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Astrocytes in development and in the injured CNS McGraw, John
Abstract
After a traumatic injury to the brain or spinal cord, the adult mammalian central nervous system (CNS) has a limited ability to repair itself. The reasons why CNS neurons are unable to grow and make functional connections after injury are beginning to be elucidated. There is evidence to suggest that both the intrinsic response of the neuron to injury and the environment the surrounding injured neuron contribute to the absence of anatomical and functional recovery after axotomy. In the developing chick embryo, the onset of myelination by oligodendrocytes is associated with a transition from a growth V permissive to a growth restrictive extraneuronal environment. This thesis examined the development of astrocytes, another glial cell, in chick development. Astrocytes begin to show a differentiated phenotype at embryonic day 12, which is just prior to the onset of myelination. In the adult, reactive astrocytes are a prominent feature of the glial scar that forms after injury. Although it has never been proven, the astroglial scar is less permissive to axonal growth than the surrounding CNS environment. It was the aim of my research to investigate different methods of reducing or removing the astroglial scar after a spinal cord injury in the adult rat. These approaches included 1) targeted antibody and complement-mediated lysis of astrocytes, 2) the reduction of transforming growth factor beta and 3) the ablation of astrocytes using 1-alpha aminoadipate (L-AAA). Of all these treatments, L-AAA was found to be the most successful at removing astrocytes from the site of injury over a one-week period. In the future, L-AAA may be useful in the investigation of the role astrocyte have in CNS development and regeneration after injury.
Item Metadata
Title |
Astrocytes in development and in the injured CNS
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
1999
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Description |
After a traumatic injury to the brain or spinal cord, the adult mammalian central nervous
system (CNS) has a limited ability to repair itself. The reasons why CNS neurons are
unable to grow and make functional connections after injury are beginning to be
elucidated. There is evidence to suggest that both the intrinsic response of the neuron to
injury and the environment the surrounding injured neuron contribute to the absence of
anatomical and functional recovery after axotomy. In the developing chick embryo, the
onset of myelination by oligodendrocytes is associated with a transition from a growth
V
permissive to a growth restrictive extraneuronal environment. This thesis examined the
development of astrocytes, another glial cell, in chick development. Astrocytes begin to
show a differentiated phenotype at embryonic day 12, which is just prior to the onset of
myelination. In the adult, reactive astrocytes are a prominent feature of the glial scar that
forms after injury. Although it has never been proven, the astroglial scar is less
permissive to axonal growth than the surrounding CNS environment. It was the aim of
my research to investigate different methods of reducing or removing the astroglial scar
after a spinal cord injury in the adult rat. These approaches included 1) targeted antibody
and complement-mediated lysis of astrocytes, 2) the reduction of transforming growth
factor beta and 3) the ablation of astrocytes using 1-alpha aminoadipate (L-AAA). Of all
these treatments, L-AAA was found to be the most successful at removing astrocytes
from the site of injury over a one-week period. In the future, L-AAA may be useful in
the investigation of the role astrocyte have in CNS development and regeneration after
injury.
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Extent |
6372737 bytes
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Genre | |
Type | |
File Format |
application/pdf
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Language |
eng
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Date Available |
2009-07-14
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0089619
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Graduation Date |
1999-11
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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Item Media
Item Citations and Data
Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.