Important role of carotid chemoreceptor afferents in control of breathing of adult and neonatal mammals

Forster, H. V.; Pan, Lawrence; Lowry, T. F.; Serra, Alexandre; Wenninger, Julie; Martino, Paul

doi:10.1016/s0034-5687(99)00115-2

Cited by 64 publications

(64 citation statements)

References 34 publications

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“…Second, why are the CBs unable to compensate for the lack of central CO 2 sensitivity, despite the fact that they contribute a still debated, but probably substantial fraction to the overall CO 2 response (Forster et al, 2000;Blain et al, 2009)? One possibility is that in the newborn period, the CBs still respond poorly to CO 2 /pH while the response to hypoxia is already well developed, although in the rat, there is evidence for a well developed peripheral CO 2 chemosensitivity at birth (Saetta and Mortola, 1987).…”

Section: Discussionmentioning

confidence: 99%

“…Cells that sense CO 2 (PCO 2 ) and O 2 (PO 2 ) partial pressure in the blood and interstitial fluid provide excitatory input to the respiratory rhythm generator (RRG) (Nattie, 1999). Elevated PCO 2 , through the attendant decrease in pH, is thought to be sensed principally by chemosensors in the brain while the carotid bodies (CBs) in the periphery are the main sensors of PO 2 and provide a substantial fraction of the CO 2 response in some species (Forster et al, 2000). In man, dysfunction of respiratory control is seen in a variety of genetic diseases.…”

Section: Introductionmentioning

confidence: 99%

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Breathing without CO₂Chemosensitivity in ConditionalPhox2bMutants

Ramanantsoa¹,

Hirsch²,

et al. 2011

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Breathing is a spontaneous, rhythmic motor behavior critical for maintaining O 2 , CO 2 , and pH homeostasis. In mammals, it is generated by a neuronal network in the lower brainstem, the respiratory rhythm generator (Feldman et al., 2003). A century-old tenet in respiratory physiology posits that the respiratory chemoreflex, the stimulation of breathing by an increase in partial pressure of CO 2 in the blood, is indispensable for rhythmic breathing. Here we have revisited this postulate with the help of mouse genetics. We have engineered a conditional mouse mutant in which the toxic PHOX2B 27Ala mutation that causes congenital central hypoventilation syndrome in man is targeted to the retrotrapezoid nucleus, a site essential for central chemosensitivity. The mutants lack a retrotrapezoid nucleus and their breathing is not stimulated by elevated CO 2 at least up to postnatal day 9 and they barely respond as juveniles, but nevertheless survive, breathe normally beyond the first days after birth, and maintain blood PCO 2 within the normal range. Input from peripheral chemoreceptors that sense PO 2 in the blood appears to compensate for the missing CO 2 response since silencing them by high O 2 abolishes rhythmic breathing. CO 2 chemosensitivity partially recovered in adulthood. Hence, during the early life of rodents, the excitatory input normally afforded by elevated CO 2 is dispensable for life-sustaining breathing and maintaining CO 2 homeostasis in the blood.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Breathing without CO₂Chemosensitivity in ConditionalPhox2bMutants

Ramanantsoa¹,

Hirsch²,

et al. 2011

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“…In cats (88) and rats (11,60,82), there is considerable recovery in the chemoreflex a few weeks after CBD and near total recovery a year later. In dogs (80), ponies (8,9), and goats (31,75), there is no significant or only a small recovery a few weeks after CBD, and in ponies there is less than 25% recovery 4 yr after CBD (Fig. 1).…”

Section: Denervation Of Peripheral Chemoreceptorsmentioning

confidence: 99%

“…Data from piglets suggest that this plasticity is due to resumption of function present at birth but lost during the neonatal period (31,57). In carotid-intact piglets, NaCN injected into the proximal descending aorta stimulates breathing until they are ϳ8 days old.…”

Section: Denervation Of Peripheral Chemoreceptorsmentioning

confidence: 99%

Invited Review: Plasticity in the control of breathing following sensory denervation

Forster

2003

Journal of Applied Physiology

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Forster, H. V. Invited Review: Plasticity in the control of breathing following sensory denervation. J Appl Physiol 94: 784-794, 2003; 10.1152/japplphysiol.00602.2002.-The purpose of this manuscript is to review the results of studies on the recovery or plasticity following a denervation-or lesion-induced change in breathing. Carotid body denervation (CBD), lung denervation (LD), cervical (CDR) and thoracic (TDR) dorsal rhizotomy, dorsal spinal column lesions, and lesions at pontine, medullary, and spinal sites all chronically alter breathing. The plasticity after these is highly variable, ranging from near complete recovery of the peripheral chemoreflex in rats after CBD to minimal recovery of the Hering-Breuer inflation reflex in ponies after LD. The degree of plasticity varies among the different functions of each pathway, and plasticity varies with the age of the animal when the lesion was made. In addition, plasticity after some lesions varies between species, and plasticity is greater in the awake than in the anesthetized state. Reinnervation is not a common mechanism of plasticity. There is evidence supporting two mechanisms of plasticity. One is through upregulation of an alternate sensory pathway, such as serotonin-mediated aortic chemoreception after CBD. The second is through upregulation on the efferent limb of a reflex, such as serotonin-mediated increased responsiveness of phrenic motoneurons after CDR, TDR, and spinal cord injury. Accordingly, numerous components of the ventilatory control system exhibit plasticity after denervation or lesion-induced changes in breathing; this plasticity is uniform neither in magnitude nor in underlying mechanisms. A major need in future research is to determine whether "reorganization" within the central nervous system contributes to plasticity following lesion-induced changes in breathing.receptors; recovery of function; redundancy; chemoreflexes; mechanoreflexes DENERVATION OR LESIONING OF a receptor or neural pathway that normally contributes to the regulation of a physiological function will result in loss of or altered function. Thereafter, a time-dependent recovery of function is a manifestation of plasticity within the regulatory system. The purpose of this review is to summarize research on this type of plasticity within the system regulating breathing. Lesions are one of several means of inducing plasticity; a review of these and a general discussion of plasticity are presented elsewhere (66). Nevertheless, it seems appropriate to emphasize here that recovery of function can be due to restoration of the same mechanism or substitution of another mechanism. Also, recovery refers specifically to the return of a function, whereas plasticity refers to the process or mechanism of the restoration (i.e., capability of building new tissue or formative). A related phenomenon, redundancy, refers to two or more mechAddress for reprint requests and other correspondence:

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“…Chemosensory nerve transection can elicit compensatory plasticity. For example, carotid denervation upregulates the impact of the aortic body chemoreceptors on ventilatory control via a serotonin-dependent mechanism (54,137,216). Carotid denervation also influences central neural chemoreflex pathways (142,143,208,209).…”

Section: Injury-induced Respiratory Plasticitymentioning

confidence: 99%

Invited Review: Neuroplasticity in respiratory motor control

Mitchell

Johnson

2003

Journal of Applied Physiology

354

313

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Although recent evidence demonstrates considerable neuroplasticity in the respiratory control system, a comprehensive conceptual framework is lacking. Our goals in this review are to define plasticity (and related neural properties) as it pertains to respiratory control and to discuss potential sites, mechanisms, and known categories of respiratory plasticity. Respiratory plasticity is defined as a persistent change in the neural control system based on prior experience. Plasticity may involve structural and/or functional alterations (most commonly both) and can arise from multiple cellular/synaptic mechanisms at different sites in the respiratory control system. Respiratory neuroplasticity is critically dependent on the establishment of necessary preconditions, the stimulus paradigm, the balance between opposing modulatory systems, age, gender, and genetics. Respiratory plasticity can be induced by hypoxia, hypercapnia, exercise, injury, stress, and pharmacological interventions or conditioning and occurs during development as well as in adults. Developmental plasticity is induced by experiences (e.g., altered respiratory gases) during sensitive developmental periods, thereby altering mature respiratory control. The same experience later in life has little or no effect. In adults, neuromodulation plays a prominent role in several forms of respiratory plasticity. For example, serotonergic modulation is thought to initiate and/or maintain respiratory plasticity following intermittent hypoxia, repeated hypercapnic exercise, spinal sensory denervation, spinal cord injury, and at least some conditioned reflexes. Considerable work is necessary before we fully appreciate the biological significance of respiratory plasticity, its underlying cellular/molecular and network mechanisms, and the potential to harness respiratory plasticity as a therapeutic tool.

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Important role of carotid chemoreceptor afferents in control of breathing of adult and neonatal mammals

Cited by 64 publications

References 34 publications

Breathing without CO₂Chemosensitivity in ConditionalPhox2bMutants

Breathing without CO₂Chemosensitivity in ConditionalPhox2bMutants

Invited Review: Plasticity in the control of breathing following sensory denervation

Invited Review: Neuroplasticity in respiratory motor control

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Important role of carotid chemoreceptor afferents in control of breathing of adult and neonatal mammals

Cited by 64 publications

References 34 publications

Breathing without CO2Chemosensitivity in ConditionalPhox2bMutants

Breathing without CO2Chemosensitivity in ConditionalPhox2bMutants

Invited Review: Plasticity in the control of breathing following sensory denervation

Invited Review: Neuroplasticity in respiratory motor control

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Product

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Breathing without CO₂Chemosensitivity in ConditionalPhox2bMutants

Breathing without CO₂Chemosensitivity in ConditionalPhox2bMutants