Chemoreflexes in Breathing

Dejours, P

doi:10.1152/physrev.1962.42.3.335

Cited by 326 publications

(183 citation statements)

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“…In normal newborn rodents, hyperoxia depresses ventilation, presumably by decreasing activity in the peripheral chemoreceptors (Hertzberg et al, 1990). Moreover, the magnitude of the hyperoxia-induced ventilatory depression provides a measure of chemoafferent drive (Dejours, 1962;Hertzberg et al, 1990). As expected, hyperoxia decreased V E on postnatal day 2.5 in bdnf ϩ/ϩ mice by 30% during periods of quiet uninterrupted breathing, indicating the presence of a significant chemoafferent drive to ventilation in normal animals.…”

Section: Bdnf-deficient Mice Exhibit Severe Developmental Deficits Insupporting

confidence: 56%

“…A large proportion of these cells innervate the carotid body (Katz et al, 1983;Katz and Black, 1986;Finley et al, 1992), a chemoreceptor organ that provides tonic excitatory drive to ventilation (Dejours, 1962) and the primary site at which hypoxemia triggers homeostatic cardiorespiratory reflexes (Heymans and Heymans, 1927;Heymans and Bouckaert, 1930). We therefore hypothesized that loss of these cells would result in abnormal breathing, possibly contributing to the lethality associated with loss of BDNF or TrkB.…”

Section: Bdnf-deficient Mice Exhibit Severe Developmental Deficits Inmentioning

confidence: 99%

“…Input from the peripheral chemoreceptors provides a tonic excitatory drive to breathing, allowing continuous reflex adjustments to changes in arterial oxygen tension (Dejours, 1962). We hypothesized, therefore, that loss of this input might account for the reduced and irregular ventilation of bdnf Ϫ/Ϫ mice.…”

Section: Bdnf-deficient Mice Exhibit Severe Developmental Deficits Inmentioning

confidence: 99%

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Mice Lacking Brain-Derived Neurotrophic Factor Exhibit Visceral Sensory Neuron Losses Distinct from Mice Lacking NT4 and Display a Severe Developmental Deficit in Control of Breathing

Erickson

Conover

Borday³

et al. 1996

J. Neurosci.

277

243

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The neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT4) act via the TrkB receptor and support survival of primary somatic and visceral sensory neurons. The major visceral sensory population, the nodose-petrosal ganglion complex (NPG), requires BDNF and NT4 for survival of a full complement of neurons, providing a unique opportunity to compare gene dosage effects between the two TrkB ligands and to explore the possibility that one ligand can compensate for loss of the other. Analysis of newborn transgenic mice lacking BDNF or NT4, or BDNF and NT4, revealed that survival of many NPG afferents is proportional to the number of functional BDNF alleles, whereas only one functional NT4 allele is required to support survival of all NT4-dependent neurons. In addition, subpopulation analysis revealed that BDNF and NT4 can compensate for the loss of the other to support a subset of dopaminergic ganglion cells. Together, these data demonstrate that the pattern of neuronal dependencies on BDNF and NT4 in vivo is far more heterogeneous than predicted from previous studies in culture. Moreover, BDNF knockout animals lack a subset of afferents involved in ventilatory control and exhibit severe respiratory abnormalities characterized by depressed and irregular breathing and reduced chemosensory drive. BDNF is therefore required for expression of normal respiratory behavior in newborn animals.

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Section: Bdnf-deficient Mice Exhibit Severe Developmental Deficits Insupporting

confidence: 56%

Section: Bdnf-deficient Mice Exhibit Severe Developmental Deficits Inmentioning

confidence: 99%

Section: Bdnf-deficient Mice Exhibit Severe Developmental Deficits Inmentioning

confidence: 99%

See 1 more Smart Citation

Mice Lacking Brain-Derived Neurotrophic Factor Exhibit Visceral Sensory Neuron Losses Distinct from Mice Lacking NT4 and Display a Severe Developmental Deficit in Control of Breathing

Erickson

Conover

Borday³

et al. 1996

J. Neurosci.

277

243

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“…The magnitude of the transient ventilatory decline in response to a brief hyperoxic exposure is used as an index of peripheral chemoreceptor, especially carotid body, sensitivity (11). Respiratory rate and phrenic nerve activity were monitored on anesthetized mice for 5 min under normoxic conditions and then for 20 sec after a hyperoxic challenge.…”

Section: Resultsmentioning

confidence: 99%

Defective carotid body function and impaired ventilatory responses to chronic hypoxia in mice partially deficient for hypoxia-inducible factor 1α

Kline

Peng

Manalo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

238

216

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To investigate whether the transcriptional activator hypoxiainducible factor 1 (HIF-1) is required for ventilatory responses to hypoxia, we analyzed mice that were either wild type or heterozygous for a loss-of-function (knockout) allele at the Hif1a locus, which encodes the O 2-regulated HIF-1␣ subunit. Although the ventilatory response to acute hypoxia was not impaired in Hif1a ϩ/Ϫ mice, the response was primarily mediated via vagal afferents, whereas in wild-type mice, carotid body chemoreceptors played a predominant role. When carotid bodies isolated from wild-type mice were exposed to either cyanide or hypoxia, a marked increase in sinus nerve activity was recorded, whereas carotid bodies from Hif1a ϩ/Ϫ mice responded to cyanide but not to hypoxia. Histologic analysis revealed no abnormalities of carotid body morphology in Hif1a ϩ/Ϫ mice. Wild-type mice exposed to hypoxia for 3 days manifested an augmented ventilatory response to a subsequent acute hypoxic challenge. In contrast, prior chronic hypoxia resulted in a diminished ventilatory response to acute hypoxia in Hif1a ϩ/Ϫ mice. Thus partial HIF-1␣ deficiency has a dramatic effect on carotid body neural activity and ventilatory adaptation to chronic hypoxia.O xygen homeostasis is mediated by the combined physiologic functioning of the circulatory and respiratory systems. Recent studies have demonstrated that the transcriptional activator hypoxia-inducible factor 1 (HIF-1) is required for both the establishment of the circulatory system during embryonic development and physiologic responses in postnatal life. Analysis of Hif1a Ϫ/Ϫ knockout mice, which are homozygous for a lossof-function mutation in the Hif1a gene encoding the O 2 -regulated HIF-1␣ subunit, revealed that complete HIF-1␣ deficiency results in embryonic lethality at midgestation with major malformations of the heart and vasculature (1-3). Hif1a ϩ/Ϫ heterozygous mice, which are partially HIF-1␣ deficient, develop normally and are indistinguishable from their wild-type littermates under normoxic conditions. However, adult Hif1a ϩ/Ϫ mice manifest impaired physiological responses to chronic hypoxia including significantly reduced rates of erythropoiesis and pulmonary vascular remodeling (4). Thus HIF-1␣ plays essential roles in cardiac, erythroid, and vascular development and physiology, i.e., all three major components of the circulatory system.An essential adaptation to both acute and chronic hypoxia is an increase in ventilation that depends on the activity of peripheral chemoreceptors, particularly those within the carotid body, which detect changes in arterial blood O 2 concentration and relay sensory information to the brainstem neurons that regulate breathing (reviewed in ref. 5). Altered ventilatory responses to hypoxia may play a critical role in asthma, diabetes, Parkinson's disease, sleep-related breathing disorders, and sudden infant death syndrome (6-8). We hypothesized that HIF-1␣ is required for carotid body function and ventilatory adaptation to chronic hypoxia. To test this hyp...

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“…To extend a somewhat unattractive jargon, C and D could be described as 'position parameters' since they define the asymptotes of the hyperbola. Rebuck & Campbell (1974) Single breath tests A single tidal breath of nitrogen in man produces transient hypoxia and a brief increase in ventilation (Dejours, 1962). A single vital capacity breath of 15% CO2 also gives a small transient response (Gabel, Kronenberg & Severinghaus, 1973).…”

Section: Inputs To the Respiratory Centrementioning

confidence: 99%

Methods in the assessment of the control of breathing.

Sauders

1980

Brit J Clinical Pharma

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Chemoreflexes in Breathing

Cited by 326 publications

References 0 publications

Mice Lacking Brain-Derived Neurotrophic Factor Exhibit Visceral Sensory Neuron Losses Distinct from Mice Lacking NT4 and Display a Severe Developmental Deficit in Control of Breathing

Mice Lacking Brain-Derived Neurotrophic Factor Exhibit Visceral Sensory Neuron Losses Distinct from Mice Lacking NT4 and Display a Severe Developmental Deficit in Control of Breathing

Defective carotid body function and impaired ventilatory responses to chronic hypoxia in mice partially deficient for hypoxia-inducible factor 1α

Methods in the assessment of the control of breathing.

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