions for entrapment syndromes. Entrapment of the auriculotemporal nerve plays a role in the pathogenesis of temporomandibular joint pain syndromes, headaches, as well as pain symptoms or paraesthesias within the external acoustic meatus and auricle. The current study was performed on 16 specimens containing the infratemporal fossa. Some variations in the nerve roots of the auriculotemporal nerve were found and described as one-, two-, three-, four-, and five-root variants. The topography of the auriculotemporal nerve and its close relationship to the structures of the temporomandibular joint were described. Individually, the variable topography of the nerve course may play a role in the symptomatology of headaches and localisation of pain in the face regions and masticatory system.

Differences in maturation of the jaw-opening reflex between rats that received early-and late-masticatory stimulation.

The jaw-opening reflex (JOR) plays an important role in the regulation of jaw movement during mastication. Previous study showed that altered masticatory function during growth impedes JOR maturation and thus may affect masticatory performance in adults. However, no studies have compared the benefit of early and delayed correction in terms of functional development. Therefore, this study tested the hypothesis that early-stimulation of masticatory function during growth can promote JOR maturation better than late-stimulation during adulthood. Soon after weaning, 120 female Wistar rats were divided into two groups and fed either solid (control group) or liquid (experimental group) diets. The experimental group was further divided into early-, late-, and non-stimulation subgroups. Early- and late-stimulation groups were fed a solid diet instead of a liquid diet at 5- and 11-week-old, respectively, whereas non-stimulation group was fed only a liquid diet until the end of the experiment. At 3, 5, 7, 9, 11 and 13 weeks, JOR recordings were conducted in anaesthetised rats of all groups. Latency and peak-to-peak amplitude of the JOR were compared between the groups. From 7 to 13 weeks, early-stimulation group showed a JOR with short latency and high amplitude similar to that of control group. In contrast, late- and non-stimulation groups showed significantly longer latency and smaller amplitude of the JOR than in control group. We demonstrated that early masticatory stimulation within the critical period for programming mastication may have greater potential to restore JOR maturation to values close to those in normal adults.

Experimental stressors alter hypertonic saline-evoked masseter muscle pain and autonomic response.

AIMS: To test in a randomized controlled trial, if hypertonic saline (HS)-evoked pain and autonomic function are modulated by either a cold pressor test (CPT) or mental arithmetic stress induced by a paced auditory serial addition task (PASAT). METHODS: Fourteen healthy women participated in three sessions. Pain was induced by two 5% HS infusions (5 minutes each, 30 minutes apart) infused into the masseter muscle. During the second HS infusion, pain was modulated by PASAT, CPT, or control (HS alone). HS-evoked pain intensity was scored on a 0 to 10 numeric rating scale (NRS). Heart rate variability (HRV) and hemodynamic measures were recorded noninvasively (Task Force Monitor). Data were analyzed using repeated measurements ANOVAs and Spearman correlation analysis. RESULTS: HS-evoked pain was significantly and similarly reduced by both PASAT (30.8 ± 27.6%; P < .001) and CPT (35.8 ± 26.6%; P < .001) compared with the control session (9.0 ± 30.5%; P > .05). PASAT and CPT increased the heart rate compared with control (P <.001). CPT reduced measures of vagal activity: Root mean square successive difference, high-frequency (HF) power, and coefficient of HF component variance compared with an internal control, ie, the first HS infusion (P < .05), while PASAT did not alter any of these HRV measures (P > .05). CONCLUSION: CPT and PASAT reduced HS-evoked masseter muscle pain and altered the autonomic response. The increase in heart rate following CPT and PASAT may be caused by different mechanisms. CPT reduced measures of efferent cardiac vagal (parasympathetic) activity, while the PASAT-induced increase in heart rate, but unchanged HRV, may suggest neurohumoral activation.

γ-Aminobutyric acid-, glycine-, and glutamate-immunopositive boutons on mesencephalic trigeminal neurons that innervate jaw-closing muscle spindles in the rat: ultrastructure and development.

Unlike other primary sensory neurons, the neurons in the mesencephalic trigeminal nucleus (Vmes) receive most of their synaptic input onto their somata. Detailed description of the synaptic boutons onto Vmes neurons is crucial for understanding the synaptic input onto these neurons and their role in the motor control of masticatory muscles. For this, we investigated the distribution of γ-aminobutyric acid (GABA)-, glycine-, and glutamate-immunopositive (+) boutons on Vmes neurons and their ultrastructural parameters that relate to transmitter release: Vmes neurons that innervate masseteric muscle spindles were identified by labeling with horseradish peroxidase injected into the muscle, and immunogold staining and quantitative ultrastructural analysis of synapses onto these neurons were performed in adult rats and during postnatal development. The bouton volume, mitochondrial volume, and active zone area of the boutons contacting labeled somata (axosomatic synapses) were similar to those of boutons forming axoaxonic synapses with Vmes neurons but smaller than those of boutons forming axodendritic or axosomatic synapses with most other neurons. GABA+ , glycine+ , and glutamate+ boutons constituted a large majority (83%) of all boutons on labeled somata. A considerable fraction of boutons (28%) was glycine(+) , and all glycine+ boutons were also GABA+ . Bouton size remained unchanged during postnatal development. These findings suggest that the excitability of Vmes neurons is determined to a great extent by GABA, glycine, and glutamate and that the relatively lower synaptic strength of axosomatic synapses may reflect the role of the Vmes neurons in modulating orofacial motor function.

Effects of changes in vertical occlusal dimension on heart rate fluctuations in guinea pigs.

BACKGROUND: We have previously reported that the decrease of the vertical occlusal dimension (VOD) led to heart failure and abnormalities in creatine phosphokinase (CPK) in guinea pigs. In the present study, we investigated the autonomic activity and the origin of the abnormality in CPK under different occlusal conditions. MATERIALS AND METHODS: Guinea pigs were separated into the following five groups: untreated control, reduced VOD, slit, restored VOD and increased VOD groups and compared for their electrocardiogram and heart rate fluctuations for two weeks using Fluclet, computer software. RESULTS: The control group revealed no changes in heart rate fluctuations or posture. The reduced VOD group exhibited a two-phase wave of heart rate fluctuations, with the first peak 0-2 days after teeth grinding, and the second peak starting from 4 days after teeth grinding until sudden death (usually 12th day), accompanied by head drop. The slit and the restored VOD groups exhibited only the first peak. The increased VOD group, with approximately 3 mm-thick acrylic pellets bonded to the posterior teeth, showed no heart rate fluctuations. Body weight loss was most prominent in the reduced VOD group, and became much milder in the order of increased VOD, restored and slit groups. The reduced VOD group exhibited transient elevation of skeletal muscle type of CPK isozyme activity within two days after treatment. CONCLUSION: The present study suggests that the first peak of heart rate fluctuations is caused by pulpal stimulation, and the second peak by excessive contraction (excessive excitation of the motor output system and the autonomic nervous system) of the masticatory muscles. On the other hand, increased VOD did not influence either the motor or the autonomic nervous system.

Development of γ-aminobutyric acid-, glycine-, and glutamate-immunopositive boutons on rat jaw-opening motoneurons.

Inhibitory and excitatory synaptic inputs onto trigeminal motoneurons play an important role in coordinating jaw movements. Previously, we reported that the phenotype of the inhibitory boutons apposing the somata of jaw-closing (JC) motoneurons changes from γ-aminobutyric acid (GABA)-positive (GABA+) to predominantly glycine-positive (Gly+) during development. In the present study, we investigated the development of inhibitory and excitatory boutons apposing antagonistic jaw-opening (JO) motoneurons (anterior digastric motoneurons) at postnatal day 2 (P2), P11, and P31 in the rat. JO motoneurons were retrogradely labeled with horseradish peroxidase. Postembedding immunogold staining with antisera against GABA, Gly, and glutamate (Glut) was performed and followed by quantitative ultrastructural analysis. The size of both small and large JO motoneurons increased during development. The number of excitatory (Glut+) and inhibitory (GABA+, Gly+, and GABA+/Gly+) boutons per JO motoneuron increased significantly from P2 to P11 and then remained unchanged until P31. The time course of inhibitory synapse formation differed between JO and JC motoneurons, whereas that of excitatory synapse formation was similar between the two neuronal populations. The fraction of GABA+ boutons decreased by 86% and the fraction of GABA+/Gly+ boutons increased by 200% from P11 to P31, suggesting a switch from GABA+ to GABA+/Gly+ phenotype. The fraction of Gly+ boutons remained unchanged. These results indicate that inhibitory synapses onto somata of JO motoneurons exhibit a developmental pattern distinct from that of synapses onto JC motoneurons, which may reflect distinctive maturation of oral motor system.