Neural mechanisms of sneeze

1975 ◽  
Vol 229 (3) ◽  
pp. 770-776 ◽  
Author(s):  
HL Batsel ◽  
AJ Lines
Keyword(s):  
High Frequency ◽  
Neural Mechanisms ◽  
Nucleus Ambiguus ◽  
Respiratory Neurons ◽  
Similar Response ◽  
Response Patterns ◽  
Nerve Activity ◽  
Inspiratory Neurons ◽  
Expiratory Neurons ◽  
Stimulation Of

Sneezes were induced in anestized cats by repetitive stimulation of the ethmoidal nerve. Activity of bulbar respiratory neurons during sneezing was recorded extracellularly through tungsten microelectrodes. Most expiratory neurons could be locked onto the stimulus pulses so that they responded either throughout inspiration as well as expiration or so that they began responding at some time during inspiration. As inspiration approached termination, multiple spiking occurred, finally to result in high-frequency bursts which just preceded active expiration. A fraction of expiratory neurons were activated only in bursts. Latent expiratory neurons were recruited in sneezing. Inspiratory neurons near nucleus ambiguus and most of those near fasciculus solitarius displayed similar response patterns consisting of silent periods followed by delayed smooth activations. Temporal characteristics of the silent periods, "inhibitory gaps," suggested that they resulted from inhibition whose source was the expiratory neurons which were driven throughout inspriation. Some inspiratory neurons in the area of fasciculus solitarius failed to exhibit inhibitory gaps.

The coordinate roles of branchial nerve activity and potassium in the stimulation of ciliary activity in Mytilus edulis: observations with phenoxybenzamine, bromolysergic acid and fluorescence histochemistry

1976 ◽  
Vol 65 (1) ◽  
pp. 109-116
Author(s):  
A. A. Paparo
Keyword(s):  
Mytilus Edulis ◽  
Nerve Stimulation ◽  
High Frequency ◽  
Low Frequency ◽  
Ciliary Activity ◽  
Nerve Activity ◽  
Basal Rate ◽  
Potassium Effect ◽  
Branchial Nerve ◽  
Stimulation Of

Potassium concentrations in excess of 30 mM increase the rate of beating of lateral cilia on the gill of Mytilus edulis. Cilioexcitation produced by low frequency (5 beats/s) electrical stimulation was potentiated with potassium but blocked with bromolysergic acid (a serotonergic inhibitor). Cilioinhibition produced by high frequency (50 beats/s) stimulation was decreased with potassium and phenoxybenzamine (a dopaminergic inhibitor). Phenoxybenzamine enhanced the cilioexcitation produced by potassium. Potassium doses incapable of maintaining a basal rate of beating (less than 30 mM) could increase ciliary activity if phenoxybenzamine was also added. After transection of the branchial nerve, the yellow-fluorophore (serotonergic storage) and cilioexcitatory effect of potassium gradually decrease. This study shows that the potassium effect on ciliary activity (a) increase with low frequency nerve stimulation, presumably through the release of serotonin and (b) decreases with high frequency nerve stimulation, presumably through the release of dopamine.

Differing activities of medullary respiratory neurons in eupnea and gasping

1991 ◽  
Vol 70 (3) ◽  
pp. 1265-1270 ◽  
Author(s):  
D. Zhou ◽  
M. J. Wasicko ◽  
J. M. Hu ◽  
W. M. St John
Keyword(s):  
Carbon Monoxide ◽  
Brain Stem ◽  
Phrenic Nerve ◽  
Peak Discharge ◽  
Discharge Frequency ◽  
Respiratory Neurons ◽  
Ventilatory Pattern ◽  
Medullary Respiratory Neurons ◽  
Inspiratory Neurons ◽  
Expiratory Neurons

Our purpose was to compare further eupneic ventilatory activity with that of gasping. Decerebrate, paralyzed, and ventilated cats were used; the vagi were sectioned within the thorax caudal to the laryngeal branches. Activities of the phrenic nerve and medullary respiratory neurons were recorded. Antidromic invasion was used to define bulbospinal, laryngeal, or not antidromically activated units. The ventilatory pattern was reversibly altered to gasping by exposure to 1% carbon monoxide in air. In eupnea, activities of inspiratory neurons commenced at various times during inspiration, and for most the discharge frequency gradually increased. In gasping, the peak discharge frequency of inspiratory neurons was unaltered. However, all commenced activities at the start of the phrenic burst and reached peak discharge almost immediately. The discharge frequencies of all groups of expiratory neurons fell in gasping, with many neurons ceasing activity entirely. These data are consistent with the hypothesis that brain stem mechanisms controlling eupnea and gasping differ fundamentally.

The Effects of Nasal Flow Stimulation on Central Respiratory Pattern

1995 ◽  
Vol 9 (4) ◽  
pp. 203-208 ◽  
Author(s):  
Satoshi Nonaka ◽  
Akihiro Katada ◽  
Kizuku Nakajima ◽  
Takashi Ohsaki ◽  
Tokuji Unno
Keyword(s):  
Cycle Time ◽  
Suppressive Effect ◽  
Respiratory Cycle ◽  
Respiratory Pattern ◽  
Respiratory Neurons ◽  
Electromyographic Activity ◽  
Inspiratory Neurons ◽  
Expiratory Neurons ◽  
Flow Stimulation ◽  
Nasal Flow

The purpose of this study was to analyze the functional role of nasal afferents on central respiratory mechanisms. The electromyographic activity of the diaphragm and the neuronal activities of respiratory neurons within the brainstem were recorded during nasal flow stimulation, using decerebrate cats. Flow stimulation delivered to the nose prolonged the respiratory cycle time and decreased the amplitude of diaphragmatic activity. The respiratory cycle time was prolonged due to prolongation of expiratory phase. Cool air flow stimulation was more effective for changing the respiratory pattern than was warm air. All recorded inspiratory neurons of the dorsal respiratory group decreased their firing rate during stimulation, but more than half of expiratory neurons of the ventral respiratory group did not change. These results suggest that nasal afferents which respond to temperature can modulate the central respiratory pattern and have a stronger suppressive effect on the activity of inspiratory neurons than that of expiratory neurons.

Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons

2006 ◽  
Vol 290 (5) ◽  
pp. R1387-R1396 ◽  
Author(s):  
Peter M. Lalley
Keyword(s):  
Action Potential ◽  
Respiratory Rhythm ◽  
Input Resistance ◽  
Membrane Depolarization ◽  
Respiratory Neurons ◽  
Response Analysis ◽  
Inspiratory Neurons ◽  
Potential Shape ◽  
Expiratory Neurons

Opiates have effects on respiratory neurons that depress tidal volume and air exchange, reduce chest wall compliance, and slow rhythm. The most dose-sensitive opioid effect is slowing of the respiratory rhythm through mechanisms that have not been thoroughly investigated. An in vivo dose-response analysis was performed on medullary respiratory neurons of adult cats to investigate two untested hypotheses related to mechanisms of opioid-mediated rhythm slowing: 1) Opiates suppress intrinsic conductances that limit discharge duration in medullary inspiratory and expiratory neurons, and 2) opiates delay the onset and lengthen the duration of discharges postsynaptically in phase-regulating postinspiratory and late-inspiratory neurons. In anesthetized and unanesthetized decerebrate cats, a threshold dose (3 μg/kg) of the μ-opioid receptor agonist fentanyl slowed respiratory rhythm by prolonging discharges of inspiratory and expiratory bulbospinal neurons. Additional doses (2–4 μg/kg) of fentanyl also lengthened the interburst silent periods in each type of neuron and delayed the rate of membrane depolarization to firing threshold without altering synaptic drive potential amplitude, input resistance, peak action potential frequency, action potential shape, or afterhyperpolarization. Fentanyl also prolonged discharges of postinspiratory and late-inspiratory neurons in doses that slowed the rhythm of inspiratory and expiratory neurons without altering peak membrane depolarization and hyperpolarization, input resistance, or action potential properties. The temporal changes evoked in the tested neurons can explain the slowing of network respiratory rhythm, but the lack of significant, direct opioid-mediated membrane effects suggests that actions emanating from other types of upstream bulbar respiratory neurons account for rhythm slowing.

Respiratory neuronal activity during apnea and poststimulatory effects of laryngeal origin in the cat

2000 ◽  
Vol 89 (3) ◽  
pp. 917-925 ◽  
Author(s):  
Fulvia Bongianni ◽  
Donatella Mutolo ◽  
Marco Carfì ◽  
Giovanni A. Fontana ◽  
Tito Pantaleo
Keyword(s):  
Respiratory Depression ◽  
Superior Laryngeal Nerve ◽  
Respiratory Neurons ◽  
Inhibitory Input ◽  
Phase Theory ◽  
Inspiratory Neurons ◽  
Three Phase ◽  
Expiratory Neurons ◽  
Inspiratory Activity ◽  
Respiratory Reflexes

We investigated the behavior of medullary respiratory neurons in cats under pentobarbitone anesthesia, vagotomized, paralysed, and artificially ventilated to elucidate neural mechanisms underlying apnea and poststimulatory respiratory depression induced by superior laryngeal nerve (SLN) stimulation. Inspiratory neurons were completely inhibited during SLN stimulation and poststimulatory apnea. During recovery of inspiratory activity, augmenting inspiratory neurons were depressed, decrementing inspiratory neurons were excited, and late inspiratory neurons displayed unchanged bursts closely locked to the end of the inspiratory phase. Augmenting expiratory neurons were either silenced or displayed different levels of tonic activity during SLN stimulation; some of them were clearly activated. These expiratory neurons displayed activity during poststimulatory apnea, before the onset of the first recovery phrenic burst. Postinspiratory or decrementing expiratory neurons were activated during SLN stimulation; their discharge continued with a decreasing trend during poststimulatory apnea. The results support the three-phase theory of rhythm generation and the view that SLN stimulation provokes a postinspiratory apnea that could represent the inhibitory component of respiratory reflexes of laryngeal origin, such as swallowing. In addition, because a subpopulation of augmenting expiratory neurons displays activation during SLN stimulation, the hypothesis can be advanced that not only postinspiratory, or decrementing expiratory neurons, but also augmenting expiratory neurons may be involved in the genesis of apnea and poststimulatory phenomena. Finally, the increase in the activity of decrementing inspiratory neurons after the end of SLN stimulation may contribute to the generation of poststimulatory respiratory depression by providing an inhibitory input to bulbospinal augmenting inspiratory neurons.

Pre-Botzinger complex in the cat

1995 ◽  
Vol 73 (4) ◽  
pp. 1452-1461 ◽  
Author(s):  
S. W. Schwarzacher ◽  
J. C. Smith ◽  
D. W. Richter
Keyword(s):  
Spinal Cord ◽  
Neuronal Activity ◽  
Membrane Depolarization ◽  
Neonatal Rat ◽  
Respiratory Neurons ◽  
Spike Discharge ◽  
Inspiratory Phase ◽  
Inspiratory Neurons ◽  
Bötzinger Complex ◽  
Expiratory Neurons

1. Patterns of respiratory neuronal activity were examined in pentobarbitone anesthetized adult cats in a circumscribed area of the ventrolateral medulla, which has previously been defined as the pre-Botzinger complex (pre-BOTC) from electrophysiological and morphological criteria in the brain stem-spinal cord preparation of the neonatal rat. The pre-BOTC has been proposed to play a critical role in respiratory rhythm generation in mammals, but electrophysiological properties of the region have not been thoroughly characterized in the adult brain stem in vivo. 2. From intra- and extracellular recordings, we verified the existence of a well-defined zone with a distinct profile of neuronal activity between the rostral Botzinger complex containing expiratory neurons and the more caudal medullary pool of inspiratory neurons of the ventral respiratory group (VRG) in the para-ambigual region. This zone corresponds to the pre-BOTC. It was characterized by a concentration of the various types of respiratory neurons, particularly those proposed to be involved in respiratory phase transitions, including neurons discharging immediately before the onset of inspiratory phase activity (pre-inspiratory neurons), early-inspiratory, and postinspiratory neurons. The majority of these neurons were presumed interneurons because they were not antidromically activated by spinal cord or cranial nerve stimulation. 3. The locus of the pre-BOTC corresponded histologically to the rostral part of the nucleus ambiguus and ventrolateral reticular formation. It was located caudal to the retrofacial nucleus and rostral to the lateral reticular nucleus, extending 3.0-3.5 mm rostral to the obex, and 3.2-4.0 mm lateral from the midline. This location was homologous to that established in the neonatal rat. 4. Pre-inspiratory neurons (pre-I neurons) were specifically found in the pre-BOTC. Intracellular recordings from these neurons revealed two types of activity patterns. Type 1 of pre-I neurons exhibited a steady membrane depolarization during expiration and a steep membrane depolarization with a high-frequency burst of action-potential discharge during the phase transition from expiration to inspiration. This was followed by a decline of depolarization and spike discharge during the remainder of the inspiratory phase. A second type of pre-I neurons exhibited a secondary graded membrane depolarization and burst discharge during the late-inspiratory period. 5. Synaptic events were examined in other respiratory neurons during the 40-160 ms preceding the onset of phrenic nerve activity when pre-I neurons exhibited peak spike discharge. Early-inspiratory, throughout-respiratory, and postinspiratory neurons were disinhibited during this period, whereas stage-2 expiratory neurons exhibited a decrease in spike activity and repolarization.(ABSTRACT TRUNCATED AT 400 WORDS)

Vasopressin V1 receptors contribute to hemodynamic and sympathoinhibitory responses evoked by stimulation of adenosine A2a receptors in NTS

2006 ◽  
Vol 290 (5) ◽  
pp. H1889-H1898 ◽  
Author(s):  
Tadeusz J. Scislo ◽  
Donal S. O'Leary
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Autonomic Response ◽  
Receptor Subtypes ◽  
Response Patterns ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Receptor Stimulation ◽  
A2a Receptors ◽  
Stimulation Of

Activation of adenosine A2a receptors in the nucleus of the solitary tract (NTS) decreases mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), whereas increases in preganglionic adrenal sympathetic nerve activity (pre-ASNA) occur, a pattern similar to that observed during hypotensive hemorrhage. Central vasopressin V1 receptors may contribute to posthemorrhagic hypotension and bradycardia. Both V1 and A2a receptors are densely expressed in the NTS, and both of these receptors are involved in cardiovascular control; thus they may interact. The responses elicited by NTS A2a receptors are mediated mostly via nonglutamatergic mechanisms, possibly via release of vasopressin. Therefore, we investigated whether blockade of NTS V1 receptors alters the autonomic response patterns evoked by stimulation of NTS A2a receptors (CGS-21680, 20 pmol/50 nl) in α-chloralose-urethane anesthetized male Sprague-Dawley rats. In addition, we compared the regional sympathetic responses to microinjections of vasopressin (0.1–100 ng/50 nl) into the NTS. Blockade of V1 receptors reversed the normal decreases in MAP into increases (−95.6 ± 28.3 vs. 51.4 ± 15.7 ∫Δ%), virtually abolished the decreases in HR (−258.3 ± 54.0 vs. 18.9 ± 57.8 ∫Δbeats/min) and RSNA (−239.3 ± 47.4 vs. 15.9 ± 36.1 ∫Δ%), and did not affect the increases in pre-ASNA (279.7 ± 48.3 vs. 233.1 ± 54.1 ∫Δ%) evoked by A2a receptor stimulation. The responses partially returned toward normal values ∼90 min after the blockade. Microinjections of vasopressin into the NTS evoked dose-dependent decreases in HR and RSNA and variable MAP and pre-ASNA responses with a tendency toward increases. We conclude that the decreases in MAP, HR, and RSNA in response to NTS A2a receptor stimulation may be mediated via release of vasopressin from neural terminals in the NTS. The differential effects of NTS V1 and A2a receptors on RSNA versus pre-ASNA support the hypothesis that these receptor subtypes are differentially located/expressed on NTS neurons/neural terminals controlling different sympathetic outputs.

Arterial pulse modulated activity is expressed in respiratory neural output

2005 ◽  
Vol 99 (2) ◽  
pp. 691-698 ◽  
Author(s):  
Thomas E. Dick ◽  
Roger Shannon ◽  
Bruce G. Lindsey ◽  
Sarah C. Nuding ◽  
Lauren S. Segers ◽  
...  
Keyword(s):  
Brain Stem ◽  
Neural Control ◽  
Respiratory Neurons ◽  
Arterial Pulse ◽  
Pulse Modulation ◽  
Nerve Activity ◽  
Data Set ◽  
Antidromic Activation ◽  
Axonal Projections ◽  
Expiratory Neurons

Although it is well-established that sympathetic activity is modulated with respiration, it is unknown whether neural control of respiration is reciprocally influenced by cardiovascular function. Even though previous studies have suggested the existence of pulse modulation in respiratory neurons, they could not exclude the possibility that such cells were involved in cardiovascular rather than respiratory motor control, owing to neuroanatomic and functional overlaps between brain stem neurons involved in respiratory and cardiovascular control. The aim of this study was to test the hypothesis that respiratory motoneurons and putative premotoneurons are modulated by arterial pulse. An existing data set composed of 72 well-characterized, respiratory-modulated brain stem motoneurons and putative premotoneurons was analyzed using δ2, a recently described statistic that quantifies the magnitude of arterial pulse-modulated spike activity [Dick TE and Morris KF. J Physiol 556: 959–970, 2004]. Neuronal activity was recorded in the rostral and caudal ventral respiratory groups of 19 decerebrate, neuromuscular-blocked, ventilated cats. Axonal projections were identified by rectified and unrectified spike-triggered averages of recurrent laryngeal nerve activity or by antidromic activation from spinal stimulation electrodes. The firing rates of ∼30% of these neurons were modulated in phase with both the respiratory and cardiac cycles. Furthermore, arterial pulse modulation occurred preferentially in the expiratory phase in that only expiratory neurons had high δ2 values and only expiratory activity had significant δ2 values after partitioning tonic activity into the inspiratory and expiratory phases. The results demonstrate that both respiratory motoneurons and putative premotoneuronal activity can be pulse modulated. We conclude that a cardiac cycle-related modulation is expressed in respiratory motor activity, complementing the long-recognized respiratory modulation of sympathetic nerve activity.

Respiratory neuron responses to hypercapnia and carotid chemoreceptor stimulation

1981 ◽  
Vol 51 (4) ◽  
pp. 816-822 ◽  
Author(s):  
W. M. St John
Keyword(s):  
Brain Stem ◽  
Reticular Formation ◽  
Phrenic Nerve ◽  
Sodium Cyanide ◽  
Respiratory Neurons ◽  
Respiratory Neuron ◽  
Nerve Activity ◽  
Dorsal Nucleus ◽  
Central Chemoreceptors ◽  
Expiratory Neurons

In decerebrate, vagotomized, paralyzed, and ventilated cats, activities were recorded from the phrenic nerve and from respiratory units within the dorsal and ventral medullary respiratory nuclei and the pontile reticular formation. These unit activities were monitored during equivalent augmentations in peak integrated phrenic nerve activity induced by stimuli acting primarily on the peripheral or central chemoreceptors. These stimuli were intracarotid infusions of sodium cyanide or nicotine and exposure to hyperoxic hypercapnia, respectively. Both stimuli caused similar increases in activities for most dorsal nucleus inspiratory units. For units of the ventral medullary nucleus, augmentations in activity were only significant (inspiratory neurons) or were of greater magnitude (expiratory neurons) during hypercapnia. As opposed to medullary units, the discharge frequencies of many pontile units were unaltered or declined during both peripheral and central chemoreceptor stimulations. These results support the concept that excitatory influences from the peripheral and central chemoreceptors are not equally distributed among all groups of brain stem respiratory neurons.

Sign in / Sign up

Export Citation Format

Share Document