Inspiratory-expiratory Neurons Research Articles

Most inspiratory neurons in the pre-Bötzinger complex are suppressed during vomiting in dogs

Pulmonary ventilation is almost completely suppressed during actual retching. Correspondingly, respiratory activity either disappears or changes to retching activity in peripheral respiratory nerves and respiratory neurons of the Bötzinger complex and the caudal part of the ventral respiratory group. These results suggest the possibility that the respiratory rhythm generator is suppressed during retching. Recently, the pre-Bötzinger complex (pre-BÖT) has been postulated to generate respiratory rhythm. To evaluate this possibility, the activities of pre-BÖT neurons were observed during fictive retching and exoulsion in decerebrate paralyzed dogs. Inspiratory (I) neurons in the pre-BÖT consisted of pre-, early-, late-, post- and throughout-subtypes, as in cats and rats. Inspiratory firing almost completely disappeared during fictive retching in about 70% of the 158 pre-BÖT I neurons examined, and changed to weak bursts produced either with retches or between retches in most of the remaining 30%. Similarly, all but one of the 21 I neurons examined did not produce any discharge with fictive expulsion. In contrast, all of the pre-BÖT expiratory and inspiratory-expiratory neurons examined produced vigorous bursts either with retches or between retches, and with expulsion. These results suggest that inspiratory outputs from the respiratory rhythm generator are almost completely suppressed during retching and expulsion, and that expiratory outputs change to retching and expulsion activities.

Cholinergic effects on spike-density and burst-duration of medullary respiration-related neurones in the rabbit: An iontophoretic study

Cholinoceptive properties of 180 medullary respiration-related neurones (RRN) were studied in urethane-anaesthetized rabbits. Acetylcholine (ACh) and agonists, as well as antagonists of muscarinic receptors and nicotinic receptors, were administered iontophoretically. Respiration-related neurones were classified with respect to the correlation of their activity with the activity of the phrenic nerve: phase-bound inspiratory (I) and expiratory (E) neurones and phase-spanning expiratory-inspiratory and inspiratory-expiratory neurones were discriminated. Acetylcholine altered the activity of 170 respiration-related neurones. In 49 cells the discharge-rate (ƒ) alone was affected. In 44 respiration-related neurones the burst-duration ( t, bd) only was altered. In 77 respiration-related neurones the discharge rate and burst duration were affected simultaneously. Inhibitory actions of ACh prevailed over excitatory actions on inspiratory neurones. In expiratory neurones the discharge rate was increased or decreased in about the same number of cases. In most phase-spanning neurones the discharge rate was increased. Cholinergic inhibition of burst duration was observed in most respiration-related neurones. In all phase-types of respiration-related neurones muscarinic as well as nicotinic actions of ACh were demonstrated. In inspiratory and expiratory-inspiratory neurones muscarinic effects on the discharge rate prevailed over nicotinic effects. More nicotinic than muscarinic effects on discharge rate were observed in expiratory and inspiratory-expiratory neurones. Cholinergic effects on burst duration in about the same number of respiration-related neurones were mediated by muscarinic or by nicotinic receptors, respectively. Various types of cholinoceptors may be involved in these effects. The results suggest that Cholinergic mechanisms play an important role in the control of the central regulation of respiratory movements. The functional significance of Cholinergic effects on respiration-related neurones is discussed with special emphasis of effects on burst duration.

Discharge patterns of bulbar respiratory neurons in response to the morphinomimetic agent, fentanyl, in chloralosed dogs

In anaesthetized, paralysed and artificially ventilated dogs, activities were recorded from the phrenic nerve and from respiratory units within the nucleus tractus solitarii (nTS), the nucleus ambiguus (nA) and the nucleus retroambigualis (nRA). The respiratory neurons were classified according to their discharge pattern and their response to lung inflation. Fentanyl injected into the vertebral artery (0.5–2 μg/kg) or intravenously (10 μg/kg) produced a depressant effect on the phrenic nerve motoneurons, on inspiratory cells (Iα and Iβ) and on phase-spanning expiratory-inspiratory neurons of the nTS and the nA. The duration of the inspiratory burst increased and the number of spikes and the peak activity were reduced. This pattern of inhibition was followed by complete blockade of spike genesis. Fentanyl also altered expiratory neurons: the duration of the expiratory discharge was enhanced. An increase followed by a decrease in the number of spikes per burst and a reduction in the peak acticity were observed. When the phrenic nerve was silent, continuous discharges appeared. High doses of fentanyl were needed to inhibit these tonic discharges. This pattern of inhibition concerns late peak expiratory units, expiratory units with a constant discharge pattern and the phase-spanning inspiratory-expiratory neurons. Naloxone antagonized these effects but induced the appearance of tonic discharges in fentanyl-treated phase-spanning expiratory-inspiratory neurons. Stimulation of peripheral chemoreceptors with almitrine (0.2 mg/kg i.v.) antagonized the effects of fentanyl. In addition, fentanyl facilitated the lung inflation reflex on respiratory neurons. In conclusion, fentanyl induces respiratory depression through a preferential effect on inspiratory neurons and alters the active inhibitory phase-switching mechanisms maintaining the expiratory periodicity. These experiments support the concept of an inhibitory influence of inspiratory neurons on expiratory cells and also support the idea that respiratory periodicity arises on a background of tonic activity for both inspiratory and expiratory neurons.

Effects of pentylenetetrazol on respiration and bulbar respiratory neurones and its interaction with K + ions and citrate

Interactions between pentylenetetrazol (PTZ) and the metabolic modifier citrate and also with K + ions were examined. When superfused onto the bulb, at low concentrations PTZ increased tidal volume and slowed down respiration; the opposite was true for higher concentrations. Addition of citrate or K + ions did not essentially alter PTZ effects. Applied microelectrophoretically, PTZ influenced the spike density of three-quarters, and K + ions and citrate of two-thirds of all cells tested. When effective, PTZ excited the majority of the inspiratory (I) and inspiratory-expiratory neurones (IE), both excited and inhibited expiratory units (E) and inhibited the majority of the non-respiratory neurones. Citrate inhibited the majority of IE and E neurones; when combined with PTZ, effects of PTZ were abolished in most respiratory but not in unspecific cells. K + ions predominantly excited IE and E units. When combined with PTZ, inhibition exerted by PTZ on unspecific neurones was reversed into activation. This was not true for respiratory cells. Since activation of respiratory cells mediated by PTZ was neutralized by the metabolic inhibitor citrate and was mimicked by K + ions, PTZ may well act as modifier of the oxidative metabolism of glucose and of the passive efflux of K + ions.

The bulbar respiratory centre in the rabbit. II. Responses of respiratory neurons to intermittent electrical bulbar stimulation during in- or expiration.

In anesthetized rabbits, spirogram and diaphragmatic activity were examined during electrical stimulation of the bulbar lateral reticular formation. The activity of bulbar respiratory neurons was recorded contra- or ipsilaterally to the stimulation site. One volley of repetitive stimuli per breath was delivered during either inspiration of expiration. 1. Each volley of about 120 ms duration at 100 pulses per second, delivered early in inspiration, caused an immediate and transient inhibition of the diaphragmatic activity. An inspiratory rebound comprising lengthening of inspiration and increase in tidal volume occurred. a) "Inspiratory" and "expiratory-inspiratory" phase-spanning neurons exhibited inhibition during the volley. The burst discharge was lengthened and the spike density increased after stimulus. The same was true of some "inspiratory-expiratory" phase-spanning units. b) The discharge of most of the "inspiratory-expiratory neurons was not inhibited. "Expiratory" units were excited. In both types of cells activation occurred which outlasted the volley. 2. When applied during expiration, the volley caused a short inspiratory twitch. a) "Inspiratory" and "expiratory-inspiratory" neurons exhibited a short post-stimulus firing and the spike density was increased. In some units of the latter type, however, the burst discharge was shortened. b) Most of the "expiratory" and "inspiratory-expiratory" neurons were not inhibited by the volley. Cells of the former type often produced post-stimulus after-discharge; the burst discharge of units belonging to the latter type was shortened. The effects of expiratory stimuli upon neuronal activity, however, were less consistent than those elicited by inspiratory volleys. 3. During spontaneous irregularities of single inspirations (short interruptions), EI and I neurons exhibited comparable burst pattern changes. The changes in pattern of IE and E units were also comparable and differed distinctly from the behaviour of the EI and I cells. No major differences in behaviour were observed between neurons which were inhibited during lung inflation (alpha units) and those which were activated during inflation (beta cells). The findings are in accord with the effects observed during electrical bulbar stimulation, suggesting that EI and I units are inspiratory-activating cells, whereas IE and E neurons may have an inspiratory-inhibitory function. 4. The conclusion is drawn that the effects of bulbar stimulation on the respiratory movements are the result of manipulation on intrinsic rhythmogenesis.