Neurophysiological investigations of medullary chemosensitive areas of respiration

Lipscomb, William T.; Boyarsky, L. L.

doi:10.1016/0034-5687(72)90065-5

Cited by 55 publications

(8 citation statements)

References 23 publications

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“…Later experiments in rats confirmed that respiratory stimulation could also be produced by superfusing CO 2 enriched solution on the ventral but not dorsal surface of the medulla oblongata (176). These methods had limited anatomical resolution and the interpretation of the results, namely, that chemoreceptors were confined to the ventral medullary surface, was quickly criticized because the pled-gets could have acidified deeper medullary structures which receive their blood supply from the ventral surface via penetrating arterioles and subsequent investigators were unable to find CO 2 -activated units within the superficial regions out-lined by Mitchell and collaborators (247). Other putatively chemosensitive superficial regions of the medulla oblongata were described by Loeschke and Schlaefke (368); the most frequently mentioned is located between the pyramidal tract and the rootlets of the hypoglossal nerve [(368) and references therein].…”

Section: The Retrotrapezoid Nucleusmentioning

confidence: 99%

Regulation of Breathing and Autonomic Outflows by Chemoreceptors

Guyenet

2014

Comprehensive Physiology

276

293

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Lung ventilation fluctuates widely with behavior but arterial PCO2 remains stable. Under normal conditions, the chemoreflexes contribute to PaCO2 stability by producing small corrective cardiorespiratory adjustments mediated by lower brainstem circuits. Carotid body (CB) information reaches the respiratory pattern generator (RPG) via nucleus solitarius (NTS) glutamatergic neurons which also target rostral ventrolateral medulla (RVLM) presympathetic neurons thereby raising sympathetic nerve activity (SNA). Chemoreceptors also regulate presympathetic neurons and cardiovagal preganglionic neurons indirectly via inputs from the RPG. Secondary effects of chemoreceptors on the autonomic outflows result from changes in lung stretch afferent and baroreceptor activity. Central respiratory chemosensitivity is caused by direct effects of acid on neurons and indirect effects of CO2 via astrocytes. Central respiratory chemoreceptors are not definitively identified but the retrotrapezoid nucleus (RTN) is a particularly strong candidate. The absence of RTN likely causes severe central apneas in congenital central hypoventilation syndrome. Like other stressors, intense chemosensory stimuli produce arousal and activate circuits that are wake- or attention-promoting. Such pathways (e.g., locus coeruleus, raphe, and orexin system) modulate the chemoreflexes in a state-dependent manner and their activation by strong chemosensory stimuli intensifies these reflexes. In essential hypertension, obstructive sleep apnea and congestive heart failure, chronically elevated CB afferent activity contributes to raising SNA but breathing is unchanged or becomes periodic (severe CHF). Extreme CNS hypoxia produces a stereotyped cardiorespiratory response (gasping, increased SNA). The effects of these various pathologies on brainstem cardiorespiratory networks are discussed, special consideration being given to the interactions between central and peripheral chemoreflexes.

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Section: The Retrotrapezoid Nucleusmentioning

confidence: 99%

Regulation of Breathing and Autonomic Outflows by Chemoreceptors

Guyenet

2014

Comprehensive Physiology

276

293

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“…Mitchell & Herbert themselves (1974b) showed that postsymaptic inhibition was present in the expiratory cells during inspiration. Whether centrally mediated excitation by C02 is direct or not must, then, be decided on the basis of other evidence (Mitchell, Loeschke, Severinghaus, Richardson & Massion, 1963;Pappenheimer, Fencl, Heisey & Held, 1965;Loeschcke, Lattre, Schlafke & Trouth, 1970;Lipscomb & Boyarsky, 1972).…”

Section: Medullary Neurone Responsesmentioning

confidence: 99%

The effect of carbon dioxide on the tonic and the rhythmic discharges of expiratory bulbospinal neurones.

Bainton¹,

Kirkwood²

1979

The Journal of Physiology

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SUMMARY1. Extracellular micro-electrodes were used to measure the responses of expiratory bulbospinal neurones to C02 in anaesthetized, paralyzed cats, ventilated with 02. Simultaneous measurements were made of phrenic nerve and intercostal nerve filament discharges.2. Hypocapnia produced tonic activity in some of the expiratory neurones and in expiratory filaments but rendered the phrenic and inspiratory filaments silent.3. A graded excitatory effect of C02 on tonic activity of both the neurones and the filaments was seen which progressed smoothly and continuously to rhythmic activity as C02 was increased and to zero as C02 was decreased.4. Increases in blood pressure produced effects which were opposite to those produced by C02, and which had a faster time course.5. The C02 response curves of those units showing tonic activity were indistinguishable from the C02 response curves of those which did not. 6. A mid line lesion in the medulla interrupted inspiratory activity, converting activity of expiratory bulbospinal neurones from periodic to tonic firing patterns.7. Following such lesions the C02 threshold for rhythmic excitation of medullary neurones was elevated and the slopes of their C02 response curves were reduced.8. These findings fully confirm the hypothesis put forward by Bainton, Kirkwood & Sears (1978b) that bulbospinal respiratory neurones convey both tonic and rhythmic excitation to spinal respiratory motoneurones and that the rhythmic excitation of expiratory muscles derives from a periodic inhibition of expiratory bulbospinal neurones which are subjected to a tonic C02 dependent excitation which is continuously variable over the physiological range.

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“…Although temperature sensitivity has been consistently noted, surface temperature has not been monitored, even though all the techniques for applying changes of Pco2 and pH involve attendant risks of temperature change. In addition, it has been proposed by others with negative findings that respiratory responses attributed to changes of pH at the medullary surface may actually be due to effects on the surface blood vessels and consequent changes in blood supply to deeper structures (Lipscomb & Boyarsky, 1972;Cragg et al 1977) or by an effect of anaesthesia on respiratory control (Cozine & Ngai, 1967), since the local application of procaine produced only 30 % reduction of ventilation in unanaesthetized, decerebrate animals but total apnoea in the anaesthetized preparation.…”

Section: Discussionmentioning

confidence: 99%

The respiratory role of the ventral surface of the medulla studied in the anaesthetized rat.

Malcolm¹,

Sarelius²,

Sinclair³

1980

The Journal of Physiology

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SUMMARY1. The respiratory role of the ventral surface of the medulla was studied in rats anaesthetized with a urethane-chloralose mixture.2. In fifty-eight studies on twelve animals, direct superfusion of the medullary surface with artificial c.s.f. made acid by the reduction of bicarbonate content or by the increase of P003 produced no significant stimulation of respiration provided that the temperature of the brain surface was unaltered.3. Superperfusion of the medullary surface with c.s.f. of low bicarbonate content produced an inhibition of respiration in fourteen of thirty-eight experiments.4. Electrical stimulation on the surface revealed a localized area lateral to the pyramids and rostral to the XIIth nerve where stimulation at low intensity produced an increase in the frequency and depth of respiration.5. The application of carbachol to a similar region increased both the frequency and amplitude of ventilation at lower concentrations than were required to obtain effects from surrounding areas.6. Sudden switching between perfusates at different temperatures produced changes of ventilation within 1-2 see of a change of surface temperature. The Q10 for the ventilation/temperature relationship was approximately 6. 7. The experiments confirm that the ventral surface of the medulla contains neural elements which, at least during urethane-chloralose anaesthesia, have a significant effect on respiration. The stimulus for these effects in the rat does not appear to be a change in H+ concentration. It appears more probable that the primary role of the area lies in the link between thermal and respiratory regulation.

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Neurophysiological investigations of medullary chemosensitive areas of respiration

Cited by 55 publications

References 23 publications

Regulation of Breathing and Autonomic Outflows by Chemoreceptors

Regulation of Breathing and Autonomic Outflows by Chemoreceptors

The effect of carbon dioxide on the tonic and the rhythmic discharges of expiratory bulbospinal neurones.

The respiratory role of the ventral surface of the medulla studied in the anaesthetized rat.

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