Glossopharyngeal Nerve Stimulation Research Articles

Antihypertensive role of glossopharyngeal nerve stimulation by nifedipine using as calcium channel blocking agent in hypertension: An experimental study

Nifedipine is a therapeutic drug in acute attacks of hypertension because of its rapid absorption from oral mucosa. Taste receptors are innervated by glossopharyngeal nerves (GPN) as well as by facial and vagal nerves. Sensory neurons of the GPNs are localised in the petrous ganglion (PG). Transection of the taste sensitive GPN fibres causes taste bud and PG degeneration and spontaneous hypertension. In this study, the role of chemical stimulation of the taste buds of the GPN by nifedipine and its role in treatment of hypertension were investigated in rabbits. Nifedipine was dropped sublingually (20 mg) for 4 days in the study group, followed by measuring blood pressures again. Then, the lingual branches of GPNs were cut. One month later, blood pressures were measured for 4 days. All animals were sacrificed humanely at the end of the experiment, and normal and degenerated neuron densities in the petrosal ganglions were enumerated stereologically. The antihypertensive effect of nifedipine decreased after GPNs denervation, in accordance with the increase of degenerated neurons in the PG. The chemical stimulation of taste buds of the GPNs by nifedipine may be an important effect of nifedipine application in addition to its calcium channel blocking effect. The rapid decrease in blood pressure following sublingual use of nifedipine may also result from the direct stimulation of taste buds innervated by the GPNs.

Characteristics of Biphasic Slow Depolarizing and Slow Hyperpolarizing Potential in Frog Taste Cell Induced by Parasympathetic Efferent Stimulation

When the velocity of capillary blood flow in the frog tongue declined to an intermediate range of 0.2-0.7 mm/s, the glossopharyngeal nerve stimulation induced a biphasic slow depolarizing and slow hyperpolarizing potential (HP) in taste cells. The objective of this work was to examine the generative mechanisms of the biphasic slow potentials. The biphasic slow response was always preceded by a slow depolarizing potential (DP) component and followed by a slow HP component. Intravenous injection of tubocurarine completely blocked the biphasic slow responses, suggesting that both components of the biphasic slow potentials are evoked by the parasympathetic nerve (PSN) fibers. Membrane conductance of taste cells increased during slow DPs and decreased during slow HPs. The reversal potential of either component of a biphasic slow response was the almost same value of -12 mV. An antagonist, L-703,606, for neurotransmitter substance P neurokinin(1) receptor completely blocked both components of the biphasic slow responses. An antagonist, flufenamic acid, for nonselective cation channels on the taste cell membrane completely blocked the biphasic slow responses. These results suggest that PSN-induced biphasic slow responses are postsynaptically elicited in taste cells by releasing substance P at the PSN axon terminals. It is concluded that the slow DP component may be generated by opening one type of nonselective cation channel on taste cells and that the slow HP component may be generated by closing the other type of nonselective cation channel. We discussed that a second messenger inositol 1,4,5-trisphosphate might be related to a slow DP component and another second messenger diacylglycerol might be related to a slow HP component.

Analysis of Slow Hyperpolarizing Potentials in Frog Taste Cells Induced by Glossopharyngeal Nerve Stimulation

Analysis of Slow Hyperpolarizing Potentials in Frog Taste Cells Induced by Glossopharyngeal Nerve Stimulation

Analysis of slow hyperpolarizing potentials in frog taste cells induced by glossopharyngeal nerve stimulation.

Electrical stimulation of the frog glossopharyngeal (GP) nerve evoked slow hyperpolarizing potentials (HPs) in taste cells. This study aimed to clarify whether slow HPs were postsynaptically induced in taste cells. The slow HPs were recorded intracellularly with a microelectrode. When Ca2+ concentration in the blood plasma was decreased to approximately 0.5 mM, the amplitude of slow HPs reduced and their latency lengthened. When the Ca2+ concentration was increased to approximately 20 mM, the amplitude of slow HPs increased and their latency shortened. Addition of Cd2+ to the plasma greatly reduced the amplitude of slow HPs and lengthened their latency. These data suggest that the slow HPs are dependent on presynaptic activities in the GP nerve terminals in the taste disk. Of various antagonists injected intravenously for blocking receptors of neurotransmitter biogenic amines and peptides, only antagonists for substance P blocked the slow HPs at 2-4 mg/kg body wt. Application of substance P of 2 mg/kg to the plasma induced hyperpolarizing responses in taste cells, whose amplitude was the same as that of the slow HPs induced by GP nerve stimulation. Application of a nonselective cation channel antagonist, flufenamic acid, to the plasma blocked the slow HPs. These results suggest that the slow HPs are generated by closing the nonselective cation channels in the postsynaptic membrane of taste cells following possible release of substance P from the GP nerve terminals in the taste disk.

Slow potentials in taste cells induced by frog glossopharyngeal nerve stimulation.

Intracellular recordings were made from the taste cells of atropinized bullfrogs while the glossopharyngeal (GP) nerve fibres were electrically stimulated. Two types of slow potential, slow hyperpolarizing potentials (HPs) and slow depolarizing potentials (DPs), were induced in the taste cells. The slow HPs appeared when the lingual capillary blood flow was kept above 0.7 mm/s, whereas the slow DPs appeared when the blood flow was slowed down below 0.7 mm/s. The membrane resistance of a taste cell increased during the generation of a slow HP, but decreased during the generation of a slow DP. The reversal potentials for the slow HPs and the slow DPs were recorded at the same membrane potential (-11 to approximately -13 mV). Activation of non-selective cation channels possibly induced the slow DP and inactivation of those channels possibly induced the slow HP in the taste cell membrane. Electrical stimulation of the GP nerve activated a population of C fibres in the nerve and possibly released neurotransmitters from the nerve terminals. Released neurotransmitters might cause modulation of the membrane conductance in taste cells that leads to generation of the slow potentials. The present data suggest that slow HPs and slow DPs evoked in the taste cells of atropinized frogs by GP nerve stimulation are induced by putative neurotransmitters in the taste disc.

The origin of slow potentials on the tongue surface induced by frog glossopharyngeal efferent fiber stimulation.

When the glossopharyngeal (GP) nerve of the frog was stimulated electrically, electropositive slow potentials were recorded from the tongue surface and depolarizing slow potentials from taste cells in the fungiform papillae. The amplitude of the slow potentials was stimulus strength- and the frequency-dependent. Generation of the slow potentials was not related to antidromic activity of myelinated afferent fibers in the GP nerve, but to orthodromic activity of autonomic post-ganglionic C fibers in the GP nerve. Intravenous injection of atropine abolished the positive and depolarizing slow potentials evoked by GP nerve stimulation, suggesting that the slow potentials were induced by the activity of parasympathetic post-ganglionic fibers. The amplitude and polarity of the slow potentials depended on the concentration of adapting NaCl solutions applied to the tongue surface. These results suggest that the slow potentials recorded from the tongue surface and taste cells are due to the liquid junction potential generated between saliva secreted from the lingual glands by GP nerve stimulation and the adapting solution on the tongue surface.

Reflex Discharges of Hypoglossal Nerve Elicited by Palatal Nerve and Glossopharyngeal Nerve Stimulation in Frogs.

Reflex discharges of the hypoglossal nerve elicited by electrical stimulation of the palatal nerve (PNS) were compared with those of the same nerve elicited by glossopharyngeal nerve stimulation (GNS) in frogs. The results were as follows: 1. threshold of the stimulation for eliciting discharges was higher in PNS than in GNS, 2. frequency and latency of the PNS-elicited discharges were lower and longer than those of GNS, respectively, 3. the PNS-elicited discharges consisted of one component with short latency, while those of GNS consisted of two components with short and long latencies, respectively, 4. the GNS-elicited discharges were facilitated by conditioning PNS, 5. PNS elicited discharges only in the hyoglossal branch of hypoglossal nerve controlling the tongue as a retractor, while GNS elicited discharges in the hyoglossal branch that functions as a retractor, and in the intrinsic and genioglossal branches as protractors, 6. the PNS-and GNS-elicited discharges were similar in characteristics to those elicited by tactile stimulation of the palate and tongue, respectively.These findings suggest that the sensory input from the palatal nerve polysynaptically elicits retraction of the tongue for transport of bolus from the oral cavity into the pharynx, while that of the glossopharyngeal nerve mono- and/or poly-synaptically elicits retraction and protraction of the tongue for bolus transport and rejection, respectively.

Parasympathetic reflex salivary secretion in the cat parotid gland.

The aim of the present study was to compare and to characterize the secretory and vasodilator effects in the parotid gland of sympathectomized cats elicited reflexly by electrical stimulation of the central cut ends of the chorda tympani (or glossopharyngeal) nerves (physiologically conveying gustatory stimuli), vagus nerve (visceral stimuli), and the lingual nerve after cutting the chorda tympani nerve (somatic stimuli). The threshold stimulus-intensity needed to elicit the salivary secretion and a blood flow increase was markedly lower for stimulation of the chorda tympani nerve and glossopharyngeal nerve (2 V for each nerve) than for the lingual nerve, inferior alveolar nerve, and vagus nerve (10 V for each nerve). The salivary and vasodilator responses to stimulation of each afferent nerve were all abolished by prior treatment with hexamethonium at a dose of 5 mg/kg, i.v. Prior treatment with scopolamine completely abolished the salivary secretion elicited by lingual nerve and glossopharyngeal nerve stimulation, but had less effect on the vasodilator response in the parotid gland. These results indicate that the secretory and vasodilator responses evoked by afferent traffic in the above nerves are mediated via an activation of the autonomic nervous system, particularly by a parasympathetic mechanism. They suggest that there is a marked difference in the ability of different sensory modalities to induce reflex salivary secretion and vasodilatation, there being low threshold nerve fibers in the chorda tympani and glossopharyngeal nerves and high threshold nerve fibers in the lingual nerve, vagus nerve, and inferior alveolar nerve.

Vasodilator responses following intracranial stimulation of the trigeminal, facial and glossopharyngeal nerves in the cat gingiva

The effects of electrical stimulation of the trigeminal, facial and glossopharyngeal nerves on gingival blood flow in the cat were studied. The intracranial part of these nerves was stimulated electrically, and gingival blood flow was measured by the laser Doppler technique. Electrical stimulation of the trigeminal, facial and glossopharyngeal nerves caused blood flow to increase in the ipsilateral gingiva both with the cranial nerve intact and after cutting it to the medulla. Stimulation of the distal cut ends of the facial and glossopharyngeal nerves elicited an increase in blood flow but no increase in systemic blood pressure. Pretreatment with hexamethonium reduced the increase in blood flow elicited by electrical stimulation of the facial and glossopharyngeal nerves, but had no effect on that elicited by stimulation of the trigeminal nerve. In contrast, pretreatment with tripelennamine attenuated the trigeminal nerve-stimulated blood flow increase, but not that elicited by stimulation of the facial and glossopharyngeal nerves. Atropine, propranolol and phentolamine had no effect on these responses. These results suggest that the autonomic nervous system, particularly the parasympathetic nervous system, is responsible for the blood flow increase elicited by facial and glossopharyngeal nerve stimulation, and that the trigeminal nerve-stimulated blood flow increase is induced by antidromic vasodilatation of the trigeminal sensory nerve.

Gustatory sensitivity of an anuran to cantharidin

Glossopharyngeal nerve stimulation of the bullfrog, Rana catesbeiana, revealed responsiveness to low levels of cantharidin (1.3 x 10(-6) M), providing a first demonstration of neural gustatory sensitivity of an animal to this defensive chemical from blister beetles (Meloidae).

Origin of the climbing fibers activated by glossopharyngeal nerve stimulation in the frog.

The origin of climbing fibers activated by electrical stimulation of the frog's glossopharyngeal (IXth) nerve was investigated using histological and electrophysiological technique. At the molecular layer near the Purkinje cell layer, where the maximum negative cerebellar field potential could be recorded following electrical stimulation of the IXth nerve, horseradish peroxidase (HRP) was iontophoretically injected through the tip of the recording micropipette. The HRP labeled cells were seen in the contralateral inferior olive (IO). In some cases, a small number of HRP-labeled cells were seen in the ipsilateral IO. Labeled cells were not found in the other areas of the brain stem. After electrolytic lesion of the contralateral IO, the negative cerebellar field potential which would be recorded in the molecular layer following electrical stimulation of the IXth nerve had almost ceased. These results demonstrate that the climbing fibers activated by the IXth nerve stimulation have their origin in the contralateral IO.

Electrical stimulation of glossopharyngeal nerve and oesophageal EMG response in the pigeon

The effects of the efferent glossopharyngeal nerve stimulation, on EMG activity of the pigeon cervical oesophagus, were studied. In control animals, stimulation caused a biphasic response characterized by an intra-stimulus excitatory component followed by a post-stimulus inhibitory one. The EMG response to glossopharyngeal stimulation appeared simultaneously throughout the cervical oesophagus. A bell-shaped mechanical wave was detected relating to the electrical excitatory component. Atropine administration antagonized the excitatory component, while the inhibitory one persisted. It occurs intra-stimulus, and its duration is increased, compared to control ones. A reduction in the oesophageal resting pressure was observed relating to the electrical inhibitory component. Hexamethonium caused complete disappearance of any EMG response to glossopharyngeal stimulation, as well as suppression of mechanical responses. The comparison between the EMG responses to swallow and to efferent glossopharyngeal stimulation suggests that in pigeon cervical oesophagus: primary peristalsis is central in origin; a dual system of glossopharyngeal fibres, excitatory and inhibitory, carries the central control for oesophageal motility; these excitatory and inhibitory fibres supply the oesophageal muscle via intramural neurons; the synaptic arrangement of the inhibitory pathway is more complex than the excitatory one.

Altered regional vasodilator responses to glossopharyngeal nerve stimulation in spontaneously hypertensive rats.

The hindlimb and renal vasodilator responses produced by electrical stimulation of the glossopharyngeal nerve were examined in adult (six to eight months) male spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) normotensive rats to ascertain whether central neurogenically activated vasodilator capacity of these regional vascular beds is altered in SHR. Changes in systemic blood pressure and regional blood flow were simultaneously measured, and vascular resistance was calculated. Glossopharyngeal nerve stimulation (3.0 volts, 0.3 ms) at the frequency of 10 Hz resulted in a significantly greater vasodilation (% decrease in resistance) in SHR than in WKY control for both the hindlimb (SHR - 13.0 +/- 1.5% versus WKY - 3.4 +/- 1.6%, P less than 0.01) and renal (SHR - 7.6 +/- 0.6% versus WKY - 1.3 +/- 0.4%, P less than 0.01) vascular beds. The linear portion of the frequency-response curves of hindlimb or renal vasodilation of SHR was shifted parallel to the left of the WKY curve. Stimulus frequencies required to produce a 20% reduction in hindlimb resistance and a 10% reduction in renal resistance were lower in SHR (hindlimb 17.0 +/- 1.8 Hz; renal 19.9 +/- 1.4 Hz) than in WKY control (hindlimb 24.6 +/- 1.1 Hz; renal 39.3 +/- 4.8 Hz; P less than 0.01). The maximal vasodilator response to glossopharyngeal nerve stimulation in the hindlimb vascular bed was similar in SHR and WKY control, but in the renal vascular bed SHR showed a greater maximal response compared to WKY normotensives (SHR - 16.3 +/- 0.9% versus WKY - 12.7 +/- 1.6%, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Reflex cardiovascular responses induced by electrical stimulation of glossopharyngeal nerves in the rat

Reflex cardiovascular responses to electrical stimulation of glossopharyngeal nerves (GPN) were studied in Dial-Urethane anesthetized rats. GPN stimulation at 3 V, 0.3 msec and 50 Hz produced maximal reflex depressor (34 ± 2 mmHg) and bradycardia (21 ± 2 beats min ) responses that were altered as follows: pentolinium (0.25 mg kg , i.a.) blocked approximately 72% and 89% of control values of depressor and bradycardia responses, respectively; tripelennamine (5 mg kg , i.a.) significantly reduced depressor responses (76%); whereas atropine (0.4 mg kg , i.a.) blocked only bradycardia (85%). Regional blood flow studies showed that GPN stimulation reduced systemic arterial pressure (approximately 25%), and increased iliac artery blood flow (5%), and decreased blood flow through the renal (14%) and superior mesenteric (13%) arteries. Hence, decreases in vascular resistance during GPN stimulation were greater in the hindlimb vascular bed (28%) than in the renal (14%) or the mesenteric vasculatures. In addition, the magnitude of decreases in hindlimb vascular resistance by GPN stimulation was reduced (80%) by pretreatment with tripelennamine, but not by atropine. The results suggest that reductions in arterial blood pressure and hindlimb vascular resistance of the rat in response to GPN stimulation may be mediated via a histaminergic vasodilator mechanism, and that there may be a differential pattern of reflex vascular adjustments of blood flow and vascular resistance among regional vasculatures of the rate.

Actions of sodium and potassium ions on baroreceptors of normotensive and spontaneously hypertensive rats.

Actions of sodium and potassium ions on baroreceptors of normotensive and spontaneously hypertensive rats.

PHYSIOLOGICAL STUDIES ON FACIAL REFLEXES IN THE RAT

Experiments were performed on 36 male albino rats anaesthetized with pentobarbitone sodium and paralyzed with gallamine triethiodide. Recordings were made with single and multibarrel glass microelectrodes in the facial nucleus and monopolar silver wire electrodes on the lingual, facial, glossopharyngeal and hypoglossal nerves. The absolute refractory period for facial motoneurones is 2-3 ms, the relative refractory period has a duration of 26-34 ms and the range in axonal conduction velocities is from 15 to 45 m.sec-1. No evidence for afferent fibres in the muscle branches of the facial and hypoglassal nerves could be found. The lingual and glossopharyngeal nerves show reflex connexions with both the facial and hypoglassal nerves. The time courses of the potentiations and depressions of test facial antidromic field potentials following lingual and glossopharyngeal conditioning stimuli are given. Evoked synaptic activity and the distribution of field potentials in the facial mucleus following lingual and glossopharyngeal nerve stimulation are also described. The observed lingual and glossopharyngeal-facial reflexes are discussed with respect to blink reflexes.

Analysis of the respiratory role of pharyngeal constrictor motoneurons of cat

The electromyogram of the middle pharyngeal constrictor muscle and the electroneurogram of the phrenic nerve was recorded in parallel with measurements of tidal inspiration and tracheal airflow in chloralose-urethane anesthetized cats. In eupnea, pharyngeal constrictor exhibited tonic and expiratory phasic activity. Lung inflation inhibited phasic pharyngeal constrictor activity to reveal its tonic component; lung deflation eliminated both phasic and tonic components. Vagotomy eliminated these static lung volume effects and increased spontaneous cyclic activity. Hypocapnia abolished phasic activity and unmasked its tonic component in vagotomized cats. Hypercapnia increased cyclic pharyngeal constrictor activity (vagi intact or cut). Weak superior laryngeal or glossopharyngeal nerve stimulation had little or no effect during inspiration; during expiration, superior laryngeal nerve stimulation evoked a short lasting attenuating effect, and glossopharyngeal nerve stimulation exerted a long lasting blocking effect. (vagi intact or cut). Pharyngeal constrictor, like laryngeal adductors, is classified as an expiratory resisting type muscle. Pharyngeal constrictor reduces dead space during hypercapnia thereby promoting the exodus of CO 2. Comparison of vagal and other respitatory motoneurons reveals some special features of neural control of respiration heretofore overlooked.

Modulation of carotid sinus baroreceptor reflex by hypothalamic defense response.

ARTICLESModulation of carotid sinus baroreceptor reflex by hypothalamic defense responseM Kumada, LP Schramm, RA Altmansberger, and K SagawaM Kumada, LP Schramm, RA Altmansberger, and K SagawaPublished Online:01 Jan 1975https://doi.org/10.1152/ajplegacy.1975.228.1.34MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByHow does homeostasis happen? Integrative physiological, systems biological, and evolutionary perspectivesDavid S. Goldstein21 March 2019 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 316, No. 4Open-loop static and dynamic characteristics of the arterial baroreflex system in rabbits and rats5 November 2015 | The Journal of Physiological Sciences, Vol. 66, No. 1Modulation of the baroreceptor reflex by stimulation of the hypothalamic defense and vigilance areasPhysiology & Behavior, Vol. 59, No. 6Modulation of neuronal firing in the medullary solitary complex by electrical stimulation of the hypothalamic defense and vigilance areas in rabbitsBrain Research, Vol. 643, No. 1-2Cardiac baroreflex dynamics during the defence reaction in freely moving ratsBrain Research, Vol. 621, No. 1Arterial Baroreceptor Regulation of Peripheral Resistance and of Cardiac PerformanceCardiac vagal and sympathetic nerve responses to baroreceptor stimulation in the dogPfl�gers Archiv European Journal of Physiology, Vol. 413, No. 4An analysis of the purinergic component of active muscle vasodilatation obtained by electrical stimulation of the hypothalamus in rabbits19 July 2012 | British Journal of Pharmacology, Vol. 83, No. 2Circulatory control in canine acrylamide neuropathyJournal of the Autonomic Nervous System, Vol. 10, No. 2Baroreflex Control of Systemic Arterial Pressure and Vascular Bed1 January 2011Interaction of Cardiovascular Reflexes in Circulatory Control1 January 2011Differential interaction between hypothalamic and bulbar mechanisms in blood flow regulation in skeletal musclesBulletin of Experimental Biology and Medicine, Vol. 96, No. 2Nonlinear summation of depressor effects of carotid sinus pressure changes and aortic nerve stimulation in the rabbit.Circulation Research, Vol. 52, No. 4Effects of isometric exercise on the carotid baroreflex in hypertensive subjects.Hypertension, Vol. 4, No. 2Effects of Central Stimulation On Reflex Bradycardia in the Spontaneously Hypertensive Rat3 July 2009 | Clinical and Experimental Hypertension. Part A: Theory and Practice, Vol. 4, No. 3Two Types of Hypotensive Effect of Beta-Blocking Agents3 July 2009 | Clinical and Experimental Hypertension. Part A: Theory and Practice, Vol. 4, No. 1-2Role of baroreceptor reflexes in the hemodynamic and heart rate responses to althesin, ketamine and thiopentone anesthesiaJournal of the Autonomic Nervous System, Vol. 3, No. 1Neural organisation and control of the baroreceptor reflex21 June 2005Reflex cardiovascular responses induced by electrical stimulation of glossopharyngeal nerves in the ratJournal of Pharmacological Methods, Vol. 5, No. 1INTEGRATIVE ROLE OF THE CENTRAL NERVOUS SYSTEM IN CARDIOVASCULAR CONTROLResponses evoked by stimulation of points in the diencephalon of unrestrained rabbitsBrain Research Bulletin, Vol. 5, No. 3Control of Vasomotor Function and the Hemodynamic Consequences of the Contractile Behavior of ArteriesGlutamate-induced fastigial pressor response in the dogNeuroscience, Vol. 2, No. 4Baroreflex sensitivity during operant blood pressure conditioningBiofeedback and Self-Regulation, Vol. 2, No. 2Interaction between the Hypothalamic Defence Reaction and Cardiac Ventricular Receptor ReflexesActa Physiologica Scandinavica, Vol. 96, No. 4Baroreceptor reflex control of arterial hemodynamics in the dog.Circulation Research, Vol. 37, No. 6 More from this issue > Volume 228Issue 1January 1975Pages 34-45 Copyright & PermissionsCopyright © 1975 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1975.228.1.34PubMed1147026History Published online 1 January 1975 Published in print 1 January 1975 Metrics

Functional significance of connections of the inferior olive.

Functional significance of connections of the inferior olive.

Spontaneous and reflexly evoked activity in pharyngeal, laryngeal, and phrenic motoneurons of cat

Experiments were performed on spontaneously breathing cats that were anesthetized with chloralose-urethane in order to study changing excitability in pharyngeal, laryngeal, and phrenic motoneurons. Pharyngeal constrictor motoneurons chiefly were spontaneously active during expiration; the stylopharyngeus and certain motoneurons serving the superior pharyngeal constrictors were inactive during either phase of tidal respiration. While confirming work of previous investigators that feeble glossopharyngeal (epipharyngeal branch) and superior laryngeal nerve stimulation transiently attenuated on-going phrenic nerve activity, such evoked afferent volleys excited laryngeal motoneurons independent of phases of respiration. On-going pharyngeal constrictor nerve activity (expiration) was attenuated for 20–50 msec by superior laryngeal nerve stimulation and for 100–300 msec by glosso-pharyngeal nerve stimulation. Intercostal nerve stimulation evoked occasional pharyngeal constrictor nerve discharges but more commonly attenuated its spontaneous nerve activity. Stylopharyngeus and an unknown portion of the superior pharyngeal constrictor motoneurons were excited by afferent volleys evoked in glossopharyngeal and superior laryngeal nerves. These aforementioned changes in excitability were unaffected by total neuromuscular paralysis while maintaining artificial respiration. It is concluded that certain pharyngeal constrictor motoneurons of the cat are spontaneously active during tidal expiration, are under central respiratory control, and that their intermittence along with those serving the diaphragm and larynx by modest afferent volleys in the ninth and tenth cranial nerves stage the act of swallow or expulsive reflexes, or both.