Time course of alterations in pre- and post-synaptic chemoreceptor function during developmental hyperoxia

Donnelly, David F.; Bavis, Ryan W.; Kim, Insook; Dbouk, Hassan A.; Carroll, John L.

doi:10.1016/j.resp.2009.05.005

Cited by 25 publications

(72 citation statements)

References 46 publications

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“…As described for single-unit activity, this profound impairment of glomus cell [Ca 2+ ] i responses to acute hypoxia can be fully reversed after 7–8 days of recovery in normoxia (Bavis et al, 2011b). As expected for the blunted calcium response, hypoxia-induced vesicle release from glomus cells is similarly reduced by hyperoxia exposure (Donnelly et al, 2009). …”

Section: Introductionsupporting

confidence: 59%

“…Although acute hypoxia generally raises intracellular calcium ([Ca 2+ ] i ) levels in glomus cells, the response is severely blunted by hyperoxia exposure. For instance, hyperoxia exposure of neonatal rats from P7 to P12 blunts the [Ca 2+ ] i response to acute hypoxia challenge and nearly abolishes the response when hyperoxia is continued to P14 (Donnelly et al, 2009). As described for single-unit activity, this profound impairment of glomus cell [Ca 2+ ] i responses to acute hypoxia can be fully reversed after 7–8 days of recovery in normoxia (Bavis et al, 2011b).…”

Section: Introductionmentioning

confidence: 99%

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Perinatal hyperoxia exposure impairs hypoxia-induced depolarization in rat carotid body glomus cells

Kim

Yang

Carroll

et al. 2013

Respiratory Physiology & Neurobiology

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Chronic post-natal hyperoxia reduces the hypoxic ventilatory response by reducing the carotid body sensitivity to acute hypoxia as demonstrated by a reduced afferent nerve response, reduced calcium response of carotid body glomus cells and reduced catecholamine secretion in response to acute hypoxia. The present study examined whether hyperoxia alters the electrophysiological characteristics of glomus cells. Rats were treated with hyperoxia for 1 week starting at P1 or P7 and for 2 weeks starting at P1 followed by harvesting and dissociation of their carotid bodies for whole cell, perforated-patch recording. As compared to glomus cells from normoxia animals, hyperoxia treated cells showed a significant reduction in the magnitude of depolarization in response to hypoxia and anoxia, despite little change in the depolarizing response to 20 mM K+. Resting cell membrane potential in glomus cells from rats exposed to hyperoxia from P1 to P15 and studied at P15 was slightly depolarized compared to other treatment groups and normoxia-treated cells, but conductance normalized to cell size was not different among groups. We conclude that postnatal hyperoxia impairs carotid chemoreceptor hypoxia transduction at a step between hypoxia sensing and membrane depolarization. This occurs without a major change in baseline electrophysiological characteristics, suggesting altered signaling or alterations in the relative abundance of different leak channel isoforms.

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Section: Introductionsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Perinatal hyperoxia exposure impairs hypoxia-induced depolarization in rat carotid body glomus cells

Kim

Yang

Carroll

et al. 2013

Respiratory Physiology & Neurobiology

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“…Indeed, Hyperoxia rats have smaller carotid bodies with fewer glomus cells and fewer chemoafferent neurons projecting to the brainstem (Erickson et al, 1998; Chavez-Valdez et al, 2012; Dmitrieff et al, 2012; Bavis et al, 2013). Futhermore, the remaining glomus cells are less sensitive to O 2 (Donnelly et al, 2005, 2009; Bavis et al, 2011b), and the spontaneous activity recorded from single-unit chemoafferent neurons may be reduced (or even silenced) at normoxic partial pressures of O 2 in Hyperoxia rats (Donnelly et al, 2005). …”

Section: Discussionmentioning

confidence: 99%

“…In addition, week-old neonatal rats exposed to 60% O 2 for 23-28 hours exhibit reduced normoxic ventilation as well (Roeser et al, 2011). Previous studies have shown enhanced glomus cell O 2 sensitivity after 24-hour hyperoxic exposures in week-old rats (Donnelly et al, 2009), and it may take several days for hyperoxia to cause measurable changes to carotid body size (Dmitrieff et al, 2012). Thus, developmental hyperoxia likely influences normoxic ventilation by eliciting plasticity/injury at additional levels of the respiratory control system.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, chronic hyperoxia inhibits postnatal growth of the carotid body (Erickson et al, 1998; Wang and Bisgard, 2005; Dmitrieff et al, 2012), causes degeneration of carotid chemoafferent neurons (Erickson et al, 1998; Chavez-Valdez et al, 2012), and diminishes carotid chemoreceptor O 2 sensitivity (Hanson et al, 1989; Bavis et al, 2011b; Kim et al, 2013). These phenotypic changes begin to appear by the fourth day of hyperoxia in rats (Donnelly et al, 2009; Bavis et al, 2011b; Dmitrieff et al, 2012), and the morphological plasticity may be permanent (Fuller et al, 2002). …”

Section: Introductionmentioning

confidence: 99%

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Postnatal development of eupneic ventilation and metabolism in rats chronically exposed to moderate hyperoxia

Bavis

Heerden

Brackett

et al. 2014

Respiratory Physiology & Neurobiology

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Newborn rats chronically exposed to moderate hyperoxia (60% O2) exhibit abnormal respiratory control, including decreased eupneic ventilation. To further characterize this plasticity and explore its proximate mechanisms, rats were exposed to either 21% O2 (Control) or 60% O2 (Hyperoxia) from birth until studied at 3 – 14 days of age (P3 – P14). Normoxic ventilation was reduced in Hyperoxia rats when studied at P3, P4, and P6-7 and this was reflected in diminished arterial O2 saturations; eupneic ventilation spontaneously recovered by P13-14 despite continuous hyperoxia, or within 24 h when Hyperoxia rats were returned to room air. Normoxic metabolism was also reduced in Hyperoxia rats but could be increased by raising inspired O2 levels (to 60% O2) or by uncoupling oxidative phosphorylation within the mitochondrion (2, 4-dinitrophenol). In contrast, moderate increases in inspired O2 had no effect on sustained ventilation which indicates that hypoventilation can be dissociated from hypometabolism. The ventilatory response to abrupt O2 inhalation was diminished in Hyperoxia rats at P4 and P6-7, consistent with smaller contributions of peripheral chemoreceptors to eupneic ventilation at these ages. Finally, the spontaneous respiratory rhythm generated in isolated brainstem-spinal cord preparations was significantly slower and more variable in P3-4 Hyperoxia rats than in age-matched Controls. We conclude that developmental hyperoxia impairs both peripheral and central components of eupneic ventilatory drive. Although developmental hyperoxia diminishes metabolism as well, this appears to be a regulated hypometabolism and contributes little to the observed changes in ventilation.

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Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

465

572

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The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article.

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Time course of alterations in pre- and post-synaptic chemoreceptor function during developmental hyperoxia

Cited by 25 publications

References 46 publications

Perinatal hyperoxia exposure impairs hypoxia-induced depolarization in rat carotid body glomus cells

Perinatal hyperoxia exposure impairs hypoxia-induced depolarization in rat carotid body glomus cells

Postnatal development of eupneic ventilation and metabolism in rats chronically exposed to moderate hyperoxia

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

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