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Expression of TrkB at the neuromuscu...

State University of New York at Buffalo.

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Expression of TrkB at the neuromuscular junction during aging .

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Expression of TrkB at the neuromuscular junction during aging ./
Author:	Parker-Wegman, Sara D.
Description:	50 p.
Notes:	Adviser: Kirkwood E. Personius.
Contained By:	Masters Abstracts International45-02.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1440025

Expression of TrkB at the neuromuscular junction during aging .
Parker-Wegman, Sara D.

Expression of TrkB at the neuromuscular junction during aging . - 50 p.

Adviser: Kirkwood E. Personius.

Thesis (M.S.)--State University of New York at Buffalo, 2007.

There is increasing evidence that age associated alterations in innervation may underlie many of the changes that occur in skeletal muscle during senescence. Aging of the neuromuscular system is associated with loss of motor neurons, altered neurotransmitter release, disruption of post-synaptic acetylcholine receptor (AChR) organization, denervation and reinnervation of muscle fibers, and motor unit remodeling. Currently the cellular mechanisms involved in the reorganization of neural innervation remain elusive. Experimental evidence supports the role of the neurotrophins, brain derived neurotrophic factor (BDNF) and neurotrophin 4/5 (NT-4/5), and their receptor TrkB, as modulators which influence the morphology and physiological function of the neuromuscular system. Recent work has shown that BDNF and NT-4/5, signaling via TrkB influences maintenance of the post-synaptic apparatus, motor neuron survival, and neuromuscular transmission. Therefore we chose to investigate whether TrkB expression at the neuromuscular junction is altered with aging and if changes in TrkB expression are correlated with disorganization of the neuromuscular junction. Immunohistochemical methods were used to label nerve terminals, AChR's, and TrkB in mouse limb muscle at age 2, 12, or 24 months. AChR area and number of discrete receptor regions were quantified to assess age-associated changes in the post-synaptic neuromuscular junction. The extent of TrkB expression and structural denervation were assessed by determining TrkB/AChR colocalization and nerve terminal/AChR colocalization respectively. As expected the AChR area expanded and fragmented with age. Changes in the soleus were greater than the changes which occurred in the EDL. Nerve terminal/AChR colocalization was decreased in the soleus but not the EDL suggesting that structural denervation was more significant in the soleus. Both EDL and soleus showed decreased TrkB. A significant linear relationship was seen between TrkB/AChR colocalization and nerve terminal/AChR colocalization in both muscle groups, however r2 values were relatively low (r2 = 0.35-0.66). Surprisingly no relationship was seen between TrkB/AChR colocalization and the number of discrete AChR regions. Together this data indicates that a loss of TrkB expression may be one of the mechanisms which contribute to structural alteration of the neuromuscular junction with aging.Subjects--Topical Terms:

1017719
Biology, Molecular.

Expression of TrkB at the neuromuscular junction during aging .
LDR:03297nam 2200289 a 45 001 852100
005 20100629
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035 $a (UMI)AAI1440025
035 $a AAI1440025
040 $a UMI $c UMI
100 1 $a Parker-Wegman, Sara D. $3 1017815
245 1 0 $a Expression of TrkB at the neuromuscular junction during aging .
300 $a 50 p.
500 $a Adviser: Kirkwood E. Personius.
500 $a Source: Masters Abstracts International, Volume: 45-02, page: 0750.
502 $a Thesis (M.S.)--State University of New York at Buffalo, 2007.
520 $a There is increasing evidence that age associated alterations in innervation may underlie many of the changes that occur in skeletal muscle during senescence. Aging of the neuromuscular system is associated with loss of motor neurons, altered neurotransmitter release, disruption of post-synaptic acetylcholine receptor (AChR) organization, denervation and reinnervation of muscle fibers, and motor unit remodeling. Currently the cellular mechanisms involved in the reorganization of neural innervation remain elusive. Experimental evidence supports the role of the neurotrophins, brain derived neurotrophic factor (BDNF) and neurotrophin 4/5 (NT-4/5), and their receptor TrkB, as modulators which influence the morphology and physiological function of the neuromuscular system. Recent work has shown that BDNF and NT-4/5, signaling via TrkB influences maintenance of the post-synaptic apparatus, motor neuron survival, and neuromuscular transmission. Therefore we chose to investigate whether TrkB expression at the neuromuscular junction is altered with aging and if changes in TrkB expression are correlated with disorganization of the neuromuscular junction. Immunohistochemical methods were used to label nerve terminals, AChR's, and TrkB in mouse limb muscle at age 2, 12, or 24 months. AChR area and number of discrete receptor regions were quantified to assess age-associated changes in the post-synaptic neuromuscular junction. The extent of TrkB expression and structural denervation were assessed by determining TrkB/AChR colocalization and nerve terminal/AChR colocalization respectively. As expected the AChR area expanded and fragmented with age. Changes in the soleus were greater than the changes which occurred in the EDL. Nerve terminal/AChR colocalization was decreased in the soleus but not the EDL suggesting that structural denervation was more significant in the soleus. Both EDL and soleus showed decreased TrkB. A significant linear relationship was seen between TrkB/AChR colocalization and nerve terminal/AChR colocalization in both muscle groups, however r2 values were relatively low (r2 = 0.35-0.66). Surprisingly no relationship was seen between TrkB/AChR colocalization and the number of discrete AChR regions. Together this data indicates that a loss of TrkB expression may be one of the mechanisms which contribute to structural alteration of the neuromuscular junction with aging.
590 $a School code: 0656.
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Biology, Physiology. $3 1017816
650 4 $a Health Sciences, General. $3 1017817
690 $a 0307
690 $a 0317
690 $a 0566
690 $a 0719
710 2 $a State University of New York at Buffalo. $3 1017814
773 0 $t Masters Abstracts International $g 45-02.
790 $a 0656
790 1 0 $a Personius, Kirkwood E., $e advisor
791 $a M.S.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1440025