Degeneration of a muscle following remote nerve damage: Physiological changes and triggering mechanisms

Persistent Link:
http://hdl.handle.net/10150/288881
Title:
Degeneration of a muscle following remote nerve damage: Physiological changes and triggering mechanisms
Author:
Personius, Kirkwood Ely, 1966-
Issue Date:
1998
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Muscle depends on innervation and contraction to maintain a differentiated state. Denervation or disuse, therefore, often leads to muscle atrophy. In grasshoppers, muscle degeneration can also be induced when a hindlimb is lost by autotomy. In this case, the thoracic muscles which degenerate are neither damaged nor denervated, suggesting the existence of transneuronal mechanisms that influence muscle survival. Arbas and Weidner (1991) found that muscle degeneration is induced when the leg nerve (which does not innervate the thoracic muscles) is severed during autotomy. To characterize this autotomy-induced degenerative process, I studied a thoracic tergotrochanteral depressor muscle (M#133b,c) subsequent to autotomy in the grasshoppers, Barytettix psolus and B. humphreysii. The degeneration of M#133b,c is generally complete by 15 days after autotomy, when muscle cross-sectional area is reduced to 4% of the contralateral-control. The rate of muscle degeneration is initially slow, but at ∼10 days post-autotomy, degeneration becomes rapid and muscle fiber number becomes reduced. During this rapid phase, degeneration of M#133b,c occurs by programmed cell death. Indicators of programmed cell death-up-regulation of ubiquitin--immunoreactivity, condensed nuclear chromatin and DNA fragmentation--are all present 10 and 15 days post-autotomy. The rapid phase of M#133b,c degeneration is also characterized by 'denervation-like' changes in fiber electrophysiology including depolarized resting membrane potentials, post-inhibitory rebound, smaller evoked excitatory junctional potentials and an increased frequency of spontaneous miniature potentials. The initial trigger for autotomy-induced muscle degeneration appears to be the loss of some proprioceptive input, since severing of afferents from the subgenual organ leads to muscle degeneration. The loss of exteroceptive chemo or mechanoreceptor input, however, does not lead to degeneration. Autotomy is also correlated with a decline in activity in the nerve innervating M#133b,c during the period of programmed cell death. The population of active motor units within the nerve is also decreased during this period. These findings suggest the transneuronal mechanisms that influence muscle degeneration following autotomy. The loss of proprioceptive input probably leads to deafferentation of motoneurons within the metathoracic ganglion. The deafferentated motoneurons have a decreased level of spontaneous activity which triggers the subsequent muscle degeneration by programmed cell death.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Biology, Neuroscience.; Biology, Cell.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Graduate College; Physiological Sciences
Degree Grantor:
University of Arizona
Advisor:
Chapman, Reginald F.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleDegeneration of a muscle following remote nerve damage: Physiological changes and triggering mechanismsen_US
dc.creatorPersonius, Kirkwood Ely, 1966-en_US
dc.contributor.authorPersonius, Kirkwood Ely, 1966-en_US
dc.date.issued1998en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractMuscle depends on innervation and contraction to maintain a differentiated state. Denervation or disuse, therefore, often leads to muscle atrophy. In grasshoppers, muscle degeneration can also be induced when a hindlimb is lost by autotomy. In this case, the thoracic muscles which degenerate are neither damaged nor denervated, suggesting the existence of transneuronal mechanisms that influence muscle survival. Arbas and Weidner (1991) found that muscle degeneration is induced when the leg nerve (which does not innervate the thoracic muscles) is severed during autotomy. To characterize this autotomy-induced degenerative process, I studied a thoracic tergotrochanteral depressor muscle (M#133b,c) subsequent to autotomy in the grasshoppers, Barytettix psolus and B. humphreysii. The degeneration of M#133b,c is generally complete by 15 days after autotomy, when muscle cross-sectional area is reduced to 4% of the contralateral-control. The rate of muscle degeneration is initially slow, but at ∼10 days post-autotomy, degeneration becomes rapid and muscle fiber number becomes reduced. During this rapid phase, degeneration of M#133b,c occurs by programmed cell death. Indicators of programmed cell death-up-regulation of ubiquitin--immunoreactivity, condensed nuclear chromatin and DNA fragmentation--are all present 10 and 15 days post-autotomy. The rapid phase of M#133b,c degeneration is also characterized by 'denervation-like' changes in fiber electrophysiology including depolarized resting membrane potentials, post-inhibitory rebound, smaller evoked excitatory junctional potentials and an increased frequency of spontaneous miniature potentials. The initial trigger for autotomy-induced muscle degeneration appears to be the loss of some proprioceptive input, since severing of afferents from the subgenual organ leads to muscle degeneration. The loss of exteroceptive chemo or mechanoreceptor input, however, does not lead to degeneration. Autotomy is also correlated with a decline in activity in the nerve innervating M#133b,c during the period of programmed cell death. The population of active motor units within the nerve is also decreased during this period. These findings suggest the transneuronal mechanisms that influence muscle degeneration following autotomy. The loss of proprioceptive input probably leads to deafferentation of motoneurons within the metathoracic ganglion. The deafferentated motoneurons have a decreased level of spontaneous activity which triggers the subsequent muscle degeneration by programmed cell death.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectBiology, Neuroscience.en_US
dc.subjectBiology, Cell.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplinePhysiological Sciencesen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorChapman, Reginald F.en_US
dc.identifier.proquest9901712en_US
dc.identifier.bibrecord.b38830620en_US
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