Chronic intermittent hypoxia induces changes in expression of synaptic proteins in the nucleus of the solitary tract

Moreau, Jason M.; Ciriello, John

doi:10.1016/j.brainres.2015.07.007

Cited by 9 publications

(8 citation statements)

References 39 publications

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“…These findings of altered BDNF/TrkB signalling in the NTS during cardiovascular disease states are supported by observations showing that chronic intermittent hypoxia alters BDNF and TrkB expression in the NTS (Ciriello et al . ; Moreau & Ciriello, ) and also increased the expression of BDNF in nodose ganglia of spontaneously hypertensive and DOCA‐salt rats (Vermehren‐Schmaedick et al . ).…”

Section: Discussionmentioning

confidence: 98%

Influence of brain‐derived neurotrophic factor‐tyrosine receptor kinase B signalling in the nucleus tractus solitarius on baroreflex sensitivity in rats with chronic heart failure

Becker

Tian

Zucker

et al. 2016

The Journal of Physiology

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Chronic heart failure (CHF) results in blunting of arterial baroreflex sensitivity (BRS), which arises from alterations to both peripheral baroreceptors and central autonomic nuclei such as the nucleus tractus solitarius (NTS). Although glutamate is known to be an important neurotransmitter released from baroreceptor afferent synapses in the NTS, the influence of other neurotransmitters and neuromodulators remains unclear. Alterations to NTS signalling in CHF remain particularly undefined. The present study aimed to evaluate the role of brain-derived neurotrophic factor (BDNF) and tyrosine receptor kinase B (TrkB) receptor signalling in the NTS on baroreflex control both in healthy and CHF rats. To this end, we microinjected BDNF or the highly selective TrkB receptor antagonist [N2-2-2-oxoazepan-3-yl amino] carbonyl phenyl benzo (b)thiophene-2-carboxamide (ANA-12) into the dorsal medial NTS (dmNTS) of male Sprague-Dawley rats with coronary artery ligation-induced CHF and sham operated controls and recorded blood pressure and renal sympathetic nerve activity responses. We subsequently measured BRS before and after bilateral dmNTS microinjections of ANA-12. In sham rats, BDNF evoked a dose-dependent depressor and sympatho-inhibitory effect and ANA-12 produced the opposite response. Both of these responses were significantly blunted in CHF rats. Furthermore, bilateral microinjection of ANA-12 into the dmNTS greatly diminished baroreflex sensitivity in sham rats, whereas it had less of an effect in CHF rats. We observed decreased levels of TrkB protein and mRNA in the dmNTS of CHF rats. These data indicate that endogenous BDNF signalling in the NTS is integral for the maintenance of BRS and that BDNF/TrkB signalling is impaired in the NTS in the CHF state.

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Section: Discussionmentioning

confidence: 98%

Influence of brain‐derived neurotrophic factor‐tyrosine receptor kinase B signalling in the nucleus tractus solitarius on baroreflex sensitivity in rats with chronic heart failure

Becker

Tian

Zucker

et al. 2016

The Journal of Physiology

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“…4;Weese-Mayer et al 2006). However, CIH and ROS production affects not only the preBötC but also other CNS sites, including the nucleus tractus solitarii (NTS; Kline, 2010), where CIH alters neurotransmission, neuromodulation (de Paula et al 2007;Kline et al 2007;Zhang et al 2008;Kline et al 2009;Costa-Silva et al 2012;Shell et al 2016), neuroprotection and plasticity by altering proteins such as TrkB and brain-derived neurotrophic factor (Almado et al 2012;Moreau & Ciriello, 2015). CIH also enhances sympathetic drive and alters the baroreflex by acting differentially on central respiratory neurons (Moraes et al 2016, 20136;Souza et al 2016Souza et al , 2017Machado et al 2017).…”

Section: The Effect Of Intermittent Hypoxia On the Cardiorespiratory mentioning

confidence: 99%

“…), neuroprotection and plasticity by altering proteins such as TrkB and brain‐derived neurotrophic factor (Almado et al . ; Moreau & Ciriello, ). CIH also enhances sympathetic drive and alters the baroreflex by acting differentially on central respiratory neurons (Moraes et al.…”

Section: Introductionmentioning

confidence: 98%

Advances in cellular and integrative control of oxygen homeostasis within the central nervous system

Ramírez

Severs

Ramirez

et al. 2018

The Journal of Physiology

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Mammals must continuously regulate the levels of O and CO , which is particularly important for the brain. Failure to maintain adequate O /CO homeostasis has been associated with numerous disorders including sleep apnoea, Rett syndrome and sudden infant death syndrome. But, O /CO homeostasis poses major regulatory challenges, even in the healthy brain. Neuronal activities change in a differentiated, spatially and temporally complex manner, which is reflected in equally complex changes in O demand. This raises important questions: is oxygen sensing an emergent property, locally generated within all active neuronal networks, and/or the property of specialized O -sensitive CNS regions? Increasing evidence suggests that the regulation of the brain's redox state involves properties that are intrinsic to many networks, but that specialized regions in the brainstem orchestrate the integrated control of respiratory and cardiovascular functions. Although the levels of O in arterial blood and the CNS are very different, neuro-glial interactions and purinergic signalling are critical for both peripheral and CNS chemosensation. Indeed, the specificity of neuroglial interactions seems to determine the differential responses to O , CO and the changes in pH.

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“…We know that the paraventricular nucleus of hypothalamus is a critical factor in setting autonomic tonus and in particular parasympathetic tonus,87 and the neurons of the NTS88 increase in the neuronal response to IH. These two brain areas activate peripheral chemoreceptors and deactivate baroreflex sensitivity, favoring an additional rise of the sympathetic tonus and a fall of parasympathetic tone.…”

Section: Deleterious Effects Of Cih: the Osa Modelmentioning

confidence: 99%

Chronic intermittent hypoxia and obstructive sleep apnea: an experimental and clinical approach

Sforza¹,

Roche²

2016

118

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Obstructive sleep apnea (OSA) is a prevalent sleep disorder considered as an independent risk factor for cardiovascular consequences, such as systemic arterial hypertension, ischemic heart disease, cardiac arrhythmias, metabolic disorders, and cognitive dysfunction. The pathogenesis of OSA-related consequence is assumed to be chronic intermittent hypoxia (IH) inducing alterations at the molecular level, oxidative stress, persistent systemic inflammation, oxygen sensor activation, and increase of sympathetic activity. Overall, these mechanisms have an effect on vessel permeability and are considered to be important factors for explaining vascular, metabolic, and cognitive OSA-related consequences. The present review attempts to examine together the research paradigms and clinical studies on the effect of acute and chronic IH and the potential link with OSA. We firstly describe the literature data on the mechanisms activated by acute and chronic IH at the experimental level, which are very helpful and beneficial to explaining OSA consequences. Then, we describe in detail the effect of IH in patients with OSA that we can consider “the human model” of chronic IH. In this way, we can better understand the specific pathophysiological mechanisms proposed to explain the consequences of IH in OSA.

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Chronic intermittent hypoxia induces changes in expression of synaptic proteins in the nucleus of the solitary tract

Cited by 9 publications

References 39 publications

Influence of brain‐derived neurotrophic factor‐tyrosine receptor kinase B signalling in the nucleus tractus solitarius on baroreflex sensitivity in rats with chronic heart failure

Influence of brain‐derived neurotrophic factor‐tyrosine receptor kinase B signalling in the nucleus tractus solitarius on baroreflex sensitivity in rats with chronic heart failure

Advances in cellular and integrative control of oxygen homeostasis within the central nervous system

Chronic intermittent hypoxia and obstructive sleep apnea: an experimental and clinical approach

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