The chemical neuroanatomy of breathing

Alheid, George F.; McCrimmon, Donald R.

doi:10.1016/j.resp.2008.07.014

Cited by 178 publications

(165 citation statements)

References 100 publications

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“…The depression of the ccRTN results not only in a reduced respiratory response to central and peripheral chemoreceptors, but also in severe hypoventilation, especially during sleep. Furthermore, a sustained normal (or perhaps increased) level of activation of non-NMDA glutamatergic receptors on pump cells of the nucleus tractus solitarius, which normally relay the inhibitory slowly adapting receptors input to the ventral respiratory column (VRC) and the pons, may contribute to the development of hypoventilation (10). In these cases, arousal might increase the breathing rate if the respiratory rhythm generators composed of the preBötzinger complex (PBötC) and the parafacial respiratory group (pRG) are operant (11).…”

Section: Discussionmentioning

confidence: 99%

“…In these cases, arousal might increase the breathing rate if the respiratory rhythm generators composed of the preBötzinger complex (PBötC) and the parafacial respiratory group (pRG) are operant (11). The PBötC neurokinin-1 receptor positive pre-inspiratory pacemaker cells express the type 2 vesicular glutamate transporter (VGlut2), indicating that these neurons play a role in glutamatergic transmission and might provide an excitatory stimulus to the remainder of the VRC, thus resulting in CNH (10). The pontine respiratory group, including the parabrachial/Kolliker fuse (PBrKF) nuclei, considered the pneumotaxic center in the older literature, contains abundant NMDA receptors and modulates breathing and ventilatory responses to hypoxia and stress (12,13).…”

Section: Discussionmentioning

confidence: 99%

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Central Neurogenic Hyperventilation in Anti-NMDA Receptor Encephalitis

et al. 2012

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Central neurogenic hyperventilation (CNH) is a rare condition that is generally associated with infiltrative tumors of the brainstem. Respiratory dysfunction, particularly central hypoventilation, is common in anti-Nmethyl D-aspartate (NMDA) receptor encephalitis. CNH, to the best of our knowledge, has not been described previously in this disease. A 24-year-old woman was diagnosed with anti-NMDA receptor encephalitis secondary to ovarian teratoma. In addition to the typical symptoms of the disease, recurrent CNH episodes were observed during the course of the illness, which subsided with midazolam and propofol infusion. Supportive and disease-specific treatments, including oopherectomy, plasmapheresis and intravenous immunoglobulin, provided excellent recovery. These observations suggest that NMDA receptors may play a role in the pathophysiology of CNH.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Central Neurogenic Hyperventilation in Anti-NMDA Receptor Encephalitis

et al. 2012

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“…The neurons of the PreBotzinger Complex in the ventrolateral medulla are now generally regarded as the initiation site for the electrical activity that culminates in normal inspiration [10,11]. However, this conclusion was only reached after two decades of experimentation and debate [12][13][14].…”

Section: Overview Of Inspiratory Neuroregulationmentioning

confidence: 99%

“…Just as sinoatrial cells receive modulating inputs from the autonomic nervous system to alter the heart rate, the preBOTc receives input from central chemoreceptors to increase ventilation in response to the decrease in pH that is associated with elevated partial pressures of CO 2 in the brain [11,22]. Although not all central chemoreceptors are found in the brainstem, many of those that are relevant to the discussion of anesthetic effects upon ventilation are located there [23].…”

Section: Central Chemoreceptorsmentioning

confidence: 99%

Sources of Inspiration: A Neurophysiologic Framework for Understanding Anesthetic Effects on Ventilatory Control

Czick

Waldman

Gross

2013

Curr Anesthesiol Rep

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Almost every medication that is presently available to provide sedation, analgesia, or general anesthesia significantly depresses one or more ventilatory control mechanisms. This places patients at risk of developing hypoventilation and hypoxemia during moderate or deep sedation as well as general anesthesia. As the neurophysiologic processes underlying normal ventilatory drive are discovered, new insights into the influence of anesthetics on ventilation have been recognized. More importantly, research into ways to circumvent these effects is underway. For example, drugs such as serotonin agonists and ampakines have been shown to counteract opioidinduced ventilatory depression without reversing the analgesic effect. On the other hand, efforts to identify agents that reverse the respiratory depression associated with propofol and the inhalation anesthetics have been less promising. Until reliable means for reversing drug-induced ventilatory depression are developed, prompt recognition of ventilatory insufficiency and initiation of resuscitative measures remain the keys to patient safety.

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“…This coordination of stereotypic movements associated with breathing and swallowing are generated by central pattern generators (CPGs) located within the brainstem of the central nervous system (CNS) (Alheid & McCrimmon, 2008;Grillner, 2006;Jean, 1990). It is hypothesized that a common pool of interneurons may exists between the respiratory CPGs, located within the pons and medulla, and the swallowing CPGs, located within the dorsal and ventrolateral medulla, due to their relative proximity within the brainstem and similar musculature they control (Chiao, Larson, Yajima, Ko, & Kahrilas, 1994;Jean, 2001;Kessler, 1993;Oku, Tanaka, & Ezure, 1994).…”

Section: Central Pattern Generatorsmentioning

confidence: 99%

Swallow and breathing coordination following suprahyoid muscle injury.

Kimbel¹

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DEDICATIONTo my wife, Kate, for all her support and patience. iv ACKNOWLEDGMENTS First, I would like to thank my thesis advisor at the University of Louisville. She provided invaluable input into the thesis process. Her knowledge base related to the scope of this paper was instrumental in its publication. Further, she was patient and forthright in her feedback. Under her tutelage, I fostered a newly found passion for research. Swallowing motility disorders (dysphagia) are a major complication following radiation treatment for head and neck cancer, affecting ~50% of those treated. One reason for this is that radiation causes muscle damage, provoking sensorimotor pathologies.Previous work has suggested that injury may cause discoordination between breathing and swallowing behaviors. We sought to determine if muscle injury provokes changes in this behavior. We hypothesized that acute suprahyoid muscle damage would alter crossbehavior excitability, causing destabilization of the respiratory-swallow pattern.Swallowing was evoked in anesthetized spontaneously breathing cats via injection of a 3cc bolus of water into the oropharyngeal cavity. A suprahyoid injury was induced unilaterally by applying a ~2mm cryoprobe to the belly of the mylohyoid muscle.Electromyography (EMG) activity (duration, amplitude) was measured concurrently in thyrohyoid, mylohyoid, thyropharyngeal, and diaphragm muscles. Swallow-breathing coordination (SBC) was measured by determining inspiration/expiration phase during the onset and offset of a swallowing event, based off the mylohyoid initiation and thyropharyngeal termination bursts, respectively. Results showed an injury-related effect in the mylohyoid muscle, as indicated by a significant decrease in the mean amplitude vi post-injury compared to pre-injury. During swallowing, the expiratory phase was found to predominate the respiratory cycle in both pre-and post-injury. No significant changes to the swallow-breathing coordination were found following injury. Results demonstrate that mylohyoid muscle injury does not appear to interfere with short-term changes in the respiratory-swallow pattern. Although deficits in muscle function were found immediately following injury, an extended time or more severe injury may be needed to adversely inhibit these behaviors. Thus, disrupting the stable coupling between respirations and swallowing, which has been found clinically, may not be apparent immediately after injury and require long-term changes in function.

show abstract

The chemical neuroanatomy of breathing

Cited by 178 publications

References 100 publications

Central Neurogenic Hyperventilation in Anti-NMDA Receptor Encephalitis

Central Neurogenic Hyperventilation in Anti-NMDA Receptor Encephalitis

Sources of Inspiration: A Neurophysiologic Framework for Understanding Anesthetic Effects on Ventilatory Control

Swallow and breathing coordination following suprahyoid muscle injury.

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