Maturational changes in neuromodulation of central pathways underlying hypoxic ventilatory response

Simakajornboon, Narong; Kuptanon, Teeradej

doi:10.1016/j.resp.2005.05.005

Cited by 43 publications

(23 citation statements)

References 104 publications

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“…In a piglet model, the decline was more marked following exposure to chronic intermittent hypoxia until day 10 after birth 26 as evidenced by a decline in phrenic electroneurograms (ENGphr). Several neurotransmitters including γ-aminobutyric acid (GABA), 27 adenosine,28 29 serotoma 30 and opioids31 are involved in the late component of the hypoxic ventilator response. Intracisternal injection of bicuculline, a GABA A antagonist, in piglets aged 2–10 days old reversed the effects of recurrent hypoxia on the ENGphr hypoxic response and eliminated apnoea during hypoxia 26.…”

Section: Discussionmentioning

confidence: 99%

Antenatal substance misuse and smoking and newborn hypoxic challenge response

Ali

Rossor

Bhat

et al. 2015

Arch Dis Child Fetal Neonatal Ed

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Interventions: Maternal and infant urine samples were tested for cotinine, cannabinoids, opiates, amphetamines, methadone, cocaine and benzodiazepines. Main out come measures:During quiet sleep, the infants were switched from breathing room air to 15% oxygen and changes in minute volume were assessed. Results:The SM infants had a greater mean increase (p=0.028, p= 0.034 respectively) and a greater magnitude of decline (p<0.001, p=0.018 respectively) in minute volume than the S infants and the controls. The rate of decline in minute volume was greater in the SM infants (p=0.008) and the S infants (p=0.011) compared to the controls. Conclusions:Both antenatal substance misuse and smoking affect the infant's ventilatory response to a hypoxic challenge.3

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Section: Discussionmentioning

confidence: 99%

Antenatal substance misuse and smoking and newborn hypoxic challenge response

Ali

Rossor

Bhat

et al. 2015

Arch Dis Child Fetal Neonatal Ed

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“…As discussed earlier, during the early stages of STP this response is mediated by enhanced glutamatergic activity, which is usually due to increased presynaptic glutamate release. In the later stages of STP, large-scale Ca 2+ influx through postsynaptic glutamatergic NMDARs, which underlies the early form of STP, leads to persistently elevated intracellular Ca 2+ , the accumulation of which not only predisposes neurons toward excitability upon subsequent stimulation, but also contributes to the sustained phosphorylation of nNOS after the removal of the hypoxic stimulus (10, 41, 192, 195, 228, 260, 263, 359). Up to several minutes are required for neuronal Ca 2+ to be returned to normal equilibrium through ion pump-mediated extrusion of the ion (183), which is a requirement for nNOS to return to its normal, inactivated state, to cease production of NO, and thereby return overall synaptic sensitivity to afferent stimulation to baseline levels.…”

Section: Physiological and Molecular Responses To Brief Hypoxic Exposmentioning

confidence: 99%

“…We focus on mammals, including humans, the HVR of nonmammalian vertebrates having been recently reviewed elsewhere (252, 316). Other aspects of the HVR that have been covered elsewhere and will not be extensively considered here include the effects of development and aging (138, 359, 394), evolution (78), gender (26, 390), measurement techniques (394), and genetic differences in laboratory animals (17, 296). …”

Section: Introductionmentioning

confidence: 99%

Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis

Pamenter

Powell

2016

Comprehensive Physiology

109

101

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Ventilatory responses to hypoxia vary widely depending on the pattern and length of hypoxic exposure. Acute, prolonged, or intermittent hypoxic episodes can increase or decrease breathing for seconds to years, both during the hypoxic stimulus, and also after its removal. These myriad effects are the result of a complicated web of molecular interactions that underlie plasticity in the respiratory control reflex circuits and ultimately control the physiology of breathing in hypoxia. Since the time domains of the physiological hypoxic ventilatory response (HVR) were identified, considerable research effort has gone toward elucidating the underlying molecular mechanisms that mediate these varied responses. This research has begun to describe complicated and plastic interactions in the relay circuits between the peripheral chemoreceptors and the ventilatory control circuits within the central nervous system. Intriguingly, many of these molecular pathways seem to share key components between the different time domains, suggesting that varied physiological HVRs are the result of specific modifications to overlapping pathways. This review highlights what has been discovered regarding the cell and molecular level control of the time domains of the HVR, and highlights key areas where further research is required. Understanding the molecular control of ventilation in hypoxia has important implications for basic physiology and is emerging as an important component of several clinical fields.

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“…Like ventilation, metabolic rate is dependent on the body size, sex, total body activities, the state of arousal, age, and several other factors, such as ambient temperature and ambient gas composition (20,42,43). Both ventilation and metabolic rate are reportedly developmentally regulated, and, in general, V CO 2 is regulated in parallel with V O 2 (21,25,53,58). However, details of postnatal development of the metabolic rate are poorly understood, because most studies focused on only a few time points.…”

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confidence: 99%

Postnatal development of metabolic rate during normoxia and acute hypoxia in rats: implication for a sensitive period

Liu¹,

Fehring²,

Lowry³

et al. 2009

Journal of Applied Physiology

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Liu Q, Fehring C, Lowry TF, Wong-Riley MTT. Postnatal development of metabolic rate during normoxia and acute hypoxia in rats: implication for a sensitive period. J Appl Physiol 106: 1212-1222, 2009. First published December 31, 2008 doi:10.1152/japplphysiol.90949.2008.-Previously, we reported that the hypoxic ventilatory response (HVR) in rats was weakest at postnatal day (P) P13, concomitant with neurochemical changes in respiratory nuclei. A major determinant of minute ventilation (V E) is reportedly the metabolic rate [O2 consumption (V O2) and CO2 production (V CO2)]. The present study aimed at testing our hypothesis that daily metabolic rates changed in parallel with ventilation during development and that a weak HVR at P13 was attributable mainly to an inadequate metabolic rate in hypoxia. Ventilation and metabolic rates were monitored daily in P0 -P21 rats. We found that 1) ventilation and metabolic rates were not always correlated, and V E/V O2 and V E/V CO2 ratios were not constant during development; 2) metabolic rate and V E/V O2 and V E/V CO2 ratios at P0 -P1 were significantly different from the remaining first postnatal week in normoxia and hypoxia; 3) at P13, metabolic rates and V E/V O2 and V E/V CO2 ratios abruptly increased in normoxia and were compromised in acute hypoxia, unlike more stable trends during the remaining second and third postnatal weeks; and 4) the respiratory quotient (V CO2/V O2) was quite stable in normoxia and fluctuated slightly in hypoxia from P0 to P21. Thus our data revealed heretofore unsuspected metabolic adjustments at P0 -P1 and P13. At P0 -P1, ventilation and metabolic rates were uncorrelated, whereas at P13, they were closely correlated under normoxia and hypoxia. The findings further strengthened the existence of a critical period of respiratory development around P13, when multiple physiological and neurochemical adjustments occur simultaneously. carbon dioxide production; critical period; oxygen consumption; respiratory quotient; ventilation PREVIOUSLY, WE CONDUCTED DETAILED, day-to-day studies of various brain stem respiratory nuclei of the rat and found that neurotransmitters and receptors underwent distinct developmental changes. Significantly, at or around postnatal day (P) 12, the expression of excitatory neurotransmitter glutamate and its N-methyl-D-aspartate receptors dropped precipitously, whereas the expression of inhibitory neurotransmitter ␥-aminobutyric acid (GABA), GABA B receptors, and glycine receptors rose sharply (27,30, 61). Concomitantly, there was a sudden fall in cytochrome oxidase activity (27,28, 61), a sensitive indicator of metabolic capacity and neuronal activity (60). We hypothesized that at and around P12 is a sensitive period in the postnatal development of the rat's respiratory control network, when a transient dominance of inhibitory over excitatory neurotransmission renders the animals less capable of overcoming exogenous respiratory stressors. Our subsequent ventilatory studies revealed striking changes in normoxic ventilation ...

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Maturational changes in neuromodulation of central pathways underlying hypoxic ventilatory response

Cited by 43 publications

References 104 publications

Antenatal substance misuse and smoking and newborn hypoxic challenge response

Antenatal substance misuse and smoking and newborn hypoxic challenge response

Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis

Postnatal development of metabolic rate during normoxia and acute hypoxia in rats: implication for a sensitive period

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