The interactions between locomotion and respiration

Gariépy, Jean-François; Missaghi, Kianoush; Dubuc, Réjean

doi:10.1016/b978-0-444-53613-6.00012-5

Cited by 33 publications

(25 citation statements)

References 97 publications

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“…However, it was later demonstrated in several animal species that the CO 2 arterial partial pressure does not increase during moderate exercise, and it even decreases (2). Other substances such as O 2 , H + ions, and Snitrosothiols are also known to modulate respiration (4-6), but there are not sufficient changes in these respiratory modulators to explain the respiratory increases during exercise (2,7).…”

mentioning

confidence: 99%

Specific neural substrate linking respiration to locomotion

Gariépy

Missaghi²,

Chevallier³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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mentioning

confidence: 99%

Specific neural substrate linking respiration to locomotion

Gariépy

Missaghi²,

Chevallier³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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“…We have shown that ACh plays an important excitatory role within the lamprey respiratory network under basal conditions and possibly under still undefined physiological conditions that imply increased respiratory drive to vagal motoneurons such as locomotion or enhanced sensory inputs (Gravel et al, 2007;Gariepy et al, 2010). This excitatory role is mediated by ␣7 nAChRs within the pTRG.…”

Section: Discussionmentioning

confidence: 99%

Identification of a Cholinergic Modulatory and Rhythmogenic Mechanism within the Lamprey Respiratory Network

Mutolo¹,

Cinelli²,

Bongianni³

et al. 2011

J. Neurosci.

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Acetylcholine (ACh) is well known to be involved in the control of breathing. However, no information is available on the role of ACh receptors (AChRs) within the lamprey respiratory network. The present study was performed on in vitro brainstem preparations of adult lampreys to investigate whether ACh affects respiratory activity possibly through an action on the paratrigeminal respiratory group (pTRG) that has been identified as an essential component of the respiratory network. Respiratory activity was monitored as vagal motor output. Bath application of 100 M physostigmine or 1 M nicotine increased respiratory frequency, while bath application of 100 M D-tubocurarine or 0.25 M ␣-bungarotoxin reduced respiratory frequency and increased the duration of vagal bursts. Since these effects were mimicked by microinjections of the same drugs into the pTRG, ACh proved to influence respiratory activity by acting on ␣7 nicotinic AChRs located within the pTRG. During apnea caused by partial blockade of ionotropic glutamate receptors at the level of the pTRG, bath application of bicuculline and strychnine restored the respiratory rhythm, although at reduced frequency. Similar results were obtained by the concurrent removal of both fast synaptic excitatory and inhibitory transmission. Blockade of pTRG ␣7 nicotinic AChRs suppressed this respiratory activity, thus indicating that pTRG neurons expressing these receptors contribute to respiratory rhythm generation. Together, these findings identify a novel cholinergic modulatory and possibly subsidiary rhythmogenic mechanism within the respiratory network of the adult lamprey and encourage further studies on the respiratory role of cholinergic receptors in different animal species.

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“…Thus, stimulation of non-respiratory muscles may represent a viable means of activating respiratory circuits (as shown in Figure 3Aii). While these experiments were conducted in spinal intact animals, the results highlight how primary afferent feedback can modulate spinal respiratory activity (Gariepy et al, 2012; Gariepy et al, 2010; Morin and Viala, 2002). In fact, more recent experiments have confirmed that stimulation of muscles in the upper extremities, and thus associated primary afferents, can restore phrenic motor output to an otherwise silent phrenic motor pool caudal to a C2 hemisection injury (Bezdudnaya et al, 2015).…”

Section: Therapeutically Shaping Respiratory Neuroplasticitymentioning

confidence: 99%

Enhancing neural activity to drive respiratory plasticity following cervical spinal cord injury

Hormigo

Zholudeva

Spruance

et al. 2017

Experimental Neurology

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Cervical spinal cord injury (SCI) results in permanent life-altering sensorimotor deficits, among which impaired breathing is one of the most devastating and life-threatening. While clinical and experimental research has revealed that some spontaneous respiratory improvement (functional plasticity) can occur post-SCI, the extent of the recovery is limited and significant deficits persist. Thus, increasing effort is being made to develop therapies that harness and enhance this neuroplastic potential to optimize long-term recovery of breathing in injured individuals. One strategy with demonstrated therapeutic potential is the use of treatments that increase neural and muscular activity (e.g. locomotor training, neural and muscular stimulation) and promote plasticity. With a focus on respiratory function post-SCI, this review will discuss advances in the use of neural interfacing strategies and activity-based treatments, and highlights some recent results from our own research.

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The interactions between locomotion and respiration

Cited by 33 publications

References 97 publications

Specific neural substrate linking respiration to locomotion

Specific neural substrate linking respiration to locomotion

Identification of a Cholinergic Modulatory and Rhythmogenic Mechanism within the Lamprey Respiratory Network

Enhancing neural activity to drive respiratory plasticity following cervical spinal cord injury

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