Elevated Body Temperature Exaggerates Laryngeal Chemoreflex Apnea in Decerebrate Piglets

Xia, Luxi; Damon, Tracey; Leiter, James C.; Bartlett, D.

doi:10.1007/978-0-387-73693-8_44

Cited by 4 publications

(3 citation statements)

References 17 publications

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“…The present results also reveal that moderate HB transiently blunted the cardiorespiratory inhibition normally observed during both laryngeal and pulmonary chemoreflexes. Such observations were somewhat unexpected, given that various postnatal stresses have been shown to increase apneas and bradycardias observed in the LCR (Lindgren et al, 1996 ; Frøen et al, 2000 ; Xia et al, 2008 , 2010 ; St-Hilaire et al, 2010 ; Carreau et al, 2011 ). Nevertheless, the blunting of LCR observed in HB lambs in the present study may be non-beneficial, due to the heightened risk of aspiration as a result of the lack of efficient glottal closure.…”

Section: Discussionmentioning

confidence: 99%

Moderate Hyperbilirubinemia Alters Neonatal Cardiorespiratory Control and Induces Inflammation in the Nucleus Tractus Solitarius

et al. 2016

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Hyperbilirubinemia (HB) occurs in 90% of preterm newborns. Moderate HB can induce acute neurological disorders while severe HB has been linked to a higher incidence of apneas of prematurity. The present study aimed to test the hypothesis that even moderate HB disrupts cardiorespiratory control in preterm lambs. Two groups of preterm lambs (born 14 days prior to term), namely control (n = 6) and HB (n = 5), were studied. At day 5 of life, moderate HB (150–250 μmol/L) was induced during 17 h in the HB group after which cardiorespiratory control as well as laryngeal and pulmonary chemoreflexes were assessed during baseline recordings and during hypoxia. Recordings were repeated 72 h after HB induction, just before euthanasia. In addition, neuropathological studies were performed to investigate for cerebral bilirubin deposition as well as for signs of glial reactivity in brainstem structures involved in cardiorespiratory control. Results revealed that sustained and moderate HB: (i) decreased baseline respiratory rate and increased the time spent in apnea; (ii) blunted the cardiorespiratory inhibition normally observed during both laryngeal and pulmonary chemoreflexes; and (iii) increased heart rate in response to acute hypoxia. These acute physiological changes were concurrent with an activation of Alzheimer type II astrocytes throughout the brain, including the brainstem. Concomitantly, bilirubin deposits were observed in the leptomeninges, but not in brain parenchyma. While most cardiorespiratory alterations returned to normal 72 h after HB normalization, the expression of glial fibrillary acid protein (GFAP) and ionized calcium binding adaptor molecule 1 (Iba1) was still increased within the nucleus tractus solitarius. In conclusion, moderate and sustained HB in preterm lambs induced cardiorespiratory alterations, the latter of which were associated with neurohistopathological changes. These changes are indicative of an inflammatory response in the brainstem neuroanatomical substrates involved in cardiorespiratory control.

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Section: Discussionmentioning

confidence: 99%

Moderate Hyperbilirubinemia Alters Neonatal Cardiorespiratory Control and Induces Inflammation in the Nucleus Tractus Solitarius

et al. 2016

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“…The LCR is also exaggerated in neonatal piglets and rats, whose body temperature rises 1–3°C above normal (150) (Figure 6). In piglets, the hyperthermic exaggeration of the LCR is most striking under postnatal day 5 and disappears by postnatal day 20 (151). Intravenous infusion of GABA A receptor blockers reverses the enhancement of laryngeal apnea by whole-body hyperthermia, suggesting that the effect of hyperthermia on the LCR is mediated by GABAergic inhibition of respiration (151a).…”

Section: The Function Of the Medullary 5-ht System And Its Relationshmentioning

confidence: 99%

The Brainstem and Serotonin in the Sudden Infant Death Syndrome

Kinney

Richerson²,

Dymecki

et al. 2009

Annu. Rev. Pathol. Mech. Dis.

270

242

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The sudden infant death syndrome (SIDS) is the sudden death of an infant under one year of age that is typically associated with sleep and that remains unexplained after a complete autopsy and death scene investigation. A leading hypothesis about its pathogenesis is that many cases result from defects in brainstem-mediated protective responses to homeostatic stressors occurring during sleep in a critical developmental period. Here we review the evidence for the brainstem hypothesis in SIDS with a focus upon abnormalities related to the neurotransmitter serotonin in the medulla oblongata, as these are the most robust pathologic findings to date. In this context, we synthesize the human autopsy data with genetic, whole-animal, and cellular data concerning the function and development of the medullary serotonergic system. These emerging data suggest an important underlying mechanism in SIDS that may help lead to identification of infants at risk and specific interventions to prevent death.

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“…The physiological meaning of the TRPV1-operated pool of vesicles is only beginning to be appreciated. This TRPV1-operated pool has been implicated as potentially playing a role in the laryngeal chemoreflex and the exaggerated apnea in animal models of Sudden Infant Death Syndrome (Curran et al, 2005; Xia et al, 2007, 2008, 2010, 2011). More comprehensive investigations are needed to fully evaluate this new form of afferent synaptic transmission and its implications in multi-system homeostatic regulation.…”

Section: Mechanism Of Distinction – Trpv1-operated Glutamate Releasementioning

confidence: 99%

Peptide and Lipid Modulation of Glutamatergic Afferent Synaptic Transmission in the Solitary Tract Nucleus

Andresen¹,

Fawley²,

Hofmann³

2013

Front. Neurosci.

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The brainstem nucleus of the solitary tract (NTS) holds the first central neurons in major homeostatic reflex pathways. These homeostatic reflexes regulate and coordinate multiple organ systems from gastrointestinal to cardiopulmonary functions. The core of many of these pathways arise from cranial visceral afferent neurons that enter the brain as the solitary tract (ST) with more than two-thirds arising from the gastrointestinal system. About one quarter of ST afferents have myelinated axons but the majority are classed as unmyelinated C-fibers. All ST afferents release the fast neurotransmitter glutamate with remarkably similar, high-probability release characteristics. Second order NTS neurons receive surprisingly limited primary afferent information with one or two individual inputs converging on single second order NTS neurons. A- and C-fiber afferents never mix at NTS second order neurons. Many transmitters modify the basic glutamatergic excitatory postsynaptic current often by reducing glutamate release or interrupting terminal depolarization. Thus, a distinguishing feature of ST transmission is presynaptic expression of G-protein coupled receptors for peptides common to peripheral or forebrain (e.g., hypothalamus) neuron sources. Presynaptic receptors for angiotensin (AT1), vasopressin (V1a), oxytocin, opioid (MOR), ghrelin (GHSR1), and cholecystokinin differentially control glutamate release on particular subsets of neurons with most other ST afferents unaffected. Lastly, lipid-like signals are transduced by two key ST presynaptic receptors, the transient receptor potential vanilloid type 1 and the cannabinoid receptor that oppositely control glutamate release. Increasing evidence suggests that peripheral nervous signaling mechanisms are repurposed at central terminals to control excitation and are major sites of signal integration of peripheral and central inputs particularly from the hypothalamus.

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Elevated Body Temperature Exaggerates Laryngeal Chemoreflex Apnea in Decerebrate Piglets

Cited by 4 publications

References 17 publications

Moderate Hyperbilirubinemia Alters Neonatal Cardiorespiratory Control and Induces Inflammation in the Nucleus Tractus Solitarius

Moderate Hyperbilirubinemia Alters Neonatal Cardiorespiratory Control and Induces Inflammation in the Nucleus Tractus Solitarius

The Brainstem and Serotonin in the Sudden Infant Death Syndrome

Peptide and Lipid Modulation of Glutamatergic Afferent Synaptic Transmission in the Solitary Tract Nucleus

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