c-Fos expression in the central nervous system elicited by phrenic nerve stimulation

Malakhova, O. E.; Davenport, Paul W.

doi:10.1152/jappl.2001.90.4.1291

Cited by 16 publications

(11 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Animal studies have been performed mainly in rats (41)(42)(43)(44)(45), cats (30,(46)(47)(48)(49)(50)(51), and dogs (31,(52)(53)(54)(55). Conditioned fear induced by hypercapnia in rats is known to cause changes in the breathing pattern (28,29).…”

Section: Animal Studiesmentioning

confidence: 99%

See 1 more Smart Citation

Pathophysiology of Dyspnea in Chronic Obstructive Pulmonary Disease: A Roundtable

O’Donnell

Banzett²,

Carrieri‐Kohlman³

et al. 2007

Proceedings of the American Thoracic Society

Self Cite

313

249

View full text Add to dashboard Cite

Effective management of dyspnea in chronic obstructive pulmonary disease (COPD) requires a clearer understanding of its underlying mechanisms. This roundtable reviews what is currently known about the neurophysiology of dyspnea with the aim of applying this knowledge to the clinical setting. Dyspnea is not a single sensation, having multiple qualitative descriptors. Primary sources of dyspnea include: (1) inputs from multiple somatic proprioceptive and bronchopulmonary afferents, and (2) centrally generated signals related to inspiratory motor command output or effort. Respiratory disruption that causes a mismatch between medullary respiratory motor discharge and peripheral mechanosensor afferent feedback gives rise to a distressing urge to breathe which is independent of muscular effort. Recent brain imaging studies have shown increased limbic system activation in response to various dyspneogenic stimuli and emphasize the affective dimension of this symptom. All of these mechanisms are likely instrumental in exertional dyspnea causation in COPD. Increased central motor drive (and effort) is required to increase ventilation during activity because the inspiratory muscles become acutely overloaded and functionally weakened. Abnormal dynamic ventilatory mechanics and excessive chemostimulation during exercise also result in a widening disparity between escalating central neural drive and restricted thoracic volume displacement. This neuromechanical uncoupling may form the basis for the distressing sensation of unsatisfied inspiration. Interventions that alleviate dyspnea in COPD do so by improving ventilatory mechanics, reducing central neural drive, or both-thereby partially restoring neuromechanical coupling of the respiratory system. Self-management strategies address the affective aspect of dyspnea and are essential to successful treatment.

show abstract

Section: Animal Studiesmentioning

confidence: 99%

“…Conditioned fear induced by hypercapnia in rats is known to cause changes in the breathing pattern (28,29). These stimuli elicit neural activation, and the activated neurons can be found using c-Fos expression in several nuclei in the central nervous system (41). Mechanical loads also stimulate these central neural fear centers.…”

Section: Animal Studiesmentioning

confidence: 99%

Pathophysiology of Dyspnea in Chronic Obstructive Pulmonary Disease: A Roundtable

O’Donnell

Banzett²,

Carrieri‐Kohlman³

et al. 2007

Proceedings of the American Thoracic Society

Self Cite

313

249

View full text Add to dashboard Cite

show abstract

“…2b). Anatomical evidence of synaptic activity between regenerated axons in the PNG and spinal cord neurons is established by an increase in the number of cFos immunoreactive neurons near the graft-host interface after electrical stimulation of the PNG [38,47].…”

Section: Experimental Approaches Using a Pngmentioning

confidence: 99%

Peripheral Nerve Grafts Support Regeneration after Spinal Cord Injury

et al. 2011

View full text Add to dashboard Cite

Summary: Traumatic insults to the spinal cord induce both immediate mechanical damage and subsequent tissue degeneration leading to a substantial physiological, biochemical, and functional reorganization of the spinal cord. Various spinal cord injury (SCI) models have shown the adaptive potential of the spinal cord and its limitations in the case of total or partial absence of supraspinal influence. Meaningful recovery of function after SCI will most likely result from a combination of therapeutic strategies, including neural tissue transplants, exogenous neurotrophic factors, elimination of inhibitory molecules, functional sensorimotor training, and/or electrical stimulation of paralyzed muscles or spinal circuits. Peripheral nerve grafts provide a growthpermissive substratum and local neurotrophic factors to enhance the regenerative effort of axotomized neurons when grafted into the site of injury. Regenerating axons can be directed via the peripheral nerve graft toward an appropriate target, but they fail to extend beyond the distal graft-host interface because of the deposition of growth inhibitors at the site of SCI. One method to facilitate the emergence of axons from a graft into the spinal cord is to digest the chondroitin sulfate proteoglycans that are associated with a glial scar. Importantly, regenerating axons that do exit the graft are capable of forming functional synaptic contacts. These results have been demonstrated in acute injury models in rats and cats and after a chronic injury in rats and have important implications for our continuing efforts to promote structural and functional repair after SCI.

show abstract

“…Anatomical studies have found that phrenic nerve afferents (of unknown type) terminate in the dorsal horn lamina I-IV of C4 and C5 spinal cord in rat (Goshgarian et al, 1986;Malakhova et al, 2001). In a brief report, Larnicol et al (1984) reported immunoflourescent evidence of dorsal root entry of phrenic nerve afferents in the dorsal horn of the cervical spinal cord.…”

Section: Introductionmentioning

confidence: 99%

Phrenic nerve afferents elicited cord dorsum potential in the cat cervical spinal cord

Chou

Davenport

2005

BMC Physiol

View full text Add to dashboard Cite

show abstract

c-Fos expression in the central nervous system elicited by phrenic nerve stimulation

Cited by 16 publications

References 38 publications

Pathophysiology of Dyspnea in Chronic Obstructive Pulmonary Disease: A Roundtable

Pathophysiology of Dyspnea in Chronic Obstructive Pulmonary Disease: A Roundtable

Peripheral Nerve Grafts Support Regeneration after Spinal Cord Injury

Phrenic nerve afferents elicited cord dorsum potential in the cat cervical spinal cord

Contact Info

Product

Resources

About