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The distribution of cell clusters in the cervical vagal nerve (CVN), superior laryngeal nerve (SLN) and recurrent laryngeal nerve (RLN), and the peptidergic features of their ganglionic neurons projecting to the larynx, were investigated in the cat using a combination of retrograde tracing by wheat germ agglutinin (WGA) and immunocytochemistry. In the CVN, a few medium sized cell clusters at a level caudal to the nodose ganglion, and some small cell clusters along the course of the vagus, were found. In the SLN and RLN, some medium sized ganglia were located close to the laryngeal framework and a few small groups of cells occupied more rostral parts. Some neurons of the cell clusters in the CVN and most of the ganglionic cells in the SLN and RLN exhibited WGA-immunoreactive (IR) cells, which projected to the larynx. In these WGA-positive ganglionic neurons, many cells showed vasoactive intestinal polypeptide-IR neurons, some neuropeptide Y-IR, and a few substance P-IR and calcitonin gene-related peptide-IR cells were also identified. The present findings indicate that neurons of the cell clusters in the laryngeal nerves, particularly those in the vicinity of the laryngeal framework, project to the larynx and may be autonomic.
The presence of ganglia associated with the laryngeal nerves is well documented. In man, these ganglia have been less well studied than in other species and, in particular, the cell types within these ganglia are less well characterized. Using a panel of antibodies to a variety of markers found in the paraganglion cells of other species, we were able to show the existence of at least two populations of cells within human laryngeal paraganglia. One population contained chromogranin and tyrosine hydroxylase representing a neurosecretory population possibly secreting dopamine. A second population of choline acetyltransferase positive cells would appear to have a putative parasympathetic function. Further work is needed to characterize these cell populations more fully before it will be possible to assign functions to these cell types but our results are consistent with the postulated functions of these ganglia as chemoreceptors, neurosecretory cells, and regulators of laryngeal mucus secretion.
Maintaining the patency of the upper airway during breathing is of vital importance. The activity of various muscles is related to the patency of the upper airway. In the present study, we examined the respiratory motor activity in the efferent nerves innervating the upper airway muscles to determine the movements of the upper airway during respiration under normocapnic conditions (pH = 7.4) and in hypercapnic acidosis (pH = 7.2). Experiments were performed on arterially perfused decerebrate rats aged between postnatal days 21-35. We recorded the efferent nerve activity in a branch of the cervical spinal nerve innervating the infrahyoid muscles (CN), the hypoglossal nerve (HGN), the external branch of the superior laryngeal nerve (SLN), and the recurrent laryngeal nerve (RLN) with the phrenic nerve (PN). Inspiratory nerve discharges were observed in all these nerves under normocapnic conditions. The onset of inspiratory discharges in the CN and HGN was slightly prior to those in the SLN and RLN. When the CO2 concentration in the perfusate was increased from 5% to 8% to prepare for hypercapnic acidosis, the peak amplitudes of the inspiratory discharges in all the recorded nerves were increased. Moreover, hypercapnic acidosis induced pre-inspiratory discharges in the CN, HGN, SLN, and RLN. The onset of pre-inspiratory discharges in the CN, HGN, and SLN was prior to that of discharges in the RLN. These results suggest that the securing of the airway that occurs a certain time before dilation of the glottis may facilitate ventilation and improve hypercapnic acidosis.
This study addresses the question of whether increased vascular permeability, which is a prominent feature of neurogenic inflammation in the respiratory tract, is mediated by sensory axons that end near venules in the airway mucosa. In these experiments, neurogenic inflammation was produced in the tracheal and bronchial mucosa of atropine-treated Long-Evans rats by electrical stimulation of the left or right superior laryngeal nerve and/or cervical vagus nerve. The particulate tracer Monastral blue was injected intravenously to localize the sites of increased vascular permeability, and microspectrophotometry was used to measure the amount of extravasated Monastral blue in the trachea and thereby quantify the increase in vascular permeability. In some rats, selective denervations were made to locate the cell bodies of neurons that mediate the increase in vascular permeability; in others, fluorescence immunohistochemistry and quantitative electron microscopic methods were used to determine which structures in the tracheal mucosa are innervated by these neurons. The study revealed that the vagally mediated increase in vascular permeability was sudden, transient (half-life = 2.4 min) and restricted to venules. Stimulation of the left or right superior laryngeal nerve increased the permeability of venules in the extrathoracic trachea, whereas stimulation of either vagus nerve increased vascular permeability in the intrathoracic trachea and bronchi. All nerves had bilateral effects in the trachea, but the vagus nerves had largely unilateral effects in the bronchi. Neurons that mediated the increase in venular permeability had their cells bodies in the jugular (superior sensory) ganglion of the vagus nerve or rostral portion of the nodose (inferior sensory) ganglion. Preganglionic autonomic vagal neurons in the brain stem were not essential for this increase in venular permeability. Few nerves identifiable by substance P-immunohistochemistry or electron microscopy were located near the affected venules, and no nerves were within 1 micron of the walls of venules. However, the epithelium and arterioles of the airway mucosa were densely innervated. All intraepithelial nerves were within 0.1 micron of epithelial cells, and at least two-thirds of nerves near arterioles were within 1 micron of the vessel walls. We conclude that the increase in venular permeability associated with neurogenic inflammation in the trachea and bronchi of rats is mediated by sensory axons that travel in the vagus nerves and superior laryngeal nerves.(ABSTRACT TRUNCATED AT 400 WORDS)
Recurrent laryngeal nerve (RLN) damage is a significant and prevalent complication of thyroid surgery. Based on the beneficial role of a human amnion/chorion membrane (HACM) allograft in wound management and nerve regeneration, we investigated whether placement of a commercially available HACM allograft on dissected RLN could reduce the occurrence and/or duration of RLN injury during thyroidectomy. Among 67 patients undergoing thyroidectomy, 100 at-risk nerves (exposure of at least 3 cm of RLN) received intraoperative placement of HACM; 205 at-risk RLNs without HACM in 134 matched patients served as controls. Patient-reported vocal analysis, physician-assessed vocal analysis, and laryngoscopic assessment of vocal-fold dysfunction were performed before and after surgery. At 24 h after surgery, 17 patients in the control group (12.5%) had documented voice changes; these changes persisted for at least 3 weeks in seven patients (5%). Only one patient (1.5%) in the HACM group had vocal changes at 24 h after surgery, which resolved within 1 week (P < 0.01). Intraoperative placement of the HACM allograft over at-risk RLNs during thyroidectomy may reduce the incidence, severity, and/or duration of intraoperative RLN injury, which could address a significant complication of head and neck surgery. A larger prospectively designed clinical study is warranted to further investigate a possible benefit of the HACM allograft in thyroid surgery and to begin to understand the mechanisms through which a clinical benefit might be mediated.
Wheat germ agglutinin conjugated to tetramethylrhodamine isothiocyanate-dextran (WGA-TRITC) was studied as a novel tracer of primary projection neurons of pharyngeal (PhN) and superior laryngeal (SLN) branches of the vagus nerve. The SLN and PhN were dissected from rat cervical tissues and the proximal end of the nerves were bathed in tracer for 60-90 min. The animals were sacrificed 42-72 h later. The tissue was fixed, sliced, mounted on slides and viewed under epifluorescence. The clarity of the fluorescent label in projection neurons was confounded in some regions of the brainstem by autofluorescence. A computer image analysis method was developed to quantify fluorescence intensity for definitive identification of labeled neurons. Brainstem neurons labeled by afferent projections of the SLN and PhN were localized to the nucleus tractus solitarius. Efferents were identified in the nucleus ambiguus. WGA-TRITC labeled cells were observed in the ipsilateral brainstem at intensities significantly different from the fluorescence observed in controls (P<0.01). The distribution and density of labeling is in agreement with results of previous investigations, suggesting that WGA-TRITC is a useful alternative for tracing SLN and PhN projections to brainstem nuclei.
In nerve regeneration studies, various animal models are used to assess nerve regeneration. However, because of the difficulties in functional nerve assessment, a visceral nerve injury model is yet to be established. The superior laryngeal nerve (SLN) plays an essential role in swallowing. Although a treatment for SLN injury following trauma and surgery is desirable, no such treatment is reported in the literature. We recently reported that stem cells derived from human exfoliated deciduous teeth (SHED) have a therapeutic effect on various tissues via macrophage polarization. Here, we established a novel animal model of SLN injury. Our model was characterized as having weight loss and drinking behavior changes. In addition, the SLN lesion caused a delay in the onset of the swallowing reflex and gain of laryngeal residue in the pharynx. Systemic administration of SHED-conditioned media (SHED-CM) promoted functional recovery of the SLN and significantly promoted axonal regeneration by converting of macrophages to the anti-inflammatory M2 phenotype. In addition, SHED-CM enhanced new blood vessel formation at the injury site. Our data suggest that the administration of SHED-CM may provide therapeutic benefits for SLN injury.
Recurrent laryngeal nerve (RLN) injury, in which hoarseness and dysphagia arise as a result of impaired vocal fold movement, is a serious complication. Misdirected regeneration is an issue for functional regeneration. In this study, we demonstrated the effect of TrkA inhibitors, which blocks the NGF-TrkA pathway that acts on the sensory/automatic nerves thus preventing misdirected regeneration among motor and sensory nerves, and thereby promoting the regeneration of motor neurons to achieve functional recovery. RLN axotomy rat models were used in this study, in which cut ends of the nerve were bridged with polyglycolic acid-collagen tube with and without TrkA inhibitor (TrkAi) infiltration. Our study revealed significant improvement in motor nerve fiber regeneration and function, in assessment of vocal fold movement, myelinated nerve regeneration, compound muscle action potential, and prevention of laryngeal muscle atrophy. Retrograde labeling demonstrated fewer labeled neurons in the vagus ganglion, which confirmed reduced misdirected regeneration among motor and sensory fibers, and a change in distribution of the labeled neurons in the nucleus ambiguus. Our study demonstrated that TrkAi have a strong potential for clinical application in the treatment of RLN injury.
In this study, we examined the effect of differing gap lengths on regeneration of transected recurrent laryngeal nerves using silicon tubes containing type I collagen gel and the ability of this regeneration to result in restoration of vocal fold movements in rats. We simulated nerve gaps in Sprague-Dawley rats by transecting the left recurrent laryngeal nerves and bridged the nerve stumps using silicon tubes containing type 1 collagen gel. Three experimental groups, in which the gap lengths between the stumps were 1, 3, or 5 mm, were compared with a control group in which the nerve was transected but was not bridged. After surgery, we observed vocal fold movements over time with a laryngoscope. At week 15, we assessed the extent of nerve regeneration in the tube, histologically and electrophysiologically. We also assessed the degree of atrophy of the thyroarytenoid muscle (T/U ratio). Restoration of vocal fold movements was observed in 9 rats in the 1-mm group, in 6 rats in the 3-mm group, and in 3 rats in the 5-mm group. However, in most rats, restoration was temporary, with only one rat demonstrating continued vocal fold movements at week 15. In electromyograph, evoked potentials were observed in rats in the 1-mm and 3-mm groups. Regenerated tissue in the tube was thickest in the 1-mm group, followed by the 3-mm and 5-mm groups. The regenerated tissue showed the presence of myelinated and unmyelinated nerve fibers. In assessment of thyroarytenoid muscle atrophy, the T/U ratio was highest in the 1-mm group, followed by the 3-mm and 5-mm groups. We successfully regenerated the nerves and produced a rat model of recurrent laryngeal nerve regeneration that demonstrated temporary recovery of vocal fold movements. This rat model could be useful for assessing novel treatments developing in the future.
Obstructive sleep apnea, similar to intermittent hypoxia (IH) during sleep, is associated with laryngeal airway hyperreactivity (LAH). IH-induced laryngeal oxidative stress may contribute to LAH, but the underlying mechanism remains unknown. Conscious rats were subjected to repetitive 75 s cycles of IH for 7 or 14 consecutive days. Reflex apneic responses to laryngeal provocations with chemical stimulants were measured to reflect laryngeal reflex reactivity. Compared with control rats, rats exposed to IH for 14 days, but not for 7 days, displayed enhanced apneic response to laryngeal chemical stimulants. The apneic response to chemical stimulants, but not to mechanical stimulation, was totally abolished by perineural capsaicin treatment of superior laryngeal nerves (SLNs) or by the sectioning of the SLNs, suggesting that the reflex was mediated through capsaicin-sensitive SLNs. Daily intraperitoneal administration of N-acetyl-L-cysteine [NAC, a reactive oxygen species (ROS) scavenger], apocynin (an inhibitor of NADPH oxidase) or YC-1 (an inhibitor of HIF-1α), but not their vehicles, largely attenuated this augmented apneic response in 14 days IH rats. Laryngeal lipid peroxidation (an index of oxidative stress) was elevated in 7 days IH rats and 14 days IH rats, and was abolished by any of these three pharmacologic interventions. The protein expression of HIF-1α (an index of HIF-1 activation) and p47phox subunit in the membrane fraction (an index of NADPH oxidase activation) in the laryngeal tissues increased in 14 days IH rats; the former was reduced by NAC, whereas the latter was inhibited by YC-1. These results suggest that 14 days of IH exposure may sensitize capsaicin-sensitive SLNs and result in exaggerated apneic reflex response to laryngeal chemical stimulants. This phenomenon depends on the action of HIF-1α-mediated, NADPH oxidase-derived ROS.
The thyroid and parathyroid glands are dually innervated by sympathetic (cervical sympathetic trunk [CST]) and parasympathetic (superior laryngeal nerve [SLN]) nerve fibers. We examined the effects of electrical stimulation of efferent or afferent nerve fibers innervating the thyroid and parathyroid glands on the secretion of immunoreactive calcitonin (iCT), parathyroid hormone (iPTH), 3,3',5-triiodothyronine (iT3), and thyroxine (iT4) from the thyroid and parathyroid glands. In anesthetized and artificially ventilated rats, thyroid venous blood was collected. The rate of hormone secretion from the glands was calculated from plasma hormone levels, measured by ELISA, and the flow rate of thyroid venous plasma. SLNs or CSTs were stimulated bilaterally with rectangular pulses with a 0.5-ms width. To define the role of unmyelinated nerve fibers (typically efferent), the cut peripheral segments were stimulated at various frequencies (up to 40 Hz) with a supramaximal intensity to excite all nerve fibers. The secretion of iCT, iT3, and iT4 increased during SLN stimulation and decreased during CST stimulation. iPTH secretion increased during CST stimulation, but was not affected by SLN stimulation. To examine the effects of selective stimulation of myelinated nerve fibers (typically afferent) in the SLN, intact SLNs were stimulated with a subthreshold intensity for unmyelinated nerve fibers. iCT, iT3, and iT4 secretion increased during stimulation of intact SLNs at 40 Hz. These results suggest that excitation of myelinated afferents induced by low intensity and high frequency stimulation of intact SLNs promotes secretion of CT and thyroid hormones from the thyroid gland, potentially via reflex activation of parasympathetic efferent nerve fibers in the SLN.
The aim of the present study was to assess the possibility and efficacy of utilizing a laminin-chitosan-poly (lactic-co-glycolic acid), otherwise known as laminin-chitosan-PLGA, nerve conduit with the co-transplantation of Schwann and neural stem cells to repair peripheral nerve defects. Previous in vitro experiments have demonstrated that the three-dimensional structure of the built in fiber filament electrospinning of laminin-chitosan-PLGA nerve conduit is beneficial to the migration and regeneration of nerve cells, and has notable mechanical strength and plasticity. It is able to provide support in the neural tissue regeneration process, and has the ability to degrade itself once peripheral nerves complete their regeneration, providing more advantages than other biological and synthetic materials. In the present study, 132 female Sprague Dawley rats were used to establish an animal model of laryngeal nerve injury, and the rats were randomly divided into six groups for experimentation. The nerve conduit was prepared and co-cultured with Schwann and neural stem cells, and micro-surgical techniques were used to repair the 5-mm-long recurrent laryngeal nerve injuries. Functional and histological assessments were performed at 8 and 12 weeks post-surgery, respectively. The results revealed that the laminin-chitosan-PLGA nerve conduit combined with Schwann and neural stem cells was able to promote nerve regeneration (P<0.05), and its effect was superior to those of the autograft (P<0.05). The results of the present study suggest that this is the ideal method for repairing peripheral nerve defects, and cells in the graft may promote nerve regeneration.
The desire to improve cosmesis has driven the introduction of robotic-assisted and video-assisted thyroidectomy techniques. We report on minimally invasive thyroidectomy (MIT) through a 2-cm incision without the added need for video assistance and hypothesize similar clinical results to standard open thyroidectomy.
The distribution of the Substance P (SP) immunoreactive nerve fibres in the canine larynx and laryngeal nerves was studied by PAP immunohistochemistry. Many individual SP immunoreactive nerve fibres with varicosities were observed within the epithelial layer and in the connective tissue below the epithelium of the laryngeal mucosa. Small numbers of SP immunoreactive nerve fibres were also found in the submucosal gland region and some of them appeared to terminate in glandular cells. These findings are consistent with the view that SP might be involved in the laryngeal sensory innervation system and the laryngeal glandular secretion. No SP immunoreactive nerve fibres were found in any intrinsic laryngeal muscles. The recurrent laryngeal nerve and the superior laryngeal nerve contained SP immunoreactive nerve fibres and were considered to lie in the pathway of the SP nerve fibres to the larynx.
Pharmacological agents that elevate dopamine and substance P concentrations have been suggested to prevent aspiration pneumonia and improve impaired swallowing processes. However, little is known about the effects of such agents on swallowing activities induced in motor nerves innervating the pharyngeal and laryngeal muscles. In this study, we examined the effects of imidapril, cilostazol, and amantadine, which are often prescribed for swallowing disorders, on swallowing motor activity. We recorded the efferent activities of the cervical vagal nerve, hypoglossal nerve, and phrenic nerve using arterially perfused rats aged between 21-35 postnatal days. The vagal nerve activity was used for evaluation of swallowing motor activity. When 1.25 ml of distilled water was injected into the oral cavity, or the superior laryngeal nerve was electrically stimulated, synchronized swallowing bursts were evoked in the vagal and hypoglossal nerves, while inspiratory discharges were inhibited in all the recorded nerves. Administration of imidapril (60 ng/ml) but not cilostazol (2.5 μg/ml) and amantadine (200 ng/ml) to the perfusate increased the mean peak amplitude of orally evoked swallowing bursts in the vagal nerve. Such increase in the peak amplitude by imidapril was antagonized by the administration of the NK1 receptor antagonist aprepitant (5 μg/ml) or the D1 receptor antagonist LE300 (2.5 μg/ml). In contrast, neither imidapril nor cilostazol caused a significant increase in swallowing bursts evoked by electrical stimulation of the superior laryngeal nerve. These results suggest that imidapril treatment may improve impaired swallowing by enhancing pharyngeal muscle activities via an increase in substance P and dopamine concentrations.
Chronic Cough (CC) is common and often associated with significant comorbidity and decreased quality of life. In up to 50% of cases, the cough is refractory despite extensive investigation and treatment trials. It is likely that the key abnormality in refractory CC is dysfunctional, hypersensitive sensory nerves, similar to conditions such as laryngeal hypersensitivity and neuropathic pain.
The effects of the pharyngeal non-noxious mechanical stimulation on the secretion of immunoreactive thyroxin (iT4), immunoreactive calcitonin (iCT), and immunoreactive parathyroid hormone (iPTH) into thyroid venous blood were examined in anesthetized rats. Secretion rates of iT4, iCT, and iPTH were calculated from their concentration in thyroid venous plasma and the plasma flow rate. A mechanical stimulation was delivered to the pharynx by a rubber balloon placed on the tongue that was intermittently pushed into the pharyngeal cavity. Pharyngeal stimulation increased iT4 and iCT secretion, but iPTH secretion was unchanged. The secretion responses were abolished by transecting the superior laryngeal nerves (SLNs) bilaterally. The activities of the thyroid parasympathetic efferent nerves and the afferent nerves in the SLN increased significantly during pharyngeal stimulation. These results indicate that pharyngeal mechanical stimulation promotes thyroxin and calcitonin secretion from the thyroid gland by a reflex increase in SLN parasympathetic efferent activity, triggered by excitation of SLN mechanoreceptive afferents.
Oropharyngeal swallowing is centrally mediated by a swallowing central pattern generator (Sw-CPG) in the medulla oblongata. The activity of the Sw-CPG depends on the sensory inputs determined by physical and chemical bolus properties. Here we investigate the sensory-motor integration during swallowing arising from different sensory sources. To do so we electrically stimulated the superior laryngeal nerve and we triggered swallowing with oral injections of distilled water or capsaicin solution and extracellularly recorded from swallowing interneurons in arterially perfused brainstem preparations of rats. We recorded the activities of 40 neurons, while monitoring the motor activities of the phrenic, vagal and hypoglossal nerves. Eighteen neurons responded to electrical stimulation of the ipsilateral superior laryngeal nerve, and 6 neurons were excited by oral fluid injection, while 16 non-respiratory neurons did not receive afferent inputs to either electrical or physiological stimuli. The cellular activities displayed by swallowing interneurons during electrical and physiological stimulation of pharyngeal and laryngeal afferent input reveal complex adaptations of the timing of firing patterns and frequencies. The modulation of neuronal activity is likely to contribute to the coordination of efficient bolus transfer during the pharyngeal stage of swallowing.
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