Invited Review: Mechanisms underlying motor unit plasticity in the respiratory system

Mantilla, Carlos B.; Sieck, Gary C.

doi:10.1152/japplphysiol.01120.2002

Cited by 65 publications

(52 citation statements)

References 153 publications

(165 reference statements)

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“…This reinnervation may potentially have been enhanced by our 5-HT 1A agonist administrations, because 5-HT 1A activation triggers functional respiratory neural plasticity (Giroux et al, 1999;Mantilla and Sieck, 2003). However, the delay in our initial administration of 5-HT 1A agonists fell far beyond the therapeutic windows for tissue preservation after SCI (Teng et al, 1997(Teng et al, , 1998(Teng et al, , 2004, precluding any hope for 5-HT 1A agonist-triggered neuroprotection in our study.…”

Section: Eventual Recovery Of Respiratory Functionmentioning

confidence: 84%

Respiratory Abnormalities Resulting from Midcervical Spinal Cord Injury and their Reversal by Serotonin 1A Agonists in Conscious Rats

Choi

Liao²,

Newton³

et al. 2005

J. Neurosci.

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Section: Eventual Recovery Of Respiratory Functionmentioning

confidence: 84%

Respiratory Abnormalities Resulting from Midcervical Spinal Cord Injury and their Reversal by Serotonin 1A Agonists in Conscious Rats

Choi

Liao²,

Newton³

et al. 2005

J. Neurosci.

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“…For example, an increase in the number of dendro-dendritic appositions and synaptically active zones is observed in the IL phrenic motor nucleus a few hours post-C2 hemisection (Goshgarian et al, 1989;Goshgarian, 2003). There is also one report suggesting that the overall soma size of IL phrenic motoneurons decreases after C2HS (preliminary evidence cited in Mantilla and Sieck, 2003). Recent preliminary experiments raise the possibility that other cells (e.g.…”

Section: The Scpp Substratementioning

confidence: 99%

“…"sighs") under anesthesia (Golder et al, 2003). Augmented breaths are associated with a large increase in respiratory neural drive that results in activation of a much larger percentage of the phrenic motor pool vs. quiet breathing (Sieck andFournier, 1989, Golder et al, 2005). Thus, the sCPP may be functionally relevant only under conditions of very high respiratory drive (Golder et al, 2003), and assessment of augmented breaths may provide an opportunity to monitor the physiological importance of the sCPP after C2HS.…”

Section: Introductionmentioning

confidence: 99%

Modest spontaneous recovery of ventilation following chronic high cervical hemisection in rats

Fuller

Doperalski

Dougherty

et al. 2008

Experimental Neurology

115

167

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Following C2 spinal hemisection (C2HS) in adult rats, ipsilateral phrenic motoneuron (PhMN) recovery occurs through a time-dependent activation of latent, crossed-spinal collaterals (i.e., spontaneous crossed phrenic phenomenon; sCPP) from contralateral bulbospinal axons. Ventilation is maintained during quiet breathing after C2HS, but the ability to increase ventilation during a respiratory stimulation (e.g. hypercapnia) is impaired. We hypothesized that long-term expression of the sCPP would correspond to a progressive normalization in ventilatory patterns during respiratory challenge. Breathing was assessed via plethsymography in unanesthetized animals and phrenic motor output was measured in urethane-anesthetized, paralyzed and vagotomized rats. At 2-week post-C2HS, minute ventilation (VE) was maintained during baseline (room air) conditions as expected but was substantially blunted during hypercapnic challenge (68±3% of VE in uninjured, weight-matched rats). However, by 12 weeks the spinal-lesioned rats achieved a hypercapnic VE response that was 85±7% of control (p = 0.017 vs. 2 wks). These rats also exhibited augmented breaths (AB's) or "sighs" more frequently (p<0.05) than controls; however, total AB volume was significantly less than control at 2-and 12-week post-injury (69±4% and 80±5%, p<0.05, respectively). We also noted that phrenic neurograms demonstrated a consistent delay in onset of the ipsilateral vs. contralateral inspiratory phrenic burst at 2-12-week post-injury. Finally, the ipsilateral phrenic response to respiratory challenge (hypoxia) was greater, though not normalized, at 4-12-vs. 2-week post-injury. We conclude that recovery of ventilation deficits occurs over 2-12-week post-C2HS; however, intrinsic neuroplasticity remains insufficient to concurrently restore a normal level of ipsilateral phrenic output.

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“…Consistent with this hypothesis, preliminary evidence suggests that activitydependent synaptic plasticity in descending inputs to respiratory cervical spinal motoneurons is shifted toward increased short-term potentiation and decreased long-term depression in spinalized turtles (29). Fourth, alterations at the level of motoneurons, neuromuscular junctions, and muscle fibers may have contributed to normal V E while breathing room air (42).…”

Section: Spinalized Turtles Compensate For Injury While Breathing Roomentioning

confidence: 99%

Spinal cord injury-induced changes in breathing are not due to supraspinal plasticity in turtles (Pseudemys scripta)

Johnson¹,

Creighton²

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Johnson, Stephen M., and Robert J. Creighton. Spinal cord injury-induced changes in breathing are not due to supraspinal plasticity in turtles (Pseudemys scripta). Am J Physiol Regul Integr Comp Physiol 289: R1550 -R1561, 2005. First published August 11, 2005; doi:10.1152/ajpregu.00397.2005-After occurrence of spinal cord injury, it is not known whether the respiratory rhythm generator undergoes plasticity to compensate for respiratory insufficiency. To test this hypothesis, respiratory variables were measured in adult semiaquatic turtles using a pneumotachograph attached to a breathing chamber on a water-filled tank. Turtles breathed room air (2 h) before being challenged with two consecutive 2-h bouts of hypercapnia (2 and 6% CO 2 or 4 and 8% CO2). Turtles were spinalized at dorsal segments D8-D10 so that only pectoral girdle movement was used for breathing. Measurements were repeated at 4 and 8 wk postinjury. For turtles breathing room air, breathing frequency, tidal volume, and ventilation were not altered by spinalization; single-breath (singlet) frequency increased sevenfold. Spinalized turtles breathing 6 -8% CO 2 had lower ventilation due to decreased frequency and tidal volume, episodic breathing (breaths/episode) was reduced, and singlet breathing was increased sevenfold. Respiratory variables in sham-operated turtles were unaltered by surgery. Isolated brain stems from control, spinalized, and sham turtles produced similar respiratory motor output and responded the same to increased bath pH. Thus spinalized turtles compensated for pelvic girdle loss while breathing room air but were unable to compensate during hypercapnic challenges. Because isolated brain stems from control and spinalized turtles had similar respiratory motor output and chemosensitivity, breathing changes in spinalized turtles in vivo were probably not due to plasticity within the respiratory rhythm generator. Instead, caudal spinal cord damage probably disrupts spinobulbar pathways that are necessary for normal breathing.control of breathing; respiration; reptile; chelonian; episodic breathing IN RESPONSE TO INJURY, THE central nervous system undergoes morphological and physiological changes to compensate for loss of function, such as altered gene expression, neuronal reorganization, and altered synaptic plasticity. Likewise, after incomplete spinal cord injury, remaining descending spinal pathways and spinal motor networks undergo reorganization and neuroplasticity to compensate for loss of function (6,20,51). Because respiratory dysfunction is the leading cause of death in spinal cord-injured patients (9, 59), understanding the mechanisms by which the respiratory control system undergoes compensatory plasticity may lead to novel therapeutic strategies for reducing respiratory complications and subsequent morbidity.After spinal cord injury, breathing pattern is altered to maintain adequate ventilation (V E). For example, high cervical spinal cord injury compromises synaptic drive to phrenic and intercostal motoneurons in mammals, r...

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Invited Review: Mechanisms underlying motor unit plasticity in the respiratory system

Cited by 65 publications

References 153 publications

Respiratory Abnormalities Resulting from Midcervical Spinal Cord Injury and their Reversal by Serotonin 1A Agonists in Conscious Rats

Respiratory Abnormalities Resulting from Midcervical Spinal Cord Injury and their Reversal by Serotonin 1A Agonists in Conscious Rats

Modest spontaneous recovery of ventilation following chronic high cervical hemisection in rats

Spinal cord injury-induced changes in breathing are not due to supraspinal plasticity in turtles (Pseudemys scripta)

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