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／     

d-serine regulation of the timing and architecture of the inspiratory burst in neonatal mice

d-serine, released from mouse medullary astrocytes in response to increased CO₂ levels, boosts the respiratory frequency to adapt breathing to physiological demands. We analyzed in mouse neonates, the influence of d-serine upon inspiratory/expiratory durations and the architecture of the inspiratory burst, assessed by pwelch's power spectrum density (PSD) and continuous wavelet transform (CWT) analyses. Suction electrode recordings were performed in slices from the ventral respiratory column (VRC), site of generation of the respiratory rhythm, and in brainstem-spinal cord (en bloc) preparations, from the C5 ventral roots, containing phrenic fibers that in vivo innervate and drive the diaphragm, the main inspiratory muscle.In en bloc and slice preparations, d-serine (100 μM) reduced the expiratory, but not the inspiratory duration, and increased the frequency and the regularity of the respiratory rhythm. In en bloc preparations, d-serine (100 μM) also increased slightly the amplitude of the integrated inspiratory burst and the area under the curve of the integrated inspiratory burst, suggesting a change in the recruitment or the firing pattern of neurons within the burst. Time-frequency analyses revealed that d-serine changed the burst architecture of phrenic roots, widening their frequency spectrum and shifting the position of the core of firing frequencies towards the onset of the inspiratory burst. At the VRC, no clear d-serine induced changes in the frequency-time domain could be established. Our results show that d-serine not only regulates the timing of the respiratory cycle, but also the recruitment strategy of phrenic motoneurons within the inspiratory burst.     

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.     

肌梭传入对呼吸的调节作用

实验用６３只麻醉、制动、切断双侧颈迷走神经、人工呼吸的家兔,以延髓呼吸相关神经元（ＲＲＮ）和膈神经放电（Ｐｈｒ．Ｄ）作为呼吸观测指标,观察了股动脉注射琥珀胆碱（Ｓｃｈ）诱发的肌梭传入活动对呼吸的影响。结果显示：（１）股动脉注射Ｓｃｈ可产生明显的呼吸易化作用,主要表现为吸气时程（Ｔｉ）延长、呼气时程（Ｔｅ）缩短不明显,Ｔｉ／Ｔｅ比值增加以及呼吸频率（ＲＦ）变化不在,称为吸气延长效应;或Ｔｅ缩短,Ｔｉ     

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.     

Simulations of a ventrolateral medullary neural network for respiratory rhythmogenesis inferred from spike train cross-correlation

Connections among ventrolateral medullary respiratory neurons inferred from spike train analysis were incorporated into a model and simulated with the program SYSTM11 (MacGregor 1987). Inspiratory (I) and expiratory (E) neurons with augmenting (AUG) and decrementing (DEC) discharge patterns and rostral I-E/I neurons exhibited varying degrees of adaptation, but no endogenous bursting properties. Simulation parameters were adjusted so that respiratory phase durations, neuronal discharge patterns, and short-time scale correlations were similar to corresponding measurements from anesthetized, vagotomized, adult cats. Rhythmogenesis persisted when the strength of each set of connections was increased 100% over a smaller effective value. Changes in phase durations and discharge patterns caused by manipulation of connection strengths or population activity led to several predictions. (a) Excitation of the I-E/I population prolongs the inspiratory phase. (b) Rhythmic activity can be reestablished in the absence of I-E/I activity by unpatterned excitation of I-DEC and I-AUG neurons. (c) An increase in I-DEC neuron activity can cause an apneustic respiratory pattern. (d) A decrease in I-DEC neuron activity increases the slope of the inspiratory ramp and shortens inspiration. (e) Excitation of the E-DEC population prolongs the expiratory phase or produces apnea; inhibition of E-DEC neurons reduces expiratory time. (f) Excitation of E-AUG cells causes I-AUG neurons to exhibit a step rather than a ramp increase in firing rate at the onset of their active phase. The results suggest mechanisms by which the duration of each phase of breathing and neuronal discharge patterns may be regulated. Received: 24 February 1993/Accepted in revised form: 8 September 1993     

Effect of ketamine on control of breathing in cats

We studied minute ventilation, breathing pattern, end-tidal CO2 partial pressure (PACO2), and tracheal occlusion pressure in cats anesthetized with ketamine (40 and 80 mg/kg) before and after CO2 inhalation. Before CO2 administration ventilation was reduced and PACO2 increased relative to unanesthetized cats at both ketamine doses. Breathing pattern was of the "apneustic" type, being characterized by 1) prolonged inspiratory duration and relatively short expiratory time and 2) markedly curvilinear (convex upward) inspiratory volume-time profile. The latter reflected a similar curvilinearity in the tracheal occlusion pressure waveform. During CO2 inhalation, the ventilatory response to CO2 was similar to that in unanesthetized cats in spite of a depressed tracheal occlusion pressure response. This discrepancy was due to the fact that in the presence of a convex upward inspiratory volume-time profile, the shortening of inspiratory duration with increasing CO2 results in a marked increase of mean inspiratory flow, and hence the ventilatory response to CO2 remains high.     

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.     

Activity of bulbar respiratory neurones during cough and other respiratory tract reflexes in cats

Changes evoked by mechanical stimulation of the relevant parts of the respiratory tract in the activity of inspiratory and expiratory neurones in the ventral respiratory group of the medulla oblongata, and in pleural pressure and the diaphragmatic electromyogram, were determined during cough, sneeze and the aspiration and expiration reflexes in 17 anaesthetized (but not paralysed) cats. The results of 72 tests of elicitation of the given reflexes showed that: Compared with the control inspiration, both the mean and the maximum discharge frequency of spontaneously active inspiratory neurones rose during the inspiratory phase of cough, sneeze and the aspiration reflex. Regular recruitment of new inspiratory units was also observed in the inspiratory phase of cough and the aspiration reflex. Compared with the control expiration, both the mean and the maximum discharge frequency of spontaneously active expiratory neurones rose during the cough, sneeze and expiration reflex effort. Recruitment of latent expiratory neurones was always observed in the expulsive phase of the given respiratory processes. The recruitment of latent expiratory neurones was accompanied by reciprocal inhibition of the activity of inspiratory units and recruitment of latent inspiratory neurones by inhibition of the activity of expiratory units and recruitment of latent inspiratory neurones by inhibition of the activity of expiratory units. Regular recruitment of the same expiratory neurones in all expulsive respiratory processes, together with the similar incidence of inspiratory neurones in the inspiratory phase of sneeze and the aspiration reflex, indicates that they are "nonspecific" in character.     

Effects of PGF2 alpha on the EMG of costal and crural parts of the diaphragm of the newborn pig

We investigated the effects of PGF2 alpha on the breathing patterns and electric activity of costal and crural parts of the diaphragm in 9 anesthetized newborn pigs. The change in diaphragmatic tension was evaluated as the change in transdiaphragmatic pressure. Because PGF2 alpha induces bronchoconstriction and an increase in respiratory resistances, the changes induced by prostaglandin were evaluated as differences between bronchoconstriction after PGF2 alpha and resistive load obtained by applying gradual occlusion to the inspiratory line of the breathing circuit. Our results show that PGF2 alpha decreased respiratory frequency with lengthening of expiratory time, while the resistive load increased both respiratory phases. The changes in breathing pattern were associated with different electrical activities of the diaphragm. While resistive load did not significantly change the EMG power spectrum, PGF2 alpha recruited new motor units. Furthermore, resistive load induced synchronization of the inspiratory time discharge of the costal and crural parts of the diaphragm, while after PGF2 alpha infusion there was an early inspiratory discharge of the crural part.     

Parameters of discharges of respiratory neurons of the ventrolateral medullary regions in early postnatal rats

In experiments on superfusedin situ semi-isolated medullo-spinal preparations (SIMSP) of newborn (1st day of life) and 4- to 5-day-old rats, we studied the parameters of extracellularly recorded spike activity of respiratory neurons of the ventrolateral medullary regions (VLMR). In SIMSP of 4- to 5-day-old rats, the frequency of discharges of pre-inspiratory, inspiratory, and expiratory neurons is shown to be significantly higher, while the dispersion of its values is considerably lower, as compared with the corresponding values for newborn animals. In the majority of pre-inspiratory and inspiratory neurons of SIMSP of newborn rats, irregular low-frequency discharges are usually generated within the interinspiration phase. The relative intensity of suppression of discharges of pre-inspiratory and expiratory neurons within an inspiration phase is much lower in SIMSP of newborn rats, as compared with that in 4- to 5-day-old preparations. The activity of most pre-inspiratory neurons manifests a trend toward transformation from a two-phase pattern in newborn rats (with two frequency peaks, pre- and post-inspiratory) to a monophasic pattern (with one pre-inspiratory frequency peak) typical of 4- to 5-day-old animals. The effects of electrical stimulation of the site of localization of pre-inspiratory neurons showed that in SIMSP of both age groups of rats an inspiratory response could be evoked in then. phrenicus only in the case when stimulation was applied within the second half of an interinspiratory phase. Therefore, it can be supposed that the respiratory network in newborn animals is to a considerable extent immature in the morphofunctional aspect. It seems probable that in early postnatal rats pre-inspiratory neurons are involved in the medullary mechanisms foron-off switching of the inspiratory and expiratory phases.Neirofiziologiya/Neurophysiology, Vol. 28, No. 4/5, pp. 207–217, July–October, 1996.     

Computer simulation of brainstem respiratory activity.

A mathematical model of the medullary respiratory oscillator, composed of two mutually inhibiting populations (inspiratory and expiratory) of computer-simulated neurons, is presented. Each population consists of randomly interconnected subpopulations of excitatory and inhibitory neurons, is presented. Each population consists of randomly interconnected subpopulations of excitatory and inhibitory neurons. Neuronal coupling is such that either the inspiratory or expiratory population alone is capable of cyclic activity. Weak inhibitory connections between inspiratory and expiratory populations provide satisfactory reciprocating activity independent of the natural frequency of either population alone. Initiation and persistence of rhythmic activity is dependent on a diffused noncyclic excitatory input. Vagal discharge, simulated by phasic inhibition of inspiratory neurons, results in increased respiratory frequency with decreased inspiratory activity. In the absence of simulated vagal discharge, uniform facilitation of synaptic connections increases averaged activities of inspiratory and expiratory populations, with minor effect on frequency. In the presence of simulated vagal discharge, facilitation of synaptic connections increases both frequency and amplitude. The simulated effects of synaptic facilitation, with and without vagal discharge, mimic the physiological response to CO2 in the intact and vagotimized animal.     

Tracheal occlusions evoke respiratory load compensation and neural activation in anesthetized rats

Airway obstruction in animals leads to compensation and avoidance behavior and elicits respiratory mechanosensation. The pattern of respiratory load compensation and neural activation in response to intrinsic, transient, tracheal occlusions (ITTO) via an inflatable tracheal cuff are unknown. We hypothesized that ITTO would cause increased diaphragm activity, decreased breathing frequency, and activation of neurons within the medullary and pontine respiratory centers without changing airway compliance. Obstructions were performed for 2-3 breaths followed by a minimum of 15 unobstructed breaths with an inflatable cuff sutured around the trachea in rats. The obstruction procedure was repeated for 10 min. The brains of obstructed and control animals were removed, fixed, sectioned, and stained for c-Fos. Respiratory pattern was measured from esophageal pressure (P(es)) and diaphragm electromyography (EMG(dia)). The obstructed breaths resulted in a prolonged inspiratory and expiratory time, an increase in EMG(dia) amplitude, and a more negative P(es) compared with control breaths. Neurons labeled with c-Fos were found in brain stem and suprapontine nuclei, with a significant increase in c-Fos expression for the occluded experimental group compared with the control groups in the nucleus ambiguus, nucleus of the solitary tract, lateral parabrachial nucleus, and periaqueductal gray matter. The results of this study demonstrate tracheal occlusion-elicited activation of neurons in brain stem respiratory nuclei and neural areas involved in stress responses and defensive behaviors, suggesting that these neurons mediate the load compensation breathing pattern response and may be part of the neural pathway for respiratory mechanosensation.     

Bradykinin stimulates respiratory drive by activating pulmonary sympathetic afferents in the rabbit.

We recently identified a vagally mediated excitatory lung reflex by injecting hypertonic saline into the lung parenchyma (Yu J, Zhang JF, and Fletcher EC. J Appl Physiol 85: 1485-1492, 1998). This reflex increased amplitude and burst rate of phrenic (inspiratory) nerve activity and suppressed external oblique abdominal (expiratory) muscle activity. In the present study, we tested the hypothesis that bradykinin may activate extravagal pathways to stimulate breathing by assessing its reflex effects on respiratory drive. Bradykinin (1 microg/kg in 0.1 ml) was injected into the lung parenchyma of anesthetized, open-chest and artificially ventilated rabbits. In most cases, bradykinin increased phrenic amplitude, phrenic burst rate, and expiratory muscle activity. However, a variety of breathing patterns resulted, ranging from hyperpnea and tachypnea to rapid shallow breathing and apnea. Bradykinin acts like hypertonic saline in producing hyperpnea and tachypnea, yet the two agents clearly differ. Bradykinin produced a higher ratio of phrenic amplitude to inspiratory time and had longer latency than hypertonic saline. Although attenuated, bradykinin-induced respiratory responses persisted after vagotomy. We conclude that bradykinin activates multiple afferent pathways in the lung; portions of its respiratory reflexes are extravagal and arise from sympathetic afferents.     

Function of different medullary neurons in respiration]

1. We have studied the activity of 162 medullary respiratory neurones in the "encephale isole bas" cat. These neurones were classed into three groups : bulbospinal inspiratory (NBSI : 39) or expiratory (NBSE : 15) neurones whose axons enter the spinal cord ; inspiratory or expiratory laryngeal motoneurones (MLI : 17; MLE : 10) antidromically activated by vagus nerve stimulation ; propriobulbar inspiratory (NPBI : 59) or expiratory (NPBE : 22) neurones whose axons lie perhaps entirely within the medulla. 2. Correlation coefficients between number of spikes delivered in each burst and the duration of the corresponding respiratory phase (inspiration for NBSI, MLI, NPBI ; expiration for NBSE, MLE, NPBE) have been calculated for each neurone. 3. The activity of most of the NBSI and MLI is significantly correlated with the duration of the inspiration. These two groups of neurones are probably homogenous. 4. On the basis of this correlation test, NPBI do not constitute an homogeneous population ; 50% of NPBI are not significantly correlated. The same results are obtained if correlations are calculated between the number of spikes delivered and the amplitude of integrated phrenic nerve acitivty. According to the discharge pattern and correlation test, we can consider three groups of NPBI : early recruited neurones with decreasing frequency and non significantly correlated activity (23,7%); early and late neurones with increasing frequency and significantly correlated activity (32,2%); early and late neurones with increasing frequency and non significantly correlated acitivty (44,1%). 5. The activity of most of the NBSE and NPBE with increasing frequency is significantly correlated with the duration of the expiration. Among the MLE and NPBE with a decreasing frequency, a great number of neurones are not significantly correlated. 6. The functional significantion of the different neuronal types is discussed from these correlation tests and from the pattern of activity and axonal pathways.     

The respiratory center--the regulator of the respiratory system

The authors consider the respiratory centre to be the regulator of the respiratory system and to consist of 3 main functional blocks: chemoregulator, respiratory rhythm autogenerator and mechanoregulator, functions of which are provided by the neurons of medulla oblongata. The main aim of chemoregulator block is to maintain the level of ventilation volume speed, which is necessary to compensate the difference between the signals of setting and the firing from the chemoreceptors. The main aim of mechanoregulator block is to provide the functioning of the regulation loop of the respiratory muscles comparing the signals which come from the respiratory autogenerator, and the firing of the mechanoreceptors. The generator unit of the respiratory centre is a set of rhythm-forming associations, the system of 4 neurons (early and late inspiratory and expiratory) are typical among them. The neurons are connected by recurrent inhibitory bonds: the neuron of each rhythm-forming group, successively becoming excited, inhibits the two preceding neurons in the cycle; for all this the neuron of the successive group is released from inhibition and in such a way the rhythmogenesis occurs. The respiratory centre forms a common unit for chemo- and mechanoreceptor loops, through which the circuits of feedback for both loops are connected, providing the regulation of breathing.     

Volume of activation of the Hering-Breuer inflation reflex in the newborn infant.

Although the Hering-Breuer inflation reflex (HBIR) is active within tidal breathing range in the neonatal period, there is no information regarding whether a critical volume has to be exceeded before any effect can be observed. To explore this, effects of multiple airway occlusions on inspiratory and expiratory timing were measured throughout tidal breathing range using a face mask and shutter system. In 20 of the 22 healthy infants studied, there was significant shortening of inspiration because the volume at which occlusion occurred rose from functional residual capacity (FRC) to end-inspiratory volume [14.9% reduction in inspiratory time (per ml/kg increase in lung volume at occlusion)]. All infants showed a significant increase in expiratory time [17.1% increase (per ml/kg increase in lung volume at occlusion)]. Polynomial regression analyses revealed a progressive increase in strength of HBIR from FRC to approximately 4 ml/kg above FRC. Eighteen infants showed no further shortening of inspiratory time and 10 infants no further lengthening of expiratory time with increasing occlusion volumes, indicating maximal stimulation of the reflex had been achieved. There was a significant relationship between strength of HBIR and respiratory rate, suggesting that HBIR modifies the breathing pattern in the neonatal period.     

Intracellular recordings of respiratory neurons in the lateral medulla of piglets

Membrane potentials of respiratory neurons in the ventral respiratory group were recorded using intracellular techniques in the medulla of newborn piglets. Three types of neurons were demonstrated: inspiratory neurons with an augmenting pattern of spike activity during inspiration; postinspiratory neurons with a short decrementing firing pattern that started immediately after inspiration ended; and stage II expiratory neurons with an augmenting spiking pattern that began shortly after inspiratory termination and ended before onset of the next inspiration. When not firing, the membrane potential trajectories of each cell type revealed two complementary patterns of relative inhibition. This latter finding suggests arrival of inhibitory synaptic potentials during these periods. These findings suggest that the respiratory control mechanisms of the newborn piglet are organized in a three-phased manner similar to that of adult cats.     

Mu-opioid receptor agonist effects on medullary respiratory neurons in the cat: evidence for involvement in certain types of ventilatory disturbances

Mu-opioid receptor agonists depress tidal volume, decrease chest wall compliance, and increase upper airway resistance. In this study, potential neuronal sites and mechanisms responsible for the disturbances were investigated, dose-response relationships were established, and it was determined whether general anesthesia plays a role. Effects of micro-opioid agonists on membrane properties and discharges of respiratory bulbospinal, vagal, and propriobulbar neurons and phrenic nerve activity were measured in pentobarbital-anesthetized and unanesthetized decerebrate cats. In all types of respiratory neurons tested, threshold intravenous doses of the micro-opioid agonist fentanyl slowed discharge frequency and prolonged duration without altering peak discharge intensity. Larger doses postsynaptically depressed discharges of inspiratory bulbospinal and inspiratory propriobulbar neurons that might account for depression of tidal volume. Iontophoresis of the micro-opioid agonist DAMGO also depressed the intensity of inspiratory bulbospinal neuron discharges. Fentanyl given intravenously prolonged discharges leading to tonic firing of bulbospinal expiratory neurons in association with reduced hyperpolarizing synaptic drive potentials, perhaps explaining decreased inspiratory phase chest wall compliance. Lowest effective doses of fentanyl had similar effects on vagal postinspiratory (laryngeal adductor) motoneurons, whereas in vagal laryngeal abductor and pharyngeal constrictor motoneurons, depression of depolarizing synaptic drive potentials led to sparse, very-low-frequency discharges. Such effects on three types of vagal motoneurons might explain tonic vocal fold closure and pharyngeal obstruction of airflow. Measurements of membrane potential and input resistance suggest the effects on bulbospinal Aug-E neurons and vagal motoneurons are mediated presynaptically. Opioid effects on the respiratory neurons were similar in anesthetized and decerebrate preparations.     

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.