Arterial chemoreceptor input to respiratory hypoglossal motoneurons

1990 ◽  
Vol 69 (2) ◽  
pp. 700-709 ◽  
Author(s):  
S. W. Mifflin
Keyword(s):  
Membrane Potential ◽  
Upper Airway ◽  
Excitatory Input ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
End Tidal ◽  
Carotid Body Chemoreceptors ◽  
Excitatory Drive ◽  
Arterial Chemoreceptor

To better understand the role of the arterial chemoreceptors in the regulation of upper airway patency at the level of the oropharynx, intracellular recordings were obtained from inspiratory hypoglossal motoneurons (IHMs), and the responses to selective activation of the carotid body chemoreceptors were examined. In pentobarbital-anesthetized, vagotomized, paralyzed, and artificially ventilated cats, chemoreceptor activation enhanced the inspiratory depolarization of membrane potential in 32 of 36 IHMs. This was manifested as an increase in either the amplitude (n = 13) or duration (n = 3) or an increase in both amplitude and duration (n = 16) of the inspiratory membrane potential depolarization. The amplitude and duration of the inspiratory membrane potential depolarization increased 98 +/- 15% (n = 29) and 78 +/- 13% (n = 19), respectively. Similar patterns of enhanced activity (increased duration and/or amplitude of membrane depolarization) were observed in five expiratory hypoglossal motoneurons (EHMs) after chemoreceptor activation. In 16 of the 32 IHMs, chemoreceptor activation also evoked changes in IHM membrane potential during expiration: enhanced post-inspiratory discharge (n = 6), expiratory depolarization/discharge (n = 6), and tonic depolarization/discharge, which persisted for several respiratory cycles (n = 4). The arterial chemoreceptors provide a powerful excitatory input to IHMs during both inspiration and expiration. This excitatory drive to IHMs and EHMs will aid in the maintenance of upper airway patency throughout the respiratory cycle during increases in end-tidal CO2.

Role of an Identified Looming-Sensitive Neuron in Triggering a Flying Locust's Escape

2006 ◽  
Vol 95 (6) ◽  
pp. 3391-3400 ◽  
Author(s):  
Roger D. Santer ◽  
F. Claire Rind ◽  
Richard Stafford ◽  
Peter J. Simmons
Keyword(s):  
Membrane Potential ◽  
Motor Neuron ◽  
High Frequency ◽  
Escape Behavior ◽  
Excitatory Input ◽  
Movement Detector ◽  
Stimulus Meaning ◽  
Contralateral Movement ◽  
Flight Motor

Flying locusts perform a characteristic gliding dive in response to predator-sized stimuli looming from one side. These visual looming stimuli trigger trains of spikes in the descending contralateral movement detector (DCMD) neuron that increase in frequency as the stimulus gets nearer. Here we provide evidence that high-frequency (>150 Hz) DCMD spikes are involved in triggering the glide: the DCMD is the only excitatory input to a key gliding motor neuron during a loom; DCMD-mediated EPSPs only summate significantly in this motor neuron when they occur at >150 Hz; when a looming stimulus ceases approach prematurely, high-frequency DCMD spikes are removed from its response and the occurrence of gliding is reduced; and an axon important for glide triggering descends in the nerve cord contralateral to the eye detecting a looming stimulus, as the DCMD does. DCMD recordings from tethered flying locusts showed that glides follow high-frequency spikes in a DCMD, but analyses could not identify a feature of the DCMD response alone that was reliably associated with glides in all trials. This was because, for a glide to be triggered, the high-frequency spikes must be timed appropriately within the wingbeat cycle to coincide with wing elevation. We interpret this as flight-gating of the DCMD response resulting from rhythmic modulation of the flight motor neuron's membrane potential during flight. This means that the locust's escape behavior can vary in response to the same looming stimulus, meaning that a predator cannot exploit predictability in the locust's collision avoidance behavior.

scholarly journals Effect of inhaled carbon dioxide on laryngeal abduction

2015 ◽  
Vol 118 (4) ◽  
pp. 489-494 ◽  
Author(s):  
Jonathan Cheetham ◽  
Amanda Jones ◽  
Manuel Martin-Flores
Keyword(s):  
Laryngeal Mask Airway ◽  
High Speed ◽  
Upper Airway ◽  
Laryngeal Mask ◽  
Maximal Response ◽  
High Temporal Resolution ◽  
Respiratory Drive ◽  
Laryngeal Function ◽  
Airway Patency ◽  
End Tidal

Hypercapnia produces a profound effect on respiratory drive and upper airway function to maintain airway patency. Previous work has evaluated the effects of hypercapnia on the sole arytenoid abductor, the posterior cricoarytenoid (PCA), using indirect measures of function, such as electromyography and direct nerve recording. Here we describe a novel method to evaluate PCA function in anesthetized animals and use this method to determine the effects of hypercapnia on PCA function. Eight dogs were anesthetized, and a laryngeal mask airway was used, in combination with high-speed videoendoscopy, to evaluate laryngeal function. A stepwise increase in inspired partial pressure of CO2 produced marked arytenoid abduction above 70-mmHg end-tidal CO2 (ETCO2) ( P < 0.001). Glottic length increased above 80-mmHg ETCO2 ( P < 0.02), and this lead to underrepresentation of changes in glottic area, if standard measures of glottic area (normalized glottic gap area) were used. Use of a known scale to determine absolute glottic area demonstrated no plateau with increasing ETCO2 up to 120 mmHg. Ventilatory parameters also continued to increase with no evidence of a maximal response. In a second anesthetic episode, repeated bursts of transient hypercapnia for 60 s with an ETCO2 of 90 mmHg produced a 43–55% increase in glottic area ( P < 0.001) at or shortly after the end of the hypercapnic burst. A laryngeal mask airway can be used in combination with videoendoscopy to precisely determine changes in laryngeal dimensions with high temporal resolution. Absolute glottic area more precisely represents PCA function than normalized glottic gap area at moderate levels of hypercapnia.

scholarly journals Intensity and frequency dependence of laryngeal afferent inputs to respiratory hypoglossal motoneurons

1997 ◽  
Vol 83 (6) ◽  
pp. 1890-1899 ◽  
Author(s):  
Steven W. Mifflin
Keyword(s):  
Frequency Dependence ◽  
Stimulus Frequency ◽  
Superior Laryngeal Nerve ◽  
Upper Airway ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
Afferent Fibers ◽  
Complex Motor ◽  
Afferent Inputs ◽  
Motor Acts

Mifflin, Steven W. Intensity and frequency dependence of laryngeal afferent inputs to respiratory hypoglossal motoneurons. J. Appl. Physiol. 83(6): 1890–1899, 1997.—Inspiratory hypoglossal motoneurons (IHMs) mediate contraction of the genioglossus muscle and contribute to the regulation of upper airway patency. Intracellular recordings were obtained from antidromically identified IHMs in anesthetized, vagotomized cats, and IHM responses to electrical activation of superior laryngeal nerve (SLN) afferent fibers at various frequencies and intensities were examined. SLN stimulus frequencies <2 Hz evoked an excitatory-inhibitory postsynaptic potential (EPSP-IPSP) sequence or only an IPSP in most IHMs that did not change in amplitude as the stimulus was maintained. During sustained stimulus frequencies of 5–10 Hz, there was a reduction in the amplitude of SLN-evoked IPSPs with time with variable changes in the EPSP. At stimulus frequencies >25 Hz, the amplitude of EPSPs and IPSPs was reduced over time. At a given stimulus frequency, increasing stimulus intensity enhanced the decay of the SLN-evoked postsynaptic potentials (PSPs). Frequency-dependent attenuation of SLN inputs to IHMs also occurred in newborn kittens. These results suggest that activation of SLN afferents evokes different PSP responses in IHMs depending on the stimulus frequency. At intermediate frequencies, inhibitory inputs are selectively filtered so that excitatory inputs predominate. At higher frequencies there was no discernible SLN-evoked PSP temporally locked to the SLN stimuli. Alterations in SLN-evoked PSPs could play a role in the coordination of genioglossal contraction during respiration, swallowing, and other complex motor acts where laryngeal afferents are activated.

scholarly journals Serotonergic Modulation of Inspiratory Hypoglossal Motoneurons in Decerebrate Dogs

2006 ◽  
Vol 95 (6) ◽  
pp. 3449-3459 ◽  
Author(s):  
Ivo F. Brandes ◽  
Edward J. Zuperku ◽  
Astrid G. Stucke ◽  
Danica Jakovcevic ◽  
Francis A. Hopp ◽  
...  
Keyword(s):  
Upper Airway ◽  
Discharge Pattern ◽  
Receptor Subtype ◽  
Drug Induced ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
Single Neuron Recording ◽  
Induced Changes

Inspiratory hypoglossal motoneurons (IHMNs) maintain upper airway patency. However, this may be compromised during sleep and by sedatives, potent analgesics, and volatile anesthetics by either depression of excitatory or enhancement of inhibitory inputs. In vitro data suggest that serotonin (5-HT), through the 5-HT2A receptor subtype, plays a key role in controlling the excitability of IHMNs. We hypothesized that in vivo 5-HT modulates IHMNs activity through the 5-HT2A receptor subtype. To test this hypothesis, we used multibarrel micropipettes for extracellular single neuron recording and pressure picoejection of 5-HT or ketanserin, a selective 5-HT2A receptor subtype antagonist, onto single IHMNs in decerebrate, vagotomized, paralyzed, and mechanically ventilated dogs. Drug-induced changes in neuronal discharge frequency ( Fn) and neuronal discharge pattern were analyzed using cycle-triggered histograms. 5-HT increased the control peak Fn to 256% and the time-averaged Fn to 340%. 5-HT increased the gain of the discharge pattern by 61% and the offset by 34 Hz. Ketanserin reduced the control peak Fn by 68%, the time-averaged Fn by 80%, and the gain by 63%. These results confirm our hypothesis that in vivo 5-HT is a potent modulator of IHMN activity through the 5-HT2A receptor subtype. Application of exogenous 5-HT shows that this mechanism is not saturated during hypercapnic hyperoxia. The two different mechanisms, gain modulation and offset change, indicate that 5-HT affects the excitability as well as the excitation of IHMNs in vivo.

scholarly journals GABA and glycine neurons from the ventral medullary region inhibit hypoglossal motoneurons

SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Olga Dergacheva ◽  
Thomaz Fleury-Curado ◽  
Vsevolod Y Polotsky ◽  
Matthew Kay ◽  
Vivek Jain ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Muscle Tone ◽  
Upper Airway ◽  
Emg Activity ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
Obstructive Sleep ◽  
Tongue Muscles

Abstract Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive sleep-related losses of upper airway patency that occur most frequently during rapid eye movement (REM) sleep. Hypoglossal motoneurons play a key role in regulating upper airway muscle tone and patency during sleep. REM sleep activates GABA and glycine neurons in the ventral medulla (VM) to induce cortical desynchronization and skeletal muscle atonia during REM sleep; however, the role of this brain region in modulating hypoglossal motor activity is unknown. We combined optogenetic and chemogenetic approaches with in-vitro and in-vivo electrophysiology, respectfully, in GAD2-Cre mice of both sexes to test the hypothesis that VM GABA/glycine neurons control the activity of hypoglossal motoneurons and tongue muscles. Here, we show that there is a pathway originating from GABA/glycine neurons in the VM that monosynaptically inhibits brainstem hypoglossal motoneurons innervating both tongue protruder genioglossus (GMNs) and retractor (RMNs) muscles. Optogenetic activation of ChR2-expressing fibers induced a greater postsynaptic inhibition in RMNs than in GMNs. In-vivo chemogenetic activation of VM GABA/glycine neurons produced an inhibitory effect on tongue electromyographic (EMG) activity, decreasing both the amplitude and duration of inspiratory-related EMG bursts without any change in respiratory rate. These results indicate that activation of GABA/glycine neurons from the VM inhibits tongue muscles via a direct pathway to both GMNs and RMNs. This inhibition may play a role in REM sleep associated upper airway obstructions that occur in patients with OSA.

Reflex modulation of airflow dynamics through the upper airway

1994 ◽  
Vol 76 (6) ◽  
pp. 2692-2700 ◽  
Author(s):  
M. M. Seelagy ◽  
A. R. Schwartz ◽  
D. B. Russ ◽  
E. D. King ◽  
R. A. Wise ◽  
...  
Keyword(s):  
Upper Airway ◽  
Major Effect ◽  
Vagal Afferents ◽  
Reflex Modulation ◽  
Airway Patency ◽  
Progressive Hypoxia ◽  
End Tidal ◽  
Inspired Oxygen ◽  
End Tidal Co2 ◽  
Respiratory Reflexes

We studied the effect of respiratory reflexes on maximal inspiratory flow (VImax) and its mechanical determinants, pharyngeal critical pressure (Pcrit) and nasal resistance, in an isolated feline upper airway preparation. Chemoreceptor reflexes were evaluated by varying inspired oxygen and end-tidal CO2 concentrations. At each gas concentration, we found that changes in VImax were related to changes in Pcrit. As CO2 increased, Pcrit became increasingly subatmospheric (P < 0.02), indicating reductions in pharyngeal collapsibility. In contrast, progressive hypoxia had no effect on Pcrit. We then examined the effects of vagal afferents and upper airway mucosal receptors on airflow dynamics at three levels of CO2. We confirmed that CO2 increased VImax (P < 0.01) and decreased Pcrit to more subatmospheric levels (P < 0.05) in both the presence and absence of vagal and airway mucosal afferent activity. Moreover, airway mucosal afferents led to smaller reductions in Pcrit (a less collapsible airway) (P < 0.05), whereas vagal afferents led to a larger increase in Pcrit (a more collapsible pharynx) under hypercapnic conditions (P < 0.01). We conclude that CO2 had a major effect on pharyngeal collapsability and that its effect was modulated by vagal and mucosal afferents. We speculate that the sensitivity and threshold to reflex CO2 responses play a major role in the maintenance of airway patency.

scholarly journals Pre- and postsynaptic modulations of hypoglossal motoneurons by α-adrenoceptor activation in wild-type and Mecp2−/Y mice

2013 ◽  
Vol 305 (10) ◽  
pp. C1080-C1090 ◽  
Author(s):  
Xiao-Tao Jin ◽  
Ningren Cui ◽  
Weiwei Zhong ◽  
Xin Jin ◽  
Zhongying Wu ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Upper Airway ◽  
Membrane Properties ◽  
Compensatory Mechanism ◽  
Tongue Movement ◽  
Wild Type ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
Therapeutical Modalities ◽  
Intrinsic Membrane Properties

Hypoglossal motoneurons (HNs) control tongue movement and play a role in maintenance of upper airway patency. Defects in these neurons may contribute to the development of sleep apnea and other cranial motor disorders including Rett syndrome (RTT). HNs are modulated by norepinephrine (NE) through α-adrenoceptors. Although postsynaptic mechanisms are known to play a role in this effect, how NE modulates the synaptic transmissions of HNs remains poorly understood. More importantly, the NE system is defective in RTT, while how the defect affects HNs is unknown. Believing that information of NE modulation of HNs may help the understanding of RTT and the design of new therapeutical interventions to motor defects in the disease, we performed these studies in which glycinergic inhibitory postsynaptic currents and intrinsic membrane properties were examined in wild-type and Mecp2 −/Y mice, a mouse of model of RTT. We found that activation of α1-adrenoceptor facilitated glycinergic synaptic transmission and excited HNs. These effects were mediated by both pre- and postsynaptic mechanisms. The latter effect involved an inhibition of barium-sensitive G protein-dependent K+ currents. The pre- and postsynaptic modulations of the HNs by α1-adrenoceptors were not only retained in Mecp2-null mice but also markedly enhanced, which appears to be a compensatory mechanism for the deficiencies in NE and GABAergic synaptic transmission. The existence of the endogenous compensatory mechanism is an encouraging finding, as it may allow therapeutical modalities to alleviate motoneuronal defects in RTT.

Effect of sleep state and hypercapnia on alae nasi and diaphragm EMGs in preterm infants

1983 ◽  
Vol 54 (6) ◽  
pp. 1590-1596 ◽  
Author(s):  
W. A. Carlo ◽  
R. J. Martin ◽  
E. F. Abboud ◽  
E. N. Bruce ◽  
K. P. Strohl
Keyword(s):  
Tidal Volume ◽  
Preterm Infants ◽  
Upper Airway ◽  
Preterm Neonates ◽  
Emg Activity ◽  
Sleep State ◽  
Quiet Sleep ◽  
Airway Patency ◽  
Temporal Relationships ◽  
End Tidal

A coordinated activation of upper airway and chest wall muscles may be crucial in maintaining airway patency and ventilation. The alae nasi (AN) and diaphragm (DIA) electromyograms (EMG) were recorded with surface electrodes in 17 unsedated healthy preterm infants during both active (AS) and quiet sleep (QS). Airflow was measured via a nasal mask pneumotachograph and integrated to obtain tidal volume. Studies were performed during inhalation of room air and mixtures of 2 and 4% CO2 in air. In room air, phasic AN EMG accompanied 45 +/- 7% of breaths during AS compared with 14 +/- 5% of breaths during QS (P less than 0.001); however, with inhalation of 4% CO2 the incidence of AN EMG increased to comparable levels in both sleep states. During room air breathing onset of AN EMG preceded that of the DIA EMG and inspiratory airflow by 41 +/- 8 ms (P less than 0.01) and 114 +/- 29 ms (P less than 0.05), respectively. Peak AN activity preceded peak DIA activity by 191 +/- 36 ms (P less than 0.01). Alteration in sleep state or increasing chemical drive did not significantly alter these temporal relationships. Nevertheless, with each increase in end-tidal CO2, peak DIA EMG and tidal volume increased while peak AN EMG only showed a consistent increase during 4% CO2 inhalation. We conclude that although there exists a mechanism that temporally coordinates AN and DIA activation, the amount of AN EMG activity with each breath is not clearly correlated with DIA activation, which may contribute to the high incidence of respiratory dysrhythmias in preterm neonates.

scholarly journals Role of Inhibitory Neurotransmission in the Control of Canine Hypoglossal Motoneuron Activity In Vivo

2009 ◽  
Vol 101 (3) ◽  
pp. 1211-1221 ◽  
Author(s):  
Antonio Sanchez ◽  
Sanda Mustapic ◽  
Edward J. Zuperku ◽  
Astrid G. Stucke ◽  
Francis A. Hopp ◽  
...  
Keyword(s):  
Upper Airway ◽  
Cellular Level ◽  
Spontaneous Discharge ◽  
Glycine Receptors ◽  
Active Neuron ◽  
Airway Patency ◽  
Inhibitory Mechanisms ◽  
Premotor Neurons

Hypoglossal motoneurons (HMNs) innervate all tongue muscles and are vital for maintenance of upper airway patency during inspiration. The relative contributions of the various synaptic inputs to the spontaneous discharge of HMNs in vivo are incompletely understood, especially at the cellular level. The purpose of this study was to determine the role of endogenously activated GABAAand glycine receptors in the control of the inspiratory HMN (IHMN) activity in a decerebrate dog model. Multibarrel micropipettes were used to record extracellular unit activity of individual IHMNs during local antagonism of GABAAreceptors with bicuculline and picrotoxin or glycine receptors with strychnine. Only bicuculline had a significant effect on peak and average discharge frequency and on the slope of the augmenting neuronal discharge pattern. These parameters were increased by 30 ± 7% ( P < 0.001), 30 ± 8% ( P < 0.001), and 25 ± 7% ( P < 0.001), respectively. The effects of picrotoxin and strychnine on the spontaneous neuronal discharge and its pattern were negligible. Our data suggest that bicuculline-sensitive GABAergic, but not picrotoxin-sensitive GABAergic or glycinergic, inhibitory mechanisms actively attenuate the activity of IHMNs in vagotomized decerebrate dogs during hyperoxic hypercapnia. The pattern of GABAergic attenuation of IHMN discharge is characteristic of gain modulation similar to that in respiratory bulbospinal premotor neurons, but the degree of attenuation (∼25%) is less than that seen in bulbospinal premotor neurons (∼60%). The current studies only assess effects on active neuron discharge and do not resolve whether the lack of effect of picrotoxin and strychnine on IHMNs also extends to the inactive expiratory phase.

Behaviors of hypoglossal hyoid motoneurons in laryngeal and vestibular reflexes and in deglutition and emesis

1998 ◽  
Vol 274 (4) ◽  
pp. R950-R955 ◽  
Author(s):  
Toshiro Umezaki ◽  
Ken Nakazawa ◽  
Alan D. Miller
Keyword(s):  
Single Cells ◽  
Upper Airway ◽  
Reflex Response ◽  
Hypoglossal Nucleus ◽  
Airway Protection ◽  
Related Activity ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
Muscle Nerve ◽  
To Receive

Reflex responses of hypoglossal motoneurons innervating the geniohyoid (GH) and thyrohyoid (TH) muscles from the superior laryngeal (SLN) and vestibular nerves and their behaviors during fictive swallowing and vomiting were examined by recording both the extracellular activities of 11 single cells in the hypoglossal nucleus and GH and TH muscle nerve activity in eight decerebrate, paralyzed, and artificially ventilated cats. The majority of TH motoneurons were either active and/or exhibited shortened antidromic latencies during early expiration. In contrast, GH motoneurons did not exhibit any respiratory-related activity. Electrical single-shock stimulation of the SLN never evoked an excitatory reflex response on GH or TH motoneurons but rather evoked inhibitory responses on the THs. Unlike other hypoglossal motoneurons, GH and TH motoneurons do not appear to receive vestibular inputs. However, they can exhibit robust activities during fictive swallowing and vomiting, particularly during expulsion. Thus these motoneurons may play an important role in airway protection during swallowing and vomiting but not in controlling upper airway patency regulated by vestibular afferents.

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