Role in the inspiratory off-switch of vagal inputs to rostral pontine inspiratory-modulated neurons

Neurons of the pontine respiratory group (PRG) in the region of the nucleus parabrachialis medialis and the Kolliker-Fuse nucleus are believed to play an important role in promoting the inspiratory (I) off-switch (IOS). In decerebrate gallamine-paralyzed cats ventilated with a cycle-triggered pump system (lung inflation during the neural I phase), we studied the effects of vagal (V) afferent inputs on firing of I-modulated neurons (the most numerous population in PRG) and on I duration. The predominant V effect on unit activity was inhibitory, as shown by two types of test: (a) withholding of inflation during an I phase, which produced increase of unit firing and of its respiratory modulation (58/66 neurons in 14 cats), indicating disinhibition due to removal of phasic V input; (b) delivery of afferent V stimulus trains during a no-inflation I phase, which produced decrease of unit firing and of its respiratory modulation (20 neurons). In addition, application of V input during the neural expiratory (E) phase, which lengthened E phase duration, produced no effect on the neurons' firing, suggesting that the inhibition during I was presynaptic in origin. The results may be interpreted by the hypothesis that the medullary late-I presumptive IOS neurons receive excitatory inputs from the PRG I-modulated neurons as well as from V afferents.. With relatively strong V input, this pontine excitatory output is reduced by inhibition, whereas with relatively weak V input that excitatory output is increased due to reduction of inhibition. Thus the pontine and the V influences on the IOS can operate in a complementary manner dependent on state.     

Responses of ventral respiratory neurones in the rat to vagus stimulation and the functional division of expiration.

In anaesthetized rats, extracellular and intracellular recordings were taken from 106 respiratory neurones in the intermediate region of the nucleus ambiguus. We observed unprovoked shortening of expiratory time accompanied, in all classes of respiratory neurone, by the elimination of the changes in membrane potential that were characteristic of stage II expiration. The demonstration of the elimination of stage II expiration in both the rat and cat strongly supports the functional division of expiration into stage I expiration (post-inspiration) and stage II expiration. In order to identify the neurones in the rat that receive inputs from vagal afferents and modulate the central respiratory rhythm, we examined whether any respiratory neurones responded to stimulation of the vagus nerve. Some post-inspiratory and stage II expiratory neurones responded. The short latency (< 2 ms) of four of the responses indicates that some vagal afferents act on post-inspiratory neurones via a disynaptic pathway. While repetitive stimulation of the vagus nerve could inhibit the phrenic rhythm, it appears that most inspiratory neurones in the intermediate region of the nucleus ambiguous complex are not directly involved in integrating the information from vagal afferents with the central respiratory rhythm.     

Role of the ventrolateral region of the nucleus of the tractus solitarius in processing respiratory afferent input from vagus and superior laryngeal nerves

Summary The role of respiratory neurons located within and adjacent to the region of the ventrolateral nucleus of the tractus solitarius (vlNTS) in processing respiratory related afferent input from the vagus and superior laryngeal nerves was examined. Responses in phrenic neural discharge to electrical stimulation of the cervical vagus or superior laryngeal nerve afferents were determined before and after lesioning the vlNTS region. Studies were conducted on anesthetized, vagotomized, paralyzed and artificially ventilated cats. Arrays of 2 to 4 tungsten microelectrodes were used to record neuronal activity and for lesioning. Constant current lesions were made in the vlNTS region where respiratory neuronal discharges were recorded. The region of the vlNTS was probed with the microelectrodes and lesions made until no further respiratory related neuronal discharge could be recorded. The size and placement of lesions was determined in subsequent microscopic examination of 50 m thick sections. Prior to making lesions, electrical stimulation of the superior laryngeal nerve (4–100 A, 10 Hz, 0.1 ms pulse duration) elicited a short latency increase in discharge of phrenic motoneurons, primarily contralateral to the stimulated nerve. This was followed by a bilateral decrease in phrenic nerve discharge and, at higher currents, a longer latency increase in discharge. Stimulation of the vagus nerve at intensities chosen to selectively activate pulmonary stretch receptor afferent fibers produced a stimulus (current) dependent shortening of inspiratory duration. Responses were compared between measurements made immediately before and immediately after each lesion so that changes in response efficacy due to lesions per se could be distinguished from other factors, such as slight changes in the level of anesthesia over the several hours necessary in some cases to complete the lesions. Neither uni- nor bi-lateral lesions altered the efficacy with which stimulation of the vagus nerve shortened inspiratory duration. The short latency excitation of the phrenic motoneurons due to stimulation of the superior laryngeal nerve was severely attenuated by unilateral lesions of the vlNTS region ipsilateral to the stimulated nerve. Neither the bilateral inhibition nor the longer latency excitation due to superior laryngeal nerve stimulation was reduced by uni- or bi-lateral lesions of the vlNTS region. These results demonstrate that extensive destruction of the region of the vlNTS: a) does not markedly affect the inspiratory terminating reflex associated with electrical stimulation of the vagus nerve in a current range selective for activation of pulmonary stretch receptor afferents, and b) abolishes the short-latency increase, but not the bilateral decrease or longer latency increase in phrenic motoneuronal discharge which follows stimulation of the superior laryngeal nerve. We conclude that respiratory neurons in the region of the vlNTS do not play an obligatory role in the respiratory phase transitions in this experimental preparation. Neurons in the vlNTS region may participate in other reflexes, such as the generation of augmented phrenic motoneuronal discharge in response to activation of certain superior laryngeal or vagus nerve afferents.     

Motor and sensory re-innervation of the lung and heart after re-anastomosis of the cervical vagus nerve in rats

There is no study in the literature dealing with re-innervation of the cardiopulmonary vagus nerve after its transection followed by re-anastomosis. In the present study, we explored the bronchomotor, heart rate and respiratory responses in rats at 2, 3 and 6 months after re-anastomosis of one cervical vagus trunk. The conduction velocity of A, B and C waves was calculated in the compound vagal action potential. We searched for afferent vagal activities in phase with pulmonary inflation to assess the persistence of pulmonary stretch receptor (PSR) discharge in re-innervated lungs. In each animal, data from the stimulation or recording of one re-anastomosed vagus nerve were compared with those obtained in the contra-lateral intact one. Two and three months after surgery, the conduction velocities of A and B waves decreased, but recovery of conduction velocity was complete at 6 months. By contrast, the conduction velocity of the C wave did not change until 6 months, when it was doubled. The PSR activity was present in 50% of re-anastomosed vagus nerves at 2 and 3 months and in 75% at 6 months. Respiratory inhibition evoked by vagal stimulation was significantly weaker from the re-anastomosed than intact nerve at 2 but not 3 months. Vagal stimulation did not elicit cardiac slowing or bronchoconstriction 6 months after re-anastomosis. Our study demonstrates the capacity of pulmonary vagal sensory neurones to regenerate after axotomy followed by re-anastomosis, and the failure of the vagal efferents to re-innervate both the lungs and heart.     

Modulation of the Hering-Breuer reflex by raphe pallidus in rabbits

Activation of the pulmonary stretch receptors by lung inflation or vagal stimulation evokes Hering-Breuer (HB) reflex, which is characterized by inspiratory inhibition and expiratory prolongation. In this work, whether the HB reflex could be modulated by the serotonergic raphe pallidus (RP) was studied by comparing the strength of this reflex before and after electrical or chemical stimulation of the RP. Experiments were performed on urethane anesthetized adult rabbits. The HB reflex was simulated with electrical stimulation of the central end of cervical vagus nerve. The RP was stimulated electrically or chemically by microinjection of glutamate. We found that after either electrical stimulation or chemical stimulation of the RP, the inspiratory inhibition and expiratory prolongation of the HB reflex were significantly attenuated. This attenuation showed post-stimulation time dependency or short-term memory, as well as RP stimulation intensity dependency. Results of the present study suggested that the serotonergic RP could exert its respiratory effects by modulating the strength of HB reflex.     

Augmentation of muscle nociceptive respiratory reflex facilitation by vagal afferents

Vagal influence on the facilitation of phrenic neural activity during respiratory phase-locked, gastrocnemius muscle nerve nociceptive electrical stimulation was examined in anesthetized, glomectomized, paralyzed, and artificially ventilated cats. (1) In the vagi-intact state, respiratory reflex facilitation was characterized by a sharp rise in peak amplitude, maximum rate of rise or slope, and mean rate of rise of integrated phrenic nerve activity. This was greater during inspiratory phase-locked (T1-locked) muscle nerve electrical stimulation than during expiratory phase-locked (TE-locked) muscle nerve electrical stimulation. "Evoked post-inspiratory phrenic activity" during the early expiratory phase was also observed during TE-locked muscle nerve electrical stimulation. (2) Bilateral vagotomy significantly attenuated the respiratory facilitation during both T1- and TE-locked muscle nerve electrical stimulation. In particular, the "evoked post-inspiratory phrenic activity" during TE-locked muscle nerve electrical stimulation was also attenuated or almost completely abolished. (3) Conditioning electrical stimulation of the vagus nerve revealed facilitatory reflexes which co-exist with inspiratory inhibitory reflexes. (4) The "evoked post-inspiratory phrenic activity" during TE-locked muscle nerve electrical stimulation, which was attenuated or abolished after vagotomy, was restored after vagal T1-locked conditioning stimuli combined with TE-locked muscle nerve electrical stimulation. The results suggest that vagal facilitatory reflexes augment the respiratory reflex facilitation during muscle nociceptive stimulation.     

Cardio-respiratory coupling depends on the pons

Cardio-respiratory coupling is reciprocal; it is expressed as respiratory-modulated sympathetic nerve activity and pulse-modulated respiratory motor activity. In the brainstem, the neuraxis controlling cardio-respiratory functions forms a ventrolateral cell column which extends to the dorsolateral (dl) pons. Our general working hypothesis is that these control systems converge at points with the common purpose of gas exchange and that neural activity along this axis coordinates both arterial pulse pressure and breathing. Here, we review the data showing that pontine nuclei modulate heart rate, blood pressure and breathing, and present new results demonstrating a vagal influence on pontine activity modulated with both arterial pulse pressure and phrenic nerve activity in the decerebrate cat. Generally with the vagi intact, dl pontine activity was weakly modulated by both arterial pulse pressure and respiratory pattern. After bilateral vagotomy, the strength and consistency of respiratory modulation increased significantly, although the strength and consistency of arterial pulse pressure modulation did not change significantly for the group; a decrease in some (62%) was offset by an increase in others (36%) neurons. Thus, the vagus shapes the envelope of the cycle-triggered averages of neural activity for both the respiratory and cardiac cycles. These data provide insight into the neural substrate for the prominent vagal effect on the cardio-respiratory coupling pattern, in particular respiratory sinus arrhythmia. While these results support convergence of inputs to neural populations controlling breathing and cardiovascular functions, the physiologic role of balancing ventilation, vascular resistance, heart rate and blood flow for the benefit of tissue oxygenation, remains hypothetical.     

Vagotomy induced changes in acetyl cholinesterase staining and substance P-like immunoreactivity in the gustatory lobes of goldfish

Summary In teleost fish, the visceral sensory nuclei of the medulla are clearly separated into gustatory lobes and a general visceral sensory nucleus. Those branches of the vagus nerve which innervate the orobranchial cavity terminate in the vagal gustatory lobe, while the general visceral component of the vagus nerve terminates in the separate general visceral nucleus. In goldfish, the vagal lobe is a complex, laminated structure containing both motor and sensory elements.Transection of the vagus nerve results in distinct changes in the pattern of acetylcholinesterase staining and substance-P-like (SPL) immunoreactivity in the vagal lobe of goldfish. Following vagotomy, cholinesterase activity is eliminated from layers 4 and 6, both being layers in which primary gustatory afferent fibers terminate. In addition, SPL immunoreactive fibers disappear from the capsular root of the vagus nerve. These results indicate that the primary afferent input to the gustatory lobe involves at least two cytochemically distinct fiber types, one containing substance-P-immunoreactive material and the other containing or inducing acetylcholinesterase activity.Vagotomy also affects immunostaining and cholinesterase activity of the motonuerons deep in the vagal lobe. Following nerve transection, acetylcholinesterase activity is diminished, and SPL-immunoreactivity increased in the affected motoneurons. Similar changes were observed in axotomized motoneurons of other cranial nerve nuclei.     

Non-respiratory neurons in the B?tzinger complex exhibiting appropriate firing patterns to generate the emetic act in dogs.

This work was performed to prove the hypothesis that the pattern generator for the emetic act exists in the B?tzinger complex (BOT) and is driven by vagal afferents via the subpostrema portion of the nucleus of the solitary tract (mNST). Non-respiratory neurons (78) intermingling with BOT respiratory neurons in decerebrate dogs responded to pulse train stimulation of vagal afferents with a mean latency of 387 ms. During retching induced by vagal stimulation, one-half of the non-respiratory neurons exhibited high frequency burst firings synchronous with each retch (SH-firing, SH-neurons) and one-third of these neurons showed similar firings synchronous with the periods between retches (BH-firing, BH-neurons). Two-thirds of the SH-neurons and one-half of the BH-neurons fired with gradually augmenting frequencies (augmenting firing) during the period prior to retching, which may correspond to the period of prodromal signs of vomiting. Three SH-neurons were observed at fictive expulsion: all 3 exhibited burst firings concomitant with expulsion. During cooling block of transmission in the mNST, stimulation of the vagus nerve ipsilateral to the cooling failed to induce not only retching but also augmenting firing and SH-firing in all 11 BOT SH-neurons observed. In contrast, contralateral vagal stimulation induced retching and neuronal firings which had been observed before the cooling. These results support the hypothesis mentioned above. Respiratory firings were changed during retching in all BOT respiratory neurons observed. Respiratory firings were depressed during retching in the majority (15/25) of inspiratory (I) neurons and in a few expiratory (E) neurons (6/45). SH-firing was exhibited by 3 I- and 13 E-neurons. A few (2) I- and half (23) E-neurons showed BH-firing. These results indicate that all BOT respiratory neurons participate in central patterning of the emetic act.     

Synaptic interactions between respiratory neurons during inspiratory on-switching evoked by vagal stimulation in decerebrate cats

To elucidate neuronal mechanisms underlying phase-switching from expiration to inspiration, or inspiratory on-switching (IonS), postsynaptic potentials (PSPs) of bulbar respiratory neurons together with phrenic nerve discharges were recorded during IonS evoked by vagal stimulation in decerebrate and vagotomized cats. A single shock stimulation of the vagus nerve applied at late-expiration developed an inspiratory discharge in the phrenic neurogram after a latency of 79+/-11 ms (n = 11). Preceding this evoked inspiratory discharge, a triphasic response was induced, consisting of an early silence (phase 1 silence), a transient burst discharge (phase 2 discharge) and a late pause (phase 3 pause). During phase 1 silence, IPSPs occurred in augmenting inspiratory (aug-I) and expiratory (E2) neurons, and EPSPs in postinspiratory (PI) neurons. During phase 2 discharge, EPSPs arose in aug-I neurons and IPSPs in PI and E2 neurons. These initial biphasic PSPs were comparable with those during inspiratory off-switching evoked by the same stimulation applied at late-inspiration. In both on- and off-switching, phase-transition in respiratory neuronal activities started to arise concomitantly with the phrenic phase 3 pause. These results suggest that vagal inputs initially produce a non-specific, biphasic response in bulbar respiratory neurons, which consecutively activates a more specific process connected to IonS.     

The location and properties of preganglionic vagal cardiomotor neurones in the rabbit

The origins of preganglionic vagal neurones which slow the heart in the rabbit have been examined with standard neurophysiological stimulation and recording techniques. The activity of 216 neurones projecting to the right cervical vagus nerve have been recorded in localized areas of the brain stem. Thirty-six of these neurones were classified as cardiomotor neurones since they had properties similar to those described for such neurones in the cat. All had efferent axons in the range of B fibers. They could be synaptically activated by electrical stimulation of the ipsilateral aortic nerve which in the rabbit is solely barosensory. The majority of these neurones (70%) were spontaneously active and those which were normally silent could be made to fire by iontophoretic application ofdl-homocysteic acid (an excitant amino acid). This spontaneous, or evoked, activity showed evidence of a pulse rhythm (of baroreceptor origin) and respiratory modulation (firing predominantly during expiration). In response to application ofdl-homocysteic acid, the neuronal excitation was usually accompanied by a small but significant bradycardia. Histological examination showed that these neurones were located in both the dorsal vagal nucleus and the nucleus ambiguus.     

The role of the vagus nerves in the respiratory and circulatory responses to intravenous histamine and phenyl diguanide in rabbits

1. The responses of rabbits, anaesthetized with pentobarbitone sodium, to intravenous injections of histamine and phenyl diguanide have been studied. Total lung conductance, lung compliance, breathing frequency, tidal volume, end-tidal CO(2)%, systemic arterial and right atrial blood pressures and heart rate were measured. Some of the rabbits were first paralysed and artificially ventilated.2. The role of vagal afferent nerves was determined by observing the responses before and after bilateral vagotomy, and before and during cooling the vagus nerves to 8-10 degrees C; such cooling selectively blocks some vagal afferent pathways.3. Histamine decreased conductance (bronchoconstriction), in spontaneously breathing and in paralysed, artificially ventilated animals, and caused rapid shallow breathing. The responses were considerably reduced or abolished by vagal cooling and vagotomy and are thought to be mainly vagal reflexes due to stimulation by histamine of irritant receptors in the lungs.4. Phenyl diguanide also decreased conductance, in spontaneously breathing and in paralysed, artificially ventilated animals, and caused rapid shallow breathing. Vagotomy abolished the respiratory changes and considerably reduced the bronchoconstriction. Vagal cooling caused an equal reduction of the bronchoconstriction but an increase in minute volume persisted. This respiratory response to phenyl diguanide which persists during vagal cooling is thought to be due to stimulation of deflation receptors in the lungs; it was associated with vagal reflex hypotension and bradycardia.5. Both histamine and phenyl diguanide decreased lung compliance when vagal conduction was unimpaired. The effects were largely secondary to changes in the pattern of breathing, although histamine also had a weak direct action on lung tissue leading to a fall in compliance.6. Both histamine and phenyl diguanide decreased end-tidal CO(2)% and increased right atrial pressure by direct (non-vagal) actions on lung tissues. Histamine also caused a non-vagal hypertension.     

Vagal stimulation and somatostatin potentiate cardiac vagal action in the toad, Bufo marinus.

Cholinergic postganglionic neurones of the cardiac vagus in the toad, Bufo marinus, have been shown to contain the peptide somatostatin (SOM), which causes direct negative inotropic and chronotropic effects on the heart. In anaesthetised toads, high frequency stimulation (10 Hz) of cardiac vagus nerves results in prolonged cardiac slowing and potentiation of the cardiac slowing measured in response to a train of vagal stimuli at low frequency. Intravenous administration of the tetradecapeptide form of SOM also results in prolonged cardiac slowing and potentiation of cardiac vagal action. Effects on heart rate of small bolus doses of acetylcholine (ACh) were unaltered by administration of SOM, at the same time as cardiac vagal slowing was enhanced. It is suggested that SOM is released from vagal nerve endings by high frequency stimulation and enhances cardiac vagal action by a presynaptic mechanism.     

Proposal for the existence of a nasogastric reflex in humans, as a potential cause of upper gastrointestinal symptoms

The nose is a gateway of air from the environment to the body and with its rich innervation from the olfactory and trigeminal nerves plays a critical role as a sensor in both human beings and primitive animals. Irritation of the nasal or paranasal mucosa may initiate a severe bradycardia, apnea, and vasoconstriction and increase the pulmonary airflow resistance. However, the interaction between nasal mucosa and the upper gastrointestinal tract is more often than not neglected in the clinical literature. We propose that a nasogastric reflex might exist with its afferent and efferent loops being the trigeminal and vagus nerves, respectively. The central connection of these loops is located at the pontomedullary level. The sensory inputs from the nasal mucosa to the general somatic afferent component of the brainstem including the pontine and medullary trigeminal nucleuses may induce the neighboring nucleus of the solitary tract and dorsal motor nucleus of the vagus. This initiates, via the efferent fibers of the vagus nerve, the manifestations of the vagal stimulation. The presence of a nasogastric reflex may warrant considerations as diseases of nose and paranasal sinuses may be the cause upper gastrointestinal symptmatology.     

Vagal modulation of responses elicited by stimulation of the aortic depressor nerve in neurons of the rostral ventrolateral medulla oblongata in the rat.

Stimulation of cervical vagal afferents inhibits central sympathetic outflows in part by inhibiting the ongoing activity of putative baroreceptive neurons in the rostral ventrolateral medulla oblongata. The aim of the present study was to examine the electrophysiological characteristics of vagal responses and their interactions with responses elicited by stimulation of the aortic nerve in neurons there. The study focused on the role of the long-lasting, late-onset vagal inhibition, which is likely to play an important role in the tonic inhibitory effects of vagal afferent stimulation. In vivo intracellular recordings were obtained from 33 neurons that received convergent inputs from aortic and vagal afferents. Sixty-four percent of these neurons exhibited a late inhibition following electrical stimulation of myelinated vagal afferents (mean onset latency of 100+/-5 ms). The average duration of late inhibition (294+/-19 ms) exceeded the duration of the cardiac cycle. As a consequence of this, sustained vagal stimulation diminished the effect of rhythmic baroreceptor inputs in neurons that exhibited late vagal inhibition. Simultaneous activation of aortic and vagal afferents significantly increased the magnitude of late inhibition, even in those neurons where stimulation of the aortic nerve alone did not elicit a response (n = 15). This suggested that the convergence between vagal and aortic afferent inputs occurred in inhibitory inteneurons antecedent to the recorded rostral ventrolateral medulla oblongata neurons. Focal stimulation of the caudal part of the nucleus of the solitary tract also elicited a late-onset inhibition in 73% of the neurons that responded to stimulation of the aortic nerve. This inhibition appeared to be similar to the late vagal inhibition, except for its shorter average onset latency (64+/-7 ms). Based on this observation, it is proposed that inhibitory inteneurons that mediate late inhibition to rostral ventrolateral medulla oblongata neurons may lie within the caudal part of the nucleus of the solitary tract. The present study established that activation of myelinated vagal afferents exerts a complex modulation over the ongoing and evoked activity of neurons that respond to stimulation of the aortic nerve. The complex interaction that occurs between aortic and vagal inputs in neurons of the rostral ventrolateral medulla may be implicated in long-term modulation of sympathetic outflows in response to changes in the activation of visceral receptors supplied by vagus afferents. The modulation elicited by late vagal inhibition may help to adjust cardiovascular outflows according to requirements set by the thoraco-abdominal visceral environment.     

The activity of lung irritant receptors during pneumothorax, hyperpnoea and pulmonary vascular congestion

1. The activity of lung irritant receptors during pneumothorax, hyperpnoea and pulmonary congestion has been studied by recording from single vagal nerve fibres from the receptors in rabbits.2. The receptors were stimulated during induction and during removal of pneumothorax.3. Pneumothorax caused a greater depression of minute volume in bilaterally vagotomized rabbits, compared with those with intact vagus nerves.4. Hyperpnoea due to breathing through an added dead space increased the discharge of the receptors. Experiments on paralysed and artificially ventilated rabbits showed that this was not a direct action of the asphyxial changes in blood gas tensions.5. Pulmonary congestion, induced by inflating a balloon in the left atrium, stimulated the receptors in paralysed artificially ventilated rabbits.6. The evidence that the receptors cause vagal reflex hyperpnoea and bronchoconstriction is discussed, together with their role in the reflex ventilatory and bronchomotor changes in the conditions studied.     

Uncoupling of rhythmic hypoglossal from phrenic activity in the rat

During eupnoea, rhythmic motor activities of the hypoglossal, vagal and phrenic nerves are linked temporally. The inspiratory discharges of the hypoglossal and vagus motor neurones commence before the onset of the phrenic burst. The vagus nerve also discharges in expiration. Upon exposure to hypocapnia or hypothermia, the hypoglossal discharge became uncoupled from that of the phrenic nerve. This uncoupling was evidenced by variable times of onset of hypoglossal discharge before or after the onset of phrenic discharge, extra bursts of hypoglossal activity in neural expiration, or complete absence of any hypoglossal discharge during a respiratory cycle. No such changes were found for vagal discharge, which remained linked to the phrenic bursts. Intracellular recordings in the hypoglossal nucleus revealed that all changes in hypoglossal discharge were due to neuronal depolarization. These results add support to the conclusion that the brainstem control of respiratory-modulated hypoglossal activity differs from control of phrenic and vagal activity. These findings have implications for any studies in which activity of the hypoglossal nerve is used as the sole index of neural inspiration. Indeed, our results establish that hypoglossal discharge alone is an equivocal index of the pattern of overall ventilatory activity and that this is accentuated by hypercapnia and hypothermia.     

Pulmonary C-fibers do not play a role in ammonia-induced brief tachypnea in the rabbit.

To determine the role of pulmonary C-fibers in evoking a brief tachypnea induced by ammonia vapor, we examined the responses of diaphragm electromyogram (DIAP EMG) to ammonia inhalation before and after procaine treatment to the contralateral vagus nerve in urethane-anesthetized, spontaneously breathing rabbits with unilateral vagotomy. Procaine treatment that blocked the conduction of vagal afferent C wave did not significantly alter the response of brief tachypnea to ammonia. Furthermore, the stimulation of pulmonary C-fibers by ammonia inhalation did not coincide with the induction of brief tachypnea. In addition, we also examined the responses of rapidly adapting receptors (RARs) and slowly adapting receptors (SARs) to ammonia inhalation in rabbits, particularly in which inhalation of this chemical gas produced a brief tachypnea. The burst activity of RARs evoked by ammonia inhalation coincided with the phase of rapid shallow breathing for a few breaths. The discharge rates of SARs during both inspiration and expiration increased when ammonia inhalation caused a brief tachypnea. From these results, it can be suggested that the ammonia-induced brief tachypnea is probably mediated by transient stimulation of both SAR and RAR activities but does not occur as a result of the pulmonary C-fiber stimulation.     

Gastric afferents to the paraventricular nucleus in the rat

Summary Extracellular recordings were made from vasopressin (AVP) and oxytocin (OXT)-secreting cells in the paraventricular nucleus (PVN) of the hypothalamus in rats anesthetized with urethane-chloralose to determine the effects of electrical stimulation of vagal gastric nerves and gastric distension on their activity. Electrical stimulation of gastric branches of the vagus nerves inhibited 5 and excited 10 of 32 phasically firing neurosecretory cells. Approximately one third of the phasically firing neuro-secretory cells (9 out of 29 cells) were transiently inhibited by gastric distension; an effect which was completely abolished by bilateral cervical vagotomy. In contrast, gastric nerve stimulation excited 45 of 72 non-phasically firing paraventricular cells. Thirteen of 77 non-phasically firing cells tested were excited by gastric distension. We conclude that there are some sensory afferent inputs originating from gastric receptors and transmitted by gastric vagal afferents which inhibit the activity of AVP- secreting neurons in the PVN although other inputs excite the cells. Similar inputs also excite some of the putative OXT-secreting neurons in the PVN.