Peripheral Chemosensitivity and Central Integration: Neuroplasticity of Catecholaminergic Cells Under Hypoxia

Soulier, V.; Gestreau, Christian; Borghini, N.; Dalmaz, Y.; Cottet-Émard, J. M.; Péquignot, Jean-Marc

doi:10.1016/s0300-9629(96)00369-6

Cited by 22 publications

(19 citation statements)

References 45 publications

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“…[11][12][13][14][15][16] This finding has been attributed to an elevation in the set point for efferent sympathetic outflow resulting from progressive carotid body hypersensitivity and altered structure and function of catecholaminergic neurons in brain stem and cortical regions involved in autonomic cardiovascular regulation. 10,[17][18][19][29][30][31][32] Johnson et al 33 have recently reviewed experimental literature demonstrating induction, by transient challenges, of long-lasting changes in synaptic function within a widely distributed network of brain regions engaged in the longterm regulation of blood pressure and the amplification of initial hemodynamic responses by subsequent rechallenge. These data indicate that short-term external stimuli can induce afferent neural and circulating hormonal changes that in turn facilitate molecular neuroplasticity in subcortical and preganglionic components of the sympathetic nervous system, resulting in an elevated prevailing set point for efferent sympathetic nerve firing and consequent norepinephrine release.…”

Section: Discussionmentioning

confidence: 99%

“…[11][12][13][14][15][16] Este hallazgo se ha atribuido a una elevación del punto de regulación del flujo simpá-tico eferente, que resulta de la hipersensibilidad progresiva del cuerpo carotídeo, y de la alteración de la estructura y función de las neuronas catecolaminérgicas del tronco cerebral y las regiones corticales involucradas en la regulación cardiovascular autónoma. 10,[17][18][19][29][30][31][32] Recientemente, Johnson et al revisaron la bibliografía experimental que demostraba inducción, mediante desafíos transitorios, de cambios duraderos de la función sináptica dentro de una red ampliamente distribuida de regiones encefálicas involucradas en la regulación a largo plazo de la presión arterial y la amplificación de las respuestas hemodinámicas iniciales por re-desafío ulterior. Estos datos indican que los estímulos externos a corto plazo pueden inducir cambios neurales aferentes y hormonales circulantes que, a su vez, facilitan la neuroplasticidad molecular de componentes subcorticales y preganglionares del sistema nervioso simpático, lo que determina un punto de regulación elevado prevalente para la descarga nerviosa simpática eferente y la consiguiente liberación de noradrenalina.…”

Section: Discussionunclassified

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Arousal From Sleep and Sympathetic Excitation During Wakefulness

et al. 2016

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Obstructive apnea during sleep elevates the set point for efferent sympathetic outflow during wakefulness. Such resetting is attributed to hypoxia-induced upregulation of peripheral chemoreceptor and brain stem sympathetic function. Whether recurrent arousal from sleep also influences daytime muscle sympathetic nerve activity is unknown. We therefore tested, in a cohort of 48 primarily nonsleepy, middle-aged, male (30) and female (18) volunteers (age: 59±1 years, mean±SE), the hypothesis that the frequency of arousals from sleep (arousal index) would relate to daytime muscle sympathetic burst incidence, independently of the frequency of apnea or its severity. Polysomnography identified 24 as having either no or mild obstructive sleep apnea (apnea–hypopnea index <15 events/h) and 24 with moderate-to-severe obstructive sleep apnea (apnea–hypopnea index >15 events/h). Burst incidence correlated significantly with arousal index ( r =0.53; P <0.001), minimum oxygen saturation ( r =−0.43; P =0.002), apnea–hypopnea index ( r =0.41; P =0.004), age ( r =0.36; P =0.013), and body mass index ( r =0.33; P =0.022) but not with oxygen desaturation index ( r =0.28; P =0.056). Arousal index was the single strongest predictor of muscle sympathetic nerve activity burst incidence, present in all best subsets regression models. The model with the highest adjusted R 2 (0.456) incorporated arousal index, minimum oxygen saturation, age, body mass index, and oxygen desaturation index but not apnea–hypopnea index. An apnea- and hypoxia-independent effect of sleep fragmentation on sympathetic discharge during wakefulness could contribute to intersubject variability, age-related increases in muscle sympathetic nerve activity, associations between sleep deprivation and insulin resistance or insomnia and future cardiovascular events, and residual adrenergic risk with persistence of hypertension should therapy eliminate obstructive apneas but not arousals.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionunclassified

Arousal From Sleep and Sympathetic Excitation During Wakefulness

et al. 2016

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“…In the subsequent minutes to days of hypoxic exposure, ventilatory activity exhibits hypoxic ventilatory decline, followed by ventilatory acclimatization to chronic hypoxia. Ventilatory acclimatization appears to be dominated by initial, peripheral chemoreceptor sensitization (21), followed by progressively increasing contributions from the central neural integration of carotid chemoafferent neurons (45,220). Thus the ventilatory response to continuous hypoxia is characterized by several unique forms of respiratory plasticity.…”

Section: Hypoxia-induced Respiratory Plasticity (Adult)mentioning

confidence: 99%

Invited Review: Neuroplasticity in respiratory motor control

Mitchell

Johnson

2003

Journal of Applied Physiology

357

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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“…In mammals, many noradrenergic neurons are hypoxia sensitive and have been implicated in the ventilatory response to hypoxia (Neubauer and Sunderram, 2004;Roux et al, 2000;Soulier et al, 1997). In pre-metamorphic tadpoles, activation of noradrenergic neurons by hypoxia would tend to facilitate both lung and buccal ventilation.…”

Section: Perspectivesmentioning

confidence: 99%

Noradrenergic modulation of respiratory motor output during tadpole development: role of α-adrenoceptors

Fournier

Kinkead

2006

Journal of Experimental Biology

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Noradrenaline (NA) is an important modulator of respiratory activity. Results from in vitro studies using immature rodents suggest that the effects exerted by NA change during development, but these investigations have been limited to neonatal stages. To address this issue, we used in vitro brainstem preparations of an ectotherm, Rana catesbeiana, at three developmental stages: premetamorphic tadpoles, metamorphic tadpoles and fully mature adult bullfrogs. We first compared the effects of NA bath application (0.02-10· mol·l -1 ) on brainstem preparations from both pre-metamorphic (Taylor-Köllros stages VII-XI) and metamorphic tadpoles (TK stages XVIII-XXIII) and adult frogs. The fictive lung ventilation frequency response to NA application was both dose-and stage-dependent. Although no net change was observed in the pre-metamorphic group, NA application decreased fictive lung burst frequency in preparations from more mature animals. These effects were attenuated by application of ␣ ␣-adrenoceptor antagonists. Conversely, NA application elicited dose-and stage-dependent increases in fictive buccal ventilation frequency. We then assessed the contribution of ␣ ␣-adrenoceptors towards these responses by applying specific agonists (␣ ␣ 1 : phenylephrine; ␣ ␣ 2 : clonidine; concentration range from 10 to 200· mol·l -1 for both). Of the two agonists used, only phenylephrine application consistently mimicked the lung burst frequency response observed during NA application in each stage group. However, both agonists decreased buccal burst frequency, thus suggesting that other (␤ ␤) adrenoceptor types mediate this response. We conclude that modulation of both buccal and lung-related motor outputs change during development. NA modulation affects both types of respiratory activities in a distinct fashion, owing to the different adrenoceptor type involved.

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Peripheral Chemosensitivity and Central Integration: Neuroplasticity of Catecholaminergic Cells Under Hypoxia

Cited by 22 publications

References 45 publications

Arousal From Sleep and Sympathetic Excitation During Wakefulness

Arousal From Sleep and Sympathetic Excitation During Wakefulness

Invited Review: Neuroplasticity in respiratory motor control

Noradrenergic modulation of respiratory motor output during tadpole development: role of α-adrenoceptors

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