Stimulation Of Superior Laryngeal Nerve Research Articles

Asymmetry of the Laryngeal Reflex Responses to Superior Laryngeal Nerve Stimulation Unrelated to the Length of the Recurrent Nerves in the Porcine Model

Electrical stimulation of the superior laryngeal nerve (SLN) can elicit reflex responses in the cricothyroid (CT) and thyroarytenoid (TA) muscles. We made bilateral recordings of the responses evoked in these muscles in piglets by the stimulation of either the right or the left superior laryngeal nerve (SLN). The stimulus intensity was gradually increased to study the ?persistence? of the responses. We observed a direct, ipsilateral response in the CT muscle, and reflex, ipsilateral and crossed responses in both CT and TA muscles. The ipsilateral or contralateral responses obtained in TA muscles, following stimulation of the left SLN, were significantly delayed in comparison with those evoked by stimulation of the right SLN. This delay cannot be explained by the difference in length between the right and the left recurrent laryngeal nerves, but rather by an asymmetry in the sensory afferent pathway. The functional significance of this observation remains to be determined.

Responses of Neurons in the Parabrachial Region of the Rat to Electrical Stimulation of the Superior Laryngeal Nerve and Chemical Stimulation of the Larynx

The responsiveness of the parabrachial region to electrical stimulation of the superior laryngeal nerve was first examined in anesthetized rats. Action potentials were recorded in 30 parabrachial sites by single and train electrical pulses to the superior laryngeal nerve. The average latency, from the onset of stimulation to the first action potentials, was 9.9 ms (range, 6.5–18.8 ms). The responsiveness of parabrachial neurons to chemical stimulation of the laryngeal region was next examined using anesthetized, immobilized, and artificially ventilated rats in which the chorda tympani and glossopharyngeal nerves were bilaterally sectioned. Taste stimuli were applied to the laryngeal region through a tracheal tube and rinsed with 0.15 NaCl. A total of 66 responses were recorded from 26 neurons. The most effective stimulus for these neurons was 0.03 M hydrochloric acid, followed by 0.01 M quinine hydrochloride, 0.5 M sodium chloride, 0.5 M sucrose, and distilled water. Seven responses were derived from 0.15 NaCl. These neurons were mainly located in a posterodorsolateral part of the parabrachial nucleus. These results suggest that chemical signals from the laryngeal region are transmitted to the parabrachial nucleus through the superior laryngeal nerve.

Differential Brainstem Fos-Like Immunoreactivity after Laryngeal-Induced Coughing and Its Reduction by Codeine

We used the expression of the immediate-early gene c-fos, a marker of neuronal activation, to localize brainstem neuronal populations functionally related to fictive cough (FC). In decerebrate, paralyzed, and ventilated cats, the level of Fos-like immunoreactivity (FLI) was examined in five groups of animals: (1) controls, sham-operated unstimulated animals; (2) coughing cats, including both animals in which FC was elicited by unilateral electrical stimulation of the superior laryngeal nerve (SLN) and (3) those in which FC was elicited by bilateral SLN stimulation; (4) stimulated-treated cats, in which bilateral SLN stimulation was applied after selective blockade of FC by codeine; and (5) codeine controls, sham-operated unstimulated cats subjected to administration of codeine. Fifteen brainstem structures were compared for numbers of labeled cells. Because codeine selectively blocks FC, brainstem nuclei activated specifically during FC were identified as regions showing increased FLI after FC and significant reductions in FLI after FC suppression by codeine in stimulated-treated cats. In coughing animals, we observed a selective immunoreactivity in the interstitial and ventrolateral subdivisions of the nucleus of the tractus solitarius, the medial part of the lateral tegmental field, the internal division of the lateral reticular nucleus, the nucleus retroambiguus, the para-ambigual region, the retrofacial nucleus, and the medial parabrachial nucleus. FLI in all these nuclei was significantly reduced in stimulated-treated cats. Our results are consistent with the involvement of neurons overlapping the main brainstem respiratory-related regions as well as the lateral tegmental field and the lateral reticular nucleus in the neural processing of laryngeal-induced FC.

Responses of distinct types of sympathetic neuron to stimulation of the superior laryngeal nerve in the cat

Stimulation of afferents in the superior laryngeal nerve (SLN) leads to apnea and evokes reflexes in sympathetic neurons. It is not clear whether these reflexes are secondary to changes in the brainstem respiratory network or due directly to the afferent input on neurons belonging to central sympathetic pathways. To clarify this question, single thoracic preganglionic sympathetic neurons projecting into the cervical sympathetic trunk (CST) were classified as described previously and then tested for their responses to electrical stimulation of the superior laryngeal nerve (SLN) in chloralose-anesthetized, paralysed and artificially ventilated cats. SLN stimulation was performed with intensities sufficient to suppress central inspiratory activity detected by phrenic and recurrent laryngeal nerve recordings. Sympathetic neurons were tested under different levels of respiratory drive. Thirteen group I (putative muscle vasoconstrictor) neurons were mostly activated by SLN stimulation when respiratory drive was low, but depressed when it was high; this was due to the change in inspiration-related activity. Ten of eleven group II (putative cutaneous vasoconstrictor) neurons were depressed during SLN stimulation. This inhibition was independent of central respiratory drive. Inhibition also occurred in those neurons which predominantly discharged during postinspiration. Eight group III neurons which showed a discharge confined to inspiration were inhibited but mostly not silenced by SLN stimulation. Group IV (functionally unclassified) neurons either showed no response ( n=5) or were slightly inhibited ( n=2). The responses of group I neurons, but not the responses of group II and group III neurons, showed a significant positive correlation with those of systemic blood pressure. The observed responses corroborate the classification made previously. The results also demonstrate that the responses of sympathetic neurons to SLN stimulation are not merely due to the respiratory modulation of their activity, but rather consist of two components, one occurring independently of and the other secondary to, the changes in respiration.

Role of nucleus retroambigualis in respiratory reflexes evoked by superior laryngeal and vestibular nerve afferents and in emesis

An ascending projection from the medullary nucleus retroambigualis (NRA) has recently been described as important for the control of the upper airway during vocalization. We evaluated the importance of this projection in other behaviors by making localized injections of the neurotoxin kainic acid in the NRA in decerebrate cats, most of which were paralyzed and artificially ventilated. In contrast to its importance for vocalization, the NRA is not essential for activation of upper airway musculature during respiration, swallowing, vomiting, or reflexes elicited by superior laryngeal or vestibular nerve afferents. However, kainic acid injections in the NRA and adjacent reticular formation prolonged the inhibitory phrenic motoneuronal response to superior laryngeal nerve stimulation and abolished or reduced abdominal motoneuronal responses during respiration, vomiting, and superior laryngeal nerve stimulation. Thus, of the behaviors we investigated, the importance of the ascending projection from the NRA appears to be limited to vocalization, while descending projections from the NRA region are important in a number of behaviors.

Characteristics of laryngeal late responses to superior laryngeal nerve stimulation in rabbits

Characteristics of laryngeal late responses to superior laryngeal nerve stimulation in rabbits

NO-containing factors mediate hindlimb vasodilation produced by superior laryngeal nerve stimulation

The electrical stimulation (ES) of the superior laryngeal nerve (SLN) produces reflex vasodilation in the rat hindlimb. This study determined whether this vasodilation is mediated by the release of nitric oxide (NO)-containing factors (NOF) from NO synthase (NOS)-positive postganglionic lumbar sympathetic fibers that innervate the rat hindlimb vasculature. ES of the SLN (1-10 Hz for 15 s) produced frequency-dependent reductions in mean arterial blood pressure (MAP) and hindlimb and mesenteric (MR) vascular resistances. The hindlimb vasodilation was not observed in rats in which the lumbar sympathetic trunk was transected 7-10 days previously. The falls in hindquarter vascular resistance (HQR) produced by lower intensity ES of the SLN were virtually abolished by the specific inhibitor of neuronal NOS 7-nitroindazole (7-NI, 45 mg/kg i.v.). The fall in HQR produced by 10 Hz ES of the SLN was not affected by 7-NI. The falls in MR produced by 1-10 Hz ES of the SLN were unaffected by 7-NI. Four consecutive episodes of ES at 10 Hz produced pronounced and equivalent reductions in MAP, HQR, and MR. After administration of 7-NI, the first ES produced similar hemodynamic responses to those observed before injection. However, each subsequent ES produced progressively and markedly smaller falls in HQR, whereas each episode of ES produced similar falls in MR. These results suggest that the reflex vasodilation in the rat hindlimb produced by ES of the SLN involves the release of newly synthesized and performed stores of NOF from NOS-positive postganglionic lumbar sympathetic nerves.

Superior laryngeal nerve stimulation in the cat: effect on oropharyngeal swallowing, oesophageal motility and lower oesophageal sphincter activity.

Superior laryngeal nerve (SLN) stimulation can activate the brainstem swallowing mechanism to produce a complete swallowing sequence consisting of oropharyngeal, oesophageal and lower oesophageal sphincter (LOS) components. However, little is known of the effect of SLN stimulation (peripheral-sensory input from the pharynx) on the characteristics of oesophageal motor activity, especially in the smooth muscle portion. The present study examined the effect of varying stimulus train length and frequency on each of the three components of the reflex. Acute studies were performed in urethane anaesthetized cats. Oesophageal motility was monitored using conventional manometric techniques, and oropharyngeal swallowing by the mylohyoid electromyogram. SLN stimulus train length (1-10 sec) and frequency (5-30 Hz) were varied independently. Increased train length or frequency resulted in (1) an increase in oropharyngeal swallowing and incidence of the complete swallowing response, (2) an increase in latency to onset of the oesophageal peristaltic wave, (3) reduction of the amplitude of the evoked peristaltic contraction in the smooth muscle portion, without altering its velocity, (4) increased LOS relaxation, and increased LOS after-contraction. The LOS contraction was abolished by atropine (100 micrograms kg-1). Therefore, increased SLN stimulation not only results in excitation of the central swallowing program and the oropharyngeal stage of swallowing, but has major effects on the oesophageal and LOS stages of swallowing. Afferent SLN stimuli can impact on the control mechanisms for each stage, to inhibit or excite the stages in different ways.

Intracellular activity of motoneurons of the rostral nucleus ambiguus during swallowing in sheep.

The nervous mechanisms that generate swallowing are still largely unknown. It has been suggested that a central pattern generator that contains a serial network of linked neurons must produce the successive excitation of motoneurons (Mns) and then the sequential activation of muscle through excitatory connections. Inhibitory connections have also been envisioned but never evidenced at the membrane level of the swallowing neurons. We investigated, by intracellular recordings, the behavior of 96 Mns in the rostral nucleus ambiguus during swallowing induced by application of superior laryngeal nerve stimulation to anesthetized sheep. The Mns were identified by antidromic activation following stimulation of glossopharyngeal, pharyngoesophageal, or cervical vagal nerves. Nine Mns showed a bell-shaped depolarization during the buccal or the early pharyngeal stage of swallowing. They probably projected to muscles of the soft palate (palatopharyngeal) and upper pharynx (stylopharyngeal, hyopharyngeal). Thirty-eight Mns exhibited a chloride-dependent hyperpolarization, indicating that they were under an active inhibition throughout the buccopharyngeal stage of swallowing. These Mns constitute a heterogeneous pool: some of them, producing spontaneous inspiratory discharges, probably innervated laryngeal or pharyngeal muscles; others might also be Mns of the esophagus, whose swallowing pattern was modified because of the anesthesia (suppression of the esophageal peristalsis). Forty-nine Mns showed a chloride-dependent hyperpolarization with a variable duration at the onset of swallowing, followed by a depolarization that could take place during either the buccopharyngeal (HD1-Mns) or the esophageal (HD2- and HD3-Mns) stage of deglutition. HD1-Mns probably projected to the median and inferior constrictors of the pharynx. HD2-Mns produced depolarizations with longer latencies and durations than those of the HD1-Mns. They probably projected to either the superior esophageal sphincter or the cervical esophagus (CE). HD3-Mns showed a buccopharyngeal hyperpolarization that was followed first by a lower-amplitude hyperpolarization accompanying the proximal CE contraction and then by a delayed depolarization. These Mns probably innervated the inferior CE or thoracic esophagus. We conclude that the initial inhibition exerted on the HD-Mns, by delaying the excitation of Mns, may play a role in the nervous mechanisms involved in temporal organization of the swallowing motor sequence. We suggest that swallowing disorders in humans such as dysphagia by failure of cricopharyngeal relaxation, diffuse esophageal spasm, and achalasia might be caused by impaired inhibitory mechanisms.

Convergence of oropharyngolaryngeal, baroreceptor and chemoreceptor afferents onto insular cortex neurons in rats.

Forty-two neurons that responded to electrical stimulation of at least one of four nerves, the chorda tympani (CT), the lingual-tonsillar branch of the glossopharyngeal (LT-IXth) nerve, the pharyngeal branch of the glossopharyngeal (PH-IXth) nerve and the superior laryngeal (SL) nerve, were identified from the insular cortex by using glass microelectrodes in paralysed and anesthetized rats. Four, 42, 41 and 40 neurons responded to the CT, LT-IXth, PH-IXth and SL nerve stimulation respectively. Of these 42 neurons, most (37/42, 88.1%) responded to three nerves (the LT-IXth, PH-IXth and SL), two (4.8%) responded to two nerves and the remaining three (7.1%) responded to all four nerves. No neurons responded to one specific stimulus. The responsiveness of these 42 neurons to baroreceptor and chemoreceptor stimulation by an i.v. injection of three drugs was investigated. For baroreceptor stimulation, methoxamine hydrochloride (Mex) and sodium nitroprusside (SNP) were used; for chemoreceptor stimulation, sodium cyanide (NaCN) was used. Of the 42 neurons, 31 (73.8%) showed an excitatory or inhibitory response to baroreceptor and chemoreceptor stimulation with at least one of the three drugs, and the remaining 11 (26.2%) showed no response. Of these 31 baroreceptor and chemoreceptor-sensitive neurons, 19 (61.3%) responded to two or all three drugs, and the rest (12; 38.7%) responded to one. Most neurons recorded were distributed in the posterior insular cortex. These results indicate that the neurons in the posterior insular cortex receive convergent inputs from the oropharyngolaryngeal region, the baroreceptors and the chemoreceptors, suggesting that the posterior insular cortex may integrate various sensory information.

鼻腔ｆｌｏｗ刺激の内喉頭筋活動への影響

During the airway reflex deriving from the nose or the larynx, the activities of the respiratory, pharyngeal and intrinsic laryngeal muscles are coordinated. In decerebrate cats, the flow stimulation delivered to the nose prolongs the respiratory cycle time and decreases the amplitude of diaphragmatic activity. The purpose of this study was to analyze whether this nasal flow stimulation influenced the activities of the intrinsic laryngeal muscles.The spontaneous activities of the intrinsic laryngeal muscles and the evoked potentials induced by electrical stimulation to the internal branch of the superior laryngeal nerve (SLN), i. e., the laryngeal reflex, were recorded during nasal flow stimulation in decerebrate cats. A laryngeal reflex was induced by a single SLN stimulation (1Hz).During quiet respiration, the magnitude of the laryngeal reflex recorded from the thyroarytenoid muscle (TA) increased in phase with expiration. In contrast, the magnitude of the laryngeal reflex recorded from the posterior cricoarytenoid muscle (PCA) increased in phase with inspiration. During the period of nasal flow stimulation, TA and PCA activity increased. Moreover, the magnitude of the laryngeal reflex from the TA and PCA during nasal stimulation also greatly increased. These results suggest that the nasal flow stimulation increased the excitability of the motoneurons innervating the laryngeal adductor and abductor muscles. Such an increase in the excitability of the intrinsic laryngeal motoneurons was observed in both the inspiratory and expiratory phases.The functional significance of this phenomenon may be that nasal flow stimulation decreases the inspiratory activity of the diaphragm so as to prevent the inhalation of foreign bodies and increases the activity of the intrinsic laryngeal muscles, thereby increasing the likelihood of the airway reflex.

Respiratory motor responses to cranial nerve afferent stimulation in rats.

It was hypothesized that, because rats appear to lack a prominent disynaptic projection from the dorsal respiratory group to phrenic motoneurons (Phr), they would lack the short-latency excitation of Phr output seen in cats in response to stimulation of some cranial nerve afferents. Single-pulse superior laryngeal nerve (SLN) stimulation elicited a short-latency bilateral excitation of glossopharyngeal (IX) and hypoglossal (XII) nerves and an ipsilateral excitation of pharyngeal branch of vagus (PhX) in 67% of rats, but no excitation of Phr. Vagus (X) stimulation elicited a bilateral excitation of Phr and a predominantly ipsilateral excitation of IX and PhX. Single-pulse stimulation of SLN or X also elicited longer-latency, bilateral decreases in activity of all recorded nerves. Repetitive stimulation (50 Hz) of SLN or X suppressed inspiratory activity and prolonged expiration. Lung inflation (7.5 cmH2O) inhibited Phr and PhX activity; X stimulation inhibited Phr but prolonged PhX activity. In conclusion, rats predictably lack the SLN-induced short latency Phr excitation but exhibit other short latency reflexes for which the underlying circuitry is not clear.

Effects of central chemical drive on poststimulatory respiratory depression of laryngeal origin in the adult cat

We investigated the influences of central CO 2-related chemosensory drive on poststimulatory respiratory phenomena induced by superior laryngeal nerve (SLN) stimulation in pentobarbitone-anesthetized, vagotomized, carotid sinusdenervated, paralyzed, and artificially ventilated adult cats. Respiratory output was monitored as integrated phrenic nerve activity. Under eucapnic conditions, apnea-producing SLN stimulations of both short (10 s) and long (30 s) duration were followed by persistent apnea and depression in phrenic motor output; the latter showed a gradual recovery that followed an exponential time course. Hypocapnia increased the duration of poststimulatory apnea and the intensity of poststimulatory depression in phrenic minute output owing to changes in peak phrenic activity. Hypercapnia did not affect the duration of poststimulatory apnea, but markedly attenuated poststimulatory depression in respiratory activity, mainly due to changes in respiratory frequency. The rate of respiratory recovery was similar under eucapnic and hypocapnic conditions, but it was slower during hypercapnia. The results provide evidence that central chemosensitivity plays a prominent role in counteracting poststimulatory depressant effects on respiration induced by SLN stimulation.

Hypothalamic modulation of laryngeal reflexes in the anaesthetized cat: role of the nucleus tractus solitarii.

1. This investigation was initiated because activation of laryngeal afferents, either by electrical stimulation of the superior laryngeal nerve (SLN) or by natural stimulation of receptors in the laryngeal mucosa, results in a cardiorespiratory response comprising bradycardia, hypotension and apnoea (phrenic nerve activity was suppressed). This pattern of response is qualitatively equivalent to the response that is evoked on activation of the arterial baroreceptors. 2. Preliminary studies indicated that the effects of activating the SLN were suppressed during stimulation in the hypothalamic defence area (HDA) at points that also blocked the effects of baroreceptor stimulation. 3. Recordings were taken from seventy-two neurones localized within the ipsilateral nucleus tractus solitarii (NTS) whose activity was modified by SLN stimulation. Sixty neurones responded with an EPSP on SLN stimulation; nine of these had an inspiratory firing pattern. Five neurones were seen to receive an IPSP on SLN stimulation. 4. Five respiratory SLN-activated neurones were unresponsive to stimulation of the other nerve inputs, whilst four received convergent EPSP inputs on sinus nerve (SN) stimulation. One cell of these four also received inputs from the aortic and the vagus nerves. Sixty-one non-respiratory SLN-activated neurones also received convergent inputs from the sinus nerve. Of these, fifty displayed an EPSP, four an IPSP and seven an EPSP-IPSP. Fifteen neurones also received inputs from the aortic nerve and seventeen from the vagus. 5. From the population of neurones affected by SLN stimulation, twenty-four of seventy were also influenced by HDA stimulation (3 were respiratory cells). Sixteen of these responses consisted of an EPSP (2 respiratory cells), five of an IPSP (1 respiratory cell) and three of an EPSP-IPSP. 6. In neurones receiving an IPSP on HDA stimulation, the SLN-evoked excitatory response was reduced throughout the period of HDA-evoked inhibition. These neurones were all shown to receive excitatory inputs from the arterial baroreceptors and laryngeal mechanoreceptors. 7. Additionally, in the thirty-seven neurones that were excited by SLN stimulation but received no direct synaptic input on HDA stimulation, a conditioning stimulus to the HDA evoked a block of SLN-evoked responses without an accompanying change in membrane potential. Several of these neurones were also affected by both baroreceptor and laryngeal mechanoreceptor stimulation. 8. These observations are discussed in the context of the role of the NTS in cardiorespiratory control. The potential importance of these interactions in respiratory distress are highlighted and the implications for the organization of central pathways for the control of autonomic and respiratory function are discussed.

Naloxone attenuates poststimulatory respiratory depression of laryngeal origin in the adult cat

Poststimulatory depression in respiratory activity induced by superior laryngeal nerve (SLN) stimulation was quantitatively investigated in 20 adult cats. The role played in this phenomenon by endogenous opioids was studied using the opiate antagonist naloxone. The effects of hypercapnia on the same phenomenon were also investigated for comparison. Experiments were performed on cats anesthetized with pentobarbitone or alpha-chloralose, vagotomized, paralyzed, and artificially ventilated with 100% O2. Some animals were also carotid sinus denervated. Respiratory output was monitored as integrated phrenic nerve activity. SLN stimulation produced apnea, which outlasted the stimulation period; when respiration resumed, it was markedly depressed as revealed mainly by a decrease in phrenic minute output, respiratory frequency, and rate of rise of inspiratory activity. Phrenic output recovered gradually to control levels following an exponential time course. These effects varied as a function of the duration of SLN stimulation. Naloxone administration (0.8 mg/kg iv) significantly reduced the duration of poststimulatory apnea and attenuated the depression of phrenic minute output of the first recovery breath as a result of changes in peak phrenic activity; it also accelerated the time course of recovery. Hypercapnia did not affect the duration of poststimulatory apnea, but attenuated the initial poststimulatory depression because of changes in respiratory frequency; the rate of recovery was reduced. The results provide characterization of poststimulatory respiratory depression of laryngeal origin in the adult cat and suggest a role of endogenous opioids in its genesis or modulation.

Short-latency excitation of phrenic motor output mediated by non-NMDA receptors

This study tested the hypothesis that the short-latency excitation of the phrenic motor output elicited by superior laryngeal nerve (SLN) stimulation requires non-NMDA receptor-mediated neurotransmission in the region of the dorsal respiratory group (DRG) of the adult cat. Injection of the non-NMDA receptor antagonist NBQX into the DRG severely attenuated or abolished the short-latency excitation, indicating that the short-latency excitation requires non-NMDA receptor-mediated neurotransmission within the DRG.

Exit jet particle velocity in the in vivo canine laryngeal model

This study extends the previous work on exit jet particle velocity in an in vivo canine laryngeal model of phonation [G. S. Berke et al., J. Voice 3, 306–313 (1989)]. In both the previous and the current study, a hot-wire anemometer was used to measure air particle velocity in the midline of the glottis at anterior, intermediate, and posterior positions. Simultaneous measurements of subglottal pressure, EGG, and PGG were also obtained. In the previous study, these measures were obtained with constant levels of recurrent laryngeal nerve (RLN) and superior laryngeal nerve (SLN) stimulation. In the current study, exit jet particle velocity profiles were obtained across multiple levels of RLN and SLN stimulation. Exit jet particle velocity was also measured at midline and off-midline positions with constant levels of RLN and SLN stimulation. The time-varying features of exit jet particle velocity as a function of subglottal pressure and glottal vibratory events will be presented.

Nitric oxide synthase blockade inhibits oropharyngeal and esophageal responses to a water bolus and superior laryngeal nerve stimulation: [formula omitted], M.J. Beyak, P.I. Collman, D.T. Valdez and N.E. Diamant. Playfair Neuroscience Unit, The Toronto Hospital; Departments of Medicine and Physiology, University of Toronto, Toronto, Ontario, Canada

Nitric oxide synthase blockade inhibits oropharyngeal and esophageal responses to a water bolus and superior laryngeal nerve stimulation: [formula omitted], M.J. Beyak, P.I. Collman, D.T. Valdez and N.E. Diamant. Playfair Neuroscience Unit, The Toronto Hospital; Departments of Medicine and Physiology, University of Toronto, Toronto, Ontario, Canada

Paradoxical phase response at late expiration by superior laryngeal nerve stimulation.

Superior laryngeal nerve (SLN) stimulation during expiration prolongs the respiratory cycle in decerebrate, vagotomized and paralysed cats. In a few animals, however, the cycle can be terminated prematurely by the same stimulus. We developed a mathematical model of the respiratory neural network to stimulate these responses. The model contained inspiratory decrementing (I-DEC), and augmenting (I-AUG) and expiratory decrementing (E-DEC), and augmenting (E-AUG) neurones. Connections were based on published findings. SLN stimulation during late expiration prolonged the cycle when it was assumed to excite principally E-DEC neurones, whereas it terminated the cycle prematurely when it was assumed to excite both I-DEC and E-DEC neurones. Therefore, phase-resetting depends on the differential strength of afferent connections on the network's elements.

A pressure-regulated model of normal and pathologic phonation.

Recent evidence suggests that the lung-thorax system functions as a constant pressure source during phonation. However, previous animal models used a constant flow source. This article describes an in vivo canine model that maintains a constant subglottic pressure during phonation to more closely simulate the pulmonary system. At any given subglottic pressure, increasing levels of recurrent laryngeal nerve stimulation resulted in a significant rise in resistance followed by a plateau. Increasing levels of superior laryngeal nerve stimulation, however, produced no significant change in glottal resistance. Three experimental conditions were studied: normal, unilateral recurrent laryngeal nerve paralysis, and paralysis followed by arytenoid adduction. In normal canines, maximal vocal efficiency values were the highest, indicating the best match between pressure and resistance. The vocal efficiency values were significantly lower in recurrent laryngeal nerve paralysis, indicating pressure-resistance mis-match. Arytenoid adduction increased the maximal vocal efficiency values and decreased the mismatch observed in the paralyzed state. These findings may provide insight into an understanding of normal and pathologic laryngeal behavior.