Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating 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 microg/kg) of the mu-opioid receptor agonist fentanyl slowed respiratory rhythm by prolonging discharges of inspiratory and expiratory bulbospinal neurons. Additional doses (2-4 microg/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.     

D1-dopamine receptor agonists prevent and reverse opiate depression of breathing but not antinociception in the cat

Opioids depress respiration and decrease chest wall compliance. A previous study in this laboratory showed that dopamine-D(1) receptor (D(1)R) agonists restored phrenic nerve activity after arrest by fentanyl in immobilized, mechanically ventilated cats. The reinstated phrenic nerve rhythm was slower than control, so it was not known whether D(1)R agonists can restore spontaneous breathing to levels that provide favorable alveolar gas exchange and blood oxygenation. It was also not known whether the agonists counteract opioid analgesia. In the present study, anesthetized, spontaneously breathing cats were given intravenous doses of fentanyl (18.0 +/- 3.4 microg/kg) that severely depressed depth and rate of respiration, lowered arterial hemoglobin oxygenation (HbO(2)), elevated end-tidal carbon dioxide (ETCO(2)), and abolished the nociceptive hind limb crossed-extensor reflex. Fentanyl (30 microg/kg) also evoked tonic discharges of caudal medullary expiratory neurons in paralyzed mechanically ventilated cats, which might explain decreased chest compliance. The selective D(1)R agonists 6-chloro APB (3 mg/kg) or dihydrexidine (DHD, 1 mg/kg) increased depth and rate of spontaneous breathing after opioid depression and returned HbO(2) and ETCO(2) to control levels. Opioid arrest of the nociceptive reflex remained intact. Pretreatment with DHD prevented significant depression of spontaneous breathing by fentanyl (17.5 +/- 4.3 microg/kg). Tonic firing evoked by fentanyl in expiratory neurons was converted to rhythmic respiratory discharges by DHD (1 mg/kg). The results suggest that D(1)R agonists might be therapeutically useful for the treatment of opioid disturbances of breathing without impeding analgesia.     

Effect of upper airway negative pressure and lung inflation on laryngeal motor unit activity in rabbit.

Distortion of the upper airway by negative transmural pressure (UANP) causes reflex vagal bradycardia. This requires activation of cardiac vagal preganglionic neurons, which exhibit postinspiratory (PI) discharge. We hypothesized that UANP would also stimulate cranial respiratory motoneurons with PI activity. We recorded 32 respiratory modulated motor units from the recurrent laryngeal nerve of seven decerebrate paralyzed rabbits and recorded their responses to UANP and to withholding lung inflation using a phrenic-triggered ventilator. The phasic inspiratory (n = 17) and PI (n = 5) neurons detected were stimulated by -10 cmH(2)O UANP and by withdrawal of lung inflation (P < 0.05, Friedman's ANOVA). Expiratory-inspiratory units (n = 10) were tonically active but transiently inhibited in postinspiration; this inhibition was more pronounced and prolonged during UANP stimuli and during no-inflation tests (P < 0.05). We conclude that, in addition to increasing inspiratory activity in the recurrent laryngeal nerve, UANP also stimulates units with PI activity.     

Ventrolateral medullary respiratory network participation in the expiration reflex in the cat.

The expiration reflex is a distinct airway defensive response characterized by a brief, intense expiratory effort and coordinated adduction and abduction of the laryngeal folds. This study addressed the hypothesis that the ventrolateral medullary respiratory network participates in the reflex. Extracellular neuron activity was recorded with microelectrode arrays in decerebrated, neuromuscular-blocked, ventilated cats. In 32 recordings (17 cats), 232 neurons were monitored in the rostral (including B?tzinger and pre-B?tzinger complexes) and caudal ventral respiratory group. Neurons were classified by firing pattern, evaluated for spinal projections, functional associations with recurrent laryngeal and lumbar nerves, and firing rate changes during brief, large increases in lumbar motor nerve discharge (fictive expiration reflex, FER) elicited during mechanical stimulation of the vocal folds. Two hundred eight neurons were respiratory modulated, and 24 were nonrespiratory; 104 of the respiratory and 6 of the nonrespiratory-modulated neurons had altered peak firing rates during the FER. Increased firing rates of bulbospinal neurons and expiratory laryngeal premotor and motoneurons during the expiratory burst of FER were accompanied by changes in the firing patterns of putative propriobulbar neurons proposed to participate in the eupneic respiratory network. The results support the hypothesis that elements of the rostral and caudal ventral respiratory groups participate in generating and shaping the motor output of the FER. A model is proposed for the participation of the respiratory network in the expiration reflex.     

Stimulation of vagal C-fibers alters timing and distribution of respiratory motor output in cats

Pulmonary vascular congestion or pulmonary embolism in humans produces shallow tachypnea, and indirect experimental evidence suggests that this characteristic breathing pattern may result from activation of vagal unmyelinated afferents from the lung. We have investigated, in decerebrate cats, reflex changes in breathing pattern and in the activation of the diaphragm, posterior cricoarytenoid, and thyroarytenoid muscles caused by activating C-fiber afferents in the vagus nerve. The right vagus nerve was sectioned distal to the origin of the recurrent laryngeal nerve, eliminating vagal afferent traffic although preserving motor innervation of the larynx on that side. The left cervical vagus was stimulated electrically, and efferent activation of the laryngeal muscles was avoided by cutting the left recurrent laryngeal nerve. Transmission to the brain of vagal afferent traffic resulting from this stimulation was controlled by graded cold block of the nerve cranial to the site of application of the stimulus. Activation of C-fibers, when A-fibers were blocked, significantly decreased respiratory period and amplitude of diaphragm inspiratory burst. In addition, this selective activation of vagal C-fibers augmented postinspiratory activity of the diaphragm and recruited phasic expiratory bursts in the thyroarytenoid. We conclude that, in unanesthetized decerebrate cats, afferent traffic of vagal C-fibers initiates a pontomedullary reflex that increases respiratory frequency, decreases tidal volume, and augments braking of expiratory airflow.     

Influences from laryngeal afferents on expiratory bulbospinal neurons and motoneurons

The purpose of this study is to analyze the reflex effects of laryngeal afferent activation on respiratory patterns in anesthetized, vagotomized, paralyzed, ventilated cats. We recorded simultaneously from the phrenic nerve, T10 internal intercostal nerve, and single bulbospinal expiratory neurons of the caudal ventral respiratory group (VRG). Laryngeal afferents were activated by electrical stimulation of the superior laryngeal nerve (SLN) or by cold-water infusion into the larynx. Both types of stimuli caused inhibition of phrenic activity and facilitation of internal intercostal nerve activity, indicating expiratory effort. The activity of 46 bulbospinal expiratory cells was depressed during SLN electrical stimulation, and 13 of them were completely inhibited. In 44 of 56 neurons tested, mean firing frequency (FFmean) was decreased in response to cold-water infusion and 8 others responded with increased FFmean; in the remaining 4 neurons, FFmean was unchanged. Possible reasons for different neuronal responses to SLN electrical stimulation and water infusion are discussed. We conclude that bulbospinal expiratory neurons of VRG were not the source of the reflex motoneuronal expiratory-like activity produced by SLN stimulation. Other, not yet identified inputs to spinal expiratory motoneurons are activated during this experimental condition.     

Arterial pulse modulated activity is expressed in respiratory neural output.

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 delta(2), 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 approximately 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 delta(2) values and only expiratory activity had significant delta(2) 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 muscle control during vomiting

The changes in thoracic and abdominal pressure that generate vomiting are produced by coordinated action of the major respiratory muscles. During vomiting, the diaphragm and external intercostal (inspiratory) muscles co-contract with abdominal (expiratory) muscles in a series of bursts of activity that culminates in expulsion. Internal intercostal (expiratory) muscles contract out of phase with these muscles during retching and are inactive during expulsion. The periesophageal portion of the diaphragm relaxes during expulsion, presumably facilitating rostral movement of gastric contents. Recent studies have begun to examine to what extent medullary respiratory neurons are involved in the control of these muscles during vomiting. Bulbospinal expiratory neurons in the ventral respiratory group caudal to the obex discharge at the appropriate time during (fictive) vomiting to activate either abdominal or internal intercostal motoneurons. The pathways that drive phrenic and external intercostal motoneurons during vomiting have yet to be identified. Most bulbospinal inspiratory neurons in the dorsal and ventral respiratory groups do not have the appropriate response pattern to initiate activation of these motoneurons during (fictive) vomiting. Relaxation of the periesophageal diaphragm during vomiting could be brought about, at least in part, by reduced firing of bulbospinal inspiratory neurons.     

Effect of five human anesthetics on respiratory control in cats

The effect of halothane, fentanyl, Innovar, thiopental, and ketamine on inspiratory output, vagal influence, and chest wall reflex was assessed in seven cats lightly anesthetized with pentobarbital, using the method of airway occlusion with and without rapid vagal cooling. All anesthetics depressed inspiratory output, as expressed by deltaP/deltat, of the first occluded inspiration. However, only halothane depressed peak inspiratory output (Pmax). Phasic vagal influence was markedly depressed by 2% halothane but was preserved under other anesthetics. The ability to induce tonic vagal influence (expiratory muscle recruitment) was lost under halothane. Inspiratory inhibitory chest wall reflex was evident in two cats during airway occlusion. Addition of any test anesthetic abolished the reflex. It is concluded that halothane should be avoided in studies dealing with assessment of vagal influence.     

Evidence that glycine and GABA mediate postsynaptic inhibition of bulbar respiratory neurons in the cat.

Experiments were carried out on decerebrate cats to identify transsynaptic mediators of spontaneous postsynaptic inhibition of bulbar inspiratory and postinspiratory neurons. Somatic membrane potentials were recorded through the central micropipette of a coaxial multibarreled electrode. Blockers of type A gamma-aminobutyric acid (GABA-A) and glycine receptors were iontophoresed extracellularly from peripheral micropipettes surrounding the central pipette. Effective antagonism was demonstrated by iontophoresis of agonists with antagonists; application of strychnine antagonized the action of glycine but not GABA, and application of bicuculline antagonized the action of GABA but not glycine. In both types of neurons, iontophoresis of either antagonist depolarized the somatic membrane and increased input resistance throughout the respiratory cycle. Bicuculline preferentially depolarized the somatic membrane in both types of neurons during inactive phases. Strychnine increased the firing rate of inspiratory neurons during inspiration despite maintenance of somatic membrane potential at preiontophoresis levels. Tetrodotoxin reduced the effects of iontophoresed bicuculline and strychnine, suggesting that the action of the antagonists required presynaptic axonal conduction. The present results suggest that presynaptic release of both GABA and glycine contributes to tonic postsynaptic inhibition of bulbar respiratory neurons. GABA-A receptors appear to contribute to inhibition during inactive phases in inspiratory and postinspiratory neurons, whereas glycinergic mechanisms appear to contribute to inspiratory inhibition in inspiratory neurons.     

Laryngeal motor control in frogs: Role of vagal and laryngeal feedback

Using decerebrate frogs (Rana catesbeiana), we investigated the role of vagal and laryngeal sensory feedback in controlling motor activation of the larynx. Vagal and laryngeal nerve afferents were activated by electrical stimulation of the intact vagal and laryngeal nerves. Pulmonary afferents were activated by lung inflation. Reflex responses were recorded by measuring efferent activity in the laryngeal branch of the vagus (Xℓ) and changes in glottal aperture. Two glottic closure reflexes were identified, one evoked by lung inflation or electrical stimulation of the main branch of the vagus (Xm), and the other by electrical stimulation of Xℓ. Lung inflation evoked a decrementing burst of Xℓ efferent activity and electrical stimulation of Xm resulted in a brief burst of Xℓ action potentials. Electrical stimulation of Xℓ evoked a triphasic mechanical response, an abrupt glottal constriction followed by glottal dilatation followed by a long-lasting glottal constriction. The first phase was inferred to be a direct (nonreflex) response to the stimulus, whereas the second and third represent reflex responses to the activation of laryngeal afferents. Intracellular recordings of membrane potential of vagal motoneurons of lung and nonlung types revealed EPSPs in both types of neurons evoked by stimulation of Xm or Xℓ, indicating activation of glottal dilator and constrictor motoneurons. In summary, we have identified two novel reflexes producing glottic closure, one stimulated by activation of pulmonary receptors and the other by laryngeal receptors. The former may be part of an inspiratory terminating reflex and the latter may represent an airway protective reflex. © 1997 John Wiley & Sons, Inc. J Neurobiol 33: 213–222, 1997     

非NMDA受体参与双相呼气和吸气神经元电活动的调节

在新生大鼠延髓脑片上同步记录舌下神经根和双相呼气神经元／吸气神经元单位的放电活动,并在灌流的改良Kredbs液中先后加以非NMDA受体的激动剂KA和拮抗剂DNQX,观察对神经元单位放电的影响,以进一步探讨非NMDA受体在对双相呼气神经元之间交互兴奋和吸气神经元兴奋性突触输入中的作用,结果表明,使用非NMDA受体激动剂KA以后,双相呼气神经元的放电频率和蜂频率都明显增大,吸气神经元中期放电的频率和非NMDA受体激动剂KA以后,双相呼气神经元的放电频率和峰频率都明显增大,吸气神经元中期放电的频率和峰频率也显著增大,而早期和晚期放电的频率无明显改变,用相应拮抗剂以后,上述效应明显被抑制,结果提示,非NMDA受体参与了双相呼气神经元之间的交互兴奋作用,并且也介导了吸气神经元的兴奋性突触输入／     

Differing activities of medullary respiratory neurons in eupnea and gasping

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.     

Influence of lung volume on activities of branches of the recurrent laryngeal nerve

To investigate the influence of inspiratory lung inflation on the respiratory activities of laryngeal motor nerves, vagally intact decerebrate paralyzed cats were ventilated by a servorespirator in accordance with their own phrenic nerve activity. Records were made of the activities of the phrenic nerve, the superior laryngeal nerve (SLN), the recurrent laryngeal nerve (RLN), and the intralaryngeal branches of the RLN serving the thyroarytenoid (TA) and posterior cricoarytenoid (PCA) muscles. Neural activities were assessed in the steady state at different end-tidal O2 and CO2 concentrations. Transient responses to withholding inspiratory lung inflation and to preventing expiratory lung emptying were also studied. Hypercapnia and hypoxia increased the inspiratory activities of the phrenic nerve, SLN, RLN, and its PCA branch. TA inspiratory activity was not changed. Expiratory activities of RLN, PCA, and TA were all increased in hypoxia. When lung inflation was withheld, neural inspiratory duration and the inspiratory activities of all nerves increased. The subsequent period of neural expiration was marked by an exaggerated burst of activity by the TA branch of the RLN. TA expiratory activity was also sharply increased after inspiratory efforts that were reflexly delayed by the prevention of lung emptying. TA activity in expiration was enhanced after vagotomy and was usually more prominent than when lung inflation was withheld before vagal section. The results demonstrate the importance and complexity of the influence of vagal afferents on laryngeal motor activity.     

Medullary neurons mediating the inhibition of inspiration by intercostal muscle tendon organs?

Studies were conducted to test the hypothesis that nonrespiratory-modulated units are last-order interneurons mediating the effects of intercostal muscle tendon organs on medullary inspiratory neuron activity. Vagotomized, anesthetized, or decerebrate cats were used. Results show the following. 1) Afferents from different receptor types (i.e., intercostal tendon organs and chest wall cutaneous receptors) that inhibit medullary inspiratory neuron activities evoke the same units. 2) Gastrocnemius muscle group I afferent fibers evoke some of the same units as intercostal afferents but do not alter respiratory activity. 3) The "pneumotaxic center" and laryngeal nerve afferents, which inhibit medullary inspiratory activity, evoke different medullary units than intercostal afferents. 4) Evoked units are not active in spontaneously breathing cats. Additional results suggest that a few respiratory neurons near the retrofacial nucleus may be involved in the mediation of the inspiratory inhibitory effects of intercostal tendon organs. These results do not establish the mechanism by which intercostal muscle tendon organs reduces medullary inspiratory activity.     

Involvement of bulbar respiratory and non-respiratory neurons in onset of expiration reflex

It was shown that excitation of high- and low-threshold superior laryngeal afferents triggers reflexes of varying complexity in a considerable proportion of non-respiratory neurons during experiments on cats anesthetized by Nembutal involving stimulation-induced expiration reflex. Systemic alterations in background firing activity were noted during this reflex in "respiratory" neurons; reflex reaction setting in as a result of low-threshold laryngeal afferent activation was also recorded in 22.4% of this group. Oligo- and polysynaptic excitatory connections were found between low-threshold laryngeal afferents and inspiratory beta neurons, P-cells, and laryngeal muscle motoneurons as opposed to inhibitory connections with inspiratory gammaneurons. This article discusses involvement of the neurons investigated in mechanisms of inspiratory inhibition, closure of the vocal chords, and adaptive decline in breathing rate occurring during expiration reflex.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 22, No. 5, pp. 670–680, September–October, 1990.     

Neural drive to tongue protrudor and retractor muscles following pulmonary C-fiber activation.

Hypoglossal (XII) nerve recordings indicate that pulmonary C-fiber (PCF) receptor activation reduces inspiratory bursting and triggers tonic discharge. We tested three hypotheses related to this observation: 1) PCF receptor activation inhibits inspiratory activity in XII branches innervating both tongue protrudor muscles (medial branch; XIImed) and retractor muscles (lateral branch; XIIlat); 2) reduced XII neurogram amplitude reflects decreased XII motoneuron discharge rate; and 3) tonic XII activity reflects recruitment of previously silent motoneurons. Phrenic, XIImed, and XIIlat neurograms were recorded in anesthetized, paralyzed, and ventilated rats. Capsaicin delivered to the jugular vein reduced phrenic bursting at doses of 0.625 and 1.25 mug/kg but augmented bursting at 5 mug/kg. All doses reduced inspiratory amplitude in XIImed and XIIlat (P < 0.05), and these effects were eliminated following bilateral vagotomy. Single-fiber recordings indicated that capsaicin causes individual XII motoneurons to either decrease discharge rate (n = 101/153) or become silent (n = 39/153). Capsaicin also altered temporal characteristics such that both XIImed and XIIlat inspiratory burst onset occurred after the phrenic burst (P < 0.05). Increases in tonic discharge after capsaicin were greater in XIImed vs. XIIlat (P < 0.05); single-fiber recordings indicated that tonic discharge reflected recruitment of previously silent motoneurons. We conclude that PCF receptor activation reduces inspiratory XII motoneuron discharge and transiently attenuates neural drive to both tongue protrudor and retractor muscles. However, tonic discharge appears to be selectively enhanced in tongue protrudor muscles. Accordingly, reductions in upper airway stiffness associated with reduced XII burst amplitude may be offset by enhanced tonic activity in tongue protrudor muscles.     

Neural organization of the ventilatory activity in the frog,Rana catesbeiana. II

The paralyzed, decerebrate frog, Rana catesbeiana, displays “fictive” oropharyngeal and pulmonary ventilations. In order to evaluate the neuronal correlates of these two centrally programmed ventilatory bursting patterns, we have performed intra-and extracellular recordings of bulbar respiratory neurons in this fictively breathing preparation. A total of 123 respiratory neurons were recorded from the caudal medulla. Of 51 antidromically activated neurons, 20 were vagal motoneurons and 31 were hypoglossal motoneurons. Respiratory neurons that depolarized during the lung (L) or non-lung (N) ventilatory phases were classified as L or N neurons, respectively. Phase spanning neurons (S) were active during both L and N phases. Some neurons showed oscillations of membrane potential synchronous with oropharyngeal ventilation. Those active during the buccal elevation phase were exclusively L neurons whereas those having buccal depressor activity were exclusively N neurons. Synaptic drive potentials were observed in all neurons recorded intracellularly. In some neurons, hyperpolarization was caused by inhibitory postsynaptic potentials, as demonstrated by reversal of membrane potential trajectory after intracellular chloride iontophoresis. Some individual motoneurons and interneurons exhibited both pulmonary and buccal ventilatory activity, indicating that both pattern generators project to a common motor control system. 1994 John Wiley & Sons, Inc.     

Respiratory cycle timing and fast inspiratory discharge rhythms in the adult decerebrate rat

In supracollicular decerebrate paralyzed adult rats, neural respiration was monitored by bilateral phrenic recordings. In the study of respiratory cycle timing, the effects of vagal afferent input (lung inflation) on respiratory phase durations resembled those seen in decerebrate cats. 1) Withholding lung inflation during neural inspiration (I) produced lengthening of I phase duration by 46% (mean, n = 11). 2) Maintaining lung inflation during neural expiration (E) produced lengthening of E phase duration by 112% (mean, n = 4). In the study of fast rhythms in inspiratory discharges, phrenic nerve autospectra and bilateral (left-right) phrenic coherences in 16 rats revealed two types of fast rhythm: 1) high-frequency oscillation (HFO), which had significant coherence peaks (n = 9, range 106-160 Hz, mean 132 Hz); and 2) medium-frequency oscillation (MFO), which had autospectral peaks but no distinct coherence peaks (n = 11, range 46-96 Hz, mean 66 Hz). These rhythms resembled MFOs and HFOs in the decerebrate cat, but the modal frequency range was about twice as large. In addition, these frequency values differed markedly from the 20-40 Hz of the rhythms found in earlier studies in neonatal in vitro preparations; the difference may be due to developmental immaturity.     

Some effects of superior laryngeal nerve stimulation on sympathetic preganglionic neuron firing

Repetitive electrical stimulation of afferent fibers in the superior laryngeal nerve (SLN) evoked depressant or excitatory effects on sympathetic preganglionic neurons of the cervical trunk in Nembutal-anesthetized, paralyzed, artifically ventilated cats. The depressant effect, which consisted of suppression of the inspiration-synchronous discharge of units with such firing pattern, was obtained at low strength and frequency of stimulation (e.g. 600 mV, 30 Hz) and was absent at end-tidal CO2 values below threshold for phrenic nerve activity. The excitatory effect required higher intensity and frequency of stimulation and was CO2 independent. The depressant effect on sympathetic preganglionic neurons with inspiratory firing pattern seemed a replica of the inspiration-inhibitory effect observed on phrenic motoneurons. Hence, it could be attributed to the known inhibition by the SLN of central inspiratory activity, if it is assumed that this is a common driver for phrenic motoneurons and some sympathetic preganglionic neurons. The excitatory effect, on the other hand, appears to be due to connections of SLN afferents with sympathetic preganglionic neurons, independent of the respiratory center.