Changes in Monoamine Release in the Ventral Horn and Hypoglossal Nucleus Linked to Pontine Inhibition of Muscle Tone: An<i>In Vivo</i>Microdialysis Study

Lai, Yuan-Yang; Kodama, Tohru; Siegel, Jerome M.

doi:10.1523/jneurosci.21-18-07384.2001

Cited by 114 publications

(89 citation statements)

References 68 publications

(68 reference statements)

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“…As reported previously (Lai et al, 2001), electrical stimulation and ACh injection into the PIA produced muscle tone suppression in both postural and respiratory muscles. The percentage decrease of integrated muscle activity in respiratory and postural muscles with PIA ACh injection was 62.5 and 67.3%, respectively (Fig.…”

Section: Stimulation and Collecting Sites In The Brainstem And Spinalsupporting

confidence: 83%

“…Suppression of muscle tone could result from activation of inhibitory systems, inactivation of excitatory systems, or both. Our previous study showed a reduction of norepinephrine and serotonin release in both the spinal ventral horn and hypoglossal (XII) nucleus during PIA stimulation in the decerebrate cat (Lai et al, 2001). This result combined with other studies that showed a facilitatory effect of these monoamines on motoneurons (Takahashi and Berger, 1990;Parkis et al, 1995;Jelev et al, 2001) indicates that disfacilitation plays an important role in muscle tone suppression.…”

Section: Introductionsupporting

confidence: 61%

“…Experiments were performed in two male and six female cats. Surgical preparation was described previously (Lai et al, 2001). Briefly, tracheotomy, arterial and venous cannulations, and decerebration at the precollicular-postmammillary level were performed under halothane-oxygen anesthesia.…”

Section: Methodsmentioning

confidence: 99%

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Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

2003

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We hypothesized that cessation of brainstem monoaminergic systems and an activation of brainstem inhibitory systems are both involved in pontine inhibitory area (PIA) stimulation-induced muscle atonia. In our previous study (Lai et al., 2001), we found a decrease in norepinephrine and serotonin release in motoneuron pools during PIA stimulation-induced muscle tone suppression. We now demonstrate an increase in inhibitory amino acid release in motor nuclei during PIA stimulation in the decerebrate cat using in vivo microdialysis and HPLC analysis techniques. Microinjection of acetylcholine into the PIA elicited muscle atonia and simultaneously produced a significant increase in both glycine and GABA release in both the hypoglossal nucleus and the lumbar ventral horn. Glycine release increased by 74% in the hypoglossal nucleus and 50% in the spinal cord. GABA release increased by 31% in the hypoglossal nucleus and 64% in the spinal cord during atonia induced by cholinergic stimulation of the PIA. As with cholinergic stimulation, 300 msec train electrical stimulation of the PIA elicited a significant increase in glycine release in the hypoglossal nucleus and ventral horn. GABA release was significantly increased in the hypoglossal nucleus but not in the spinal cord during electrical stimulation of the PIA. Glutamate release in the motor nuclei was not significantly altered during atonia induced by electrical or acetylcholine stimulation of the PIA. We suggest that both glycine and GABA play important roles in the regulation of upper airway and postural muscle tone. A combination of decreased monoamine and increased inhibitory amino acid release in motoneuron pools causes PIA-induced atonia and may be involved in atonia linked to rapid eye-movement sleep.

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Section: Stimulation and Collecting Sites In The Brainstem And Spinalsupporting

confidence: 83%

Section: Introductionsupporting

confidence: 61%

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Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

2003

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“…Thus, although a reduced release of norepinephrine was observed in the XII nucleus region during the REM sleep-like suppression of motor activity (35), our results show that few or no A5 cell projections target XII motoneurons and the activity of A5 cells makes little or no contribution to the activity of XII motoneurons under our experimental conditions. By exclusion, norepinephrine cells of the A7 group and/or sub-LC region may play a larger role in withdrawing noradrenergic excitation from XII motoneurons during REM sleep, whereas the silencing of A5 neurons may be important in regulating afferent transmission in the NTS and elsewhere.…”

Section: Discussioncontrasting

confidence: 54%

“…Consistent with these findings, the extracellular level of norepinephrine is reduced in the XII nucleus during the motor atonia produced by electrical stimulation of the pontine reticular formation region implicated in the triggering of REM sleep (35). The noradrenergic cells of the A5 group may be similarly modulated with the sleep-wake cycle, but this has not been tested.…”

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confidence: 88%

A5 cells are silenced when REM sleep-like signs are elicited by pontine carbachol

Fenik

Marchenko

Janssen

et al. 2002

Journal of Applied Physiology

111

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. A5 cells are silenced when REM sleep-like signs are elicited by pontine carbachol. J Appl Physiol 93: 1448-1456, 2002. First published June 14, 2002 10.1152/japplphysiol.00225.2002The A5 noradrenergic neurons are considered important for cardiorespiratory regulation. We hypothesized that A5 cells are silenced during rapid eye movement (REM) sleep, thereby contributing to cardiorespiratory changes and suppression of hypoglossal (XII) motoneuronal activity. We used an anesthetized, paralyzed, and artificially ventilated rat in which pontine microinjections of carbachol trigger signs of REM sleep, including hippocampal theta rhythm, motor suppression, and silencing of locus coeruleus neurons. All 16 putative noradrenergic A5 cells recorded were strongly suppressed when the REM sleep-like episodes were elicited and also after intravenous clonidine. Antidromic mapping showed that none of six neurons tested projected to the XII nucleus, whereas three of five projected to the nucleus of the solitary tract and two of four to the rostral ventrolateral medulla. Bilateral microinjections of clonidine into the A5 regions did not alter XII nerve activity. These data suggest that A5 neurons are silenced during natural REM sleep. This will lead to decreased norepinephrine release and may alter synaptic transmission in the nucleus of the solitary tract and rostral ventrolateral medulla without, however, a detectable impact on XII motoneurons. hypoglossal motoneurons; norepinephrine; nucleus of the solitary tract; pons; rapid eye movement sleep THE NOREPINEPHRINE-CONTAINING neurons of the A5 group, located in the ventrolateral pons between the root of the facial nerve and the superior olive, are considered important regulators of cardiorespiratory function (reviewed in Refs. 11,24,25,45,46). They have extensive axonal projections that include cardiorespiratory and motor regions of the brain stem and spinal cord (1,8,9,23,36). Through these projections, they may control, among others, sympathetic and respiratory outputs and, via projection to the hypoglossal (XII) motor nucleus, may mediate noradrenergic excitation of XII motoneurons (5,22,27,40,49). XII motoneurons are of particular interest because they innervate the genioglossus muscle of the tongue, an important airway dilator. Its decreased activity during sleep contributes, in predisposed individuals, to the pathophysiology of the obstructive sleep apnea syndrome (34).The noradrenergic neurons of the locus coeruleus (LC) and the sub-LC region show a robust relationship of their firing frequency with the sleep-wake cycle: the highest activity occurs during wakefulness, and the lowest during the rapid eye movement (REM) stage of sleep (6,43). Consistent with these findings, the extracellular level of norepinephrine is reduced in the XII nucleus during the motor atonia produced by electrical stimulation of the pontine reticular formation region implicated in the triggering of REM sleep (35). The noradrenergic cells of the A5 group may be similarly modulated with the sleep-wa...

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Neural Control of the Upper Airway: Respiratory and State‐Dependent Mechanisms

Kubin

2016

Comprehensive Physiology

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Upper airway muscles subserve many essential for survival orofacial behaviors, including their important role as accessory respiratory muscles. In the face of certain predisposition of craniofacial anatomy, both tonic and phasic inspiratory activation of upper airway muscles is necessary to protect the upper airway against collapse. This protective action is adequate during wakefulness, but fails during sleep which results in recurrent episodes of hypopneas and apneas, a condition known as the obstructive sleep apnea syndrome (OSA). Although OSA is almost exclusively a human disorder, animal models help unveil the basic principles governing the impact of sleep on breathing and upper airway muscle activity. This article discusses the neuroanatomy, neurochemistry, and neurophysiology of the different neuronal systems whose activity changes with sleep-wake states, such as the noradrenergic, serotonergic, cholinergic, orexinergic, histaminergic, GABAergic and glycinergic, and their impact on central respiratory neurons and upper airway motoneurons. Observations of the interactions between sleep-wake states and upper airway muscles in healthy humans and OSA patients are related to findings from animal models with normal upper airway, and various animal models of OSA, including the chronic-intermittent hypoxia model. Using a framework of upper airway motoneurons being under concurrent influence of central respiratory, reflex and state-dependent inputs, different neurotransmitters, and neuropeptides are considered as either causing a sleep-dependent withdrawal of excitation from motoneurons or mediating an active, sleep-related inhibition of motoneurons. Information about the neurochemistry of state-dependent control of upper airway muscles accumulated to date reveals fundamental principles and may help understand and treat OSA.

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Changes in Monoamine Release in the Ventral Horn and Hypoglossal Nucleus Linked to Pontine Inhibition of Muscle Tone: AnIn VivoMicrodialysis Study

Cited by 114 publications

References 68 publications

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

A5 cells are silenced when REM sleep-like signs are elicited by pontine carbachol

Neural Control of the Upper Airway: Respiratory and State‐Dependent Mechanisms

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