ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012
Effect of chronic intermittent hypoxia on noradrenergic activation of hypoglossal motoneurons.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 21 citations in OpenAlex.
- Chronic intermittent hypoxia attenuates noradrenergic innervation of hypoglossal motor nucleus.Respiratory physiology & neurobiology · 2024Article
- Understanding Pathophysiological Concepts Leading to Obstructive Apnea.Obesity surgery · 2018Review
- Noradrenergic Activation of Hypoglossal Nucleus Modulates the Central Regulation of Genioglossus in Chronic Intermittent Hypoxic Rats.Frontiers in neurology · 2017Article
- Chronic intermittent hypoxia affects endogenous serotonergic inputs and expression of synaptic proteins in rat hypoglossal nucleus.American journal of translational research · 2017Article
- Neural Control of the Upper Airway: Respiratory and State-Dependent Mechanisms.Comprehensive Physiology · 2016Review
- Sleep-wake control of the upper airway by noradrenergic neurons, with and without intermittent hypoxia.Progress in brain research · 2014Article
- Respiratory modulation of lingual muscle activity across sleep-wake states in rats.Respiratory physiology & neurobiology · 2013Article
- Intermittent hypoxia, respiratory plasticity and sleep apnea in humans: present knowledge and future investigations.Respiratory physiology & neurobiology · 2013Review
- Reduced c-Fos expression in medullary catecholaminergic neurons in rats 20 h after exposure to chronic intermittent hypoxia.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Antagonism of orexin receptors in the posterior hypothalamus reduces hypoglossal and cardiorespiratory excitation from the perifornical hypothalamus.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Effect of chronic intermittent hypoxia on noradrenergic activation of hypoglossal motoneurons.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Glucoregulatory consequences and cardiorespiratory parameters in rats exposed to chronic-intermittent hypoxia: effects of the duration of exposure and losartan.Frontiers in neurology · 2012Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
In obstructive sleep apnea patients, elevated activity of the lingual muscles during wakefulness protects the upper airway against occlusions. A possibly related form of respiratory neuroplasticity is present in rats exposed to acute and chronic intermittent hypoxia (CIH). Since rats exposed to CIH have increased density of noradrenergic terminals and increased α(1)-adrenoceptor immunoreactivity in the hypoglossal (XII) nucleus, we investigated whether these anatomic indexes of increased noradrenergic innervation translate to increased sensitivity of XII motoneurons to noradrenergic activation. Adult male Sprague-Dawley rats were subjected to CIH for 35 days, with O(2) level varying between 24% and 7% with 180-s period for 10 h/day. They were then anesthetized, vagotomized, paralyzed, and artificially ventilated. The dorsal medulla was exposed, and phenylephrine (2 mM, 10 nl) and then the α(1)-adrenoceptor antagonist prazosin (0.2 mM, 3 × 40 nl) were microinjected into the XII nucleus while XII nerve activity (XIIa) was recorded. The area under integrated XIIa was measured before and at different times after microinjections. The excitatory effect of phenylephrine on XII motoneurons was similar in sham- and CIH-treated rats. In contrast, spontaneous XIIa was more profoundly reduced following prazosin injections in CIH- than sham-treated rats [to 21 ± 7% (SE) vs. 40 ± 8% of baseline, P < 0.05] without significant changes in central respiratory rate, arterial blood pressure, or heart rate. Thus, consistent with increased neuroanatomic measures of noradrenergic innervation of XII motoneurons following exposure to CIH, prazosin injections revealed a stronger endogenous noradrenergic excitatory drive to XII motoneurons in CIH- than sham-treated anesthetized rats.
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