IGF-I specifically enhances axon outgrowth of corticospinal motor neurons

2006 ◽  
Vol 9 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
P Hande Özdinler ◽  
Jeffrey D Macklis
Keyword(s):  
Motor Neurons ◽  
Axon Outgrowth ◽  
Igf I ◽  
Corticospinal Motor Neurons

scholarly journals Poor Corticospinal Motor Neuron Health Is Associated with Increased Symptom Severity in the Acute Phase Following Repetitive Mild TBI and Predicts Early ALS Onset in Genetically Predisposed Rodents

2021 ◽  
Vol 11 (2) ◽  
pp. 160
Author(s):  
Mor R. Alkaslasi ◽  
Noell E. Cho ◽  
Navpreet K. Dhillon ◽  
Oksana Shelest ◽  
Patricia S. Haro-Lopez ◽  
...  
Keyword(s):  
Risk Factor ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Disease Onset ◽  
Poor Health ◽  
Disease Symptoms ◽  
Established Risk Factor ◽  
Early Injury ◽  
Corticospinal Motor Neurons ◽  
Lateral Sclerosis

Traumatic brain injury (TBI) is a well-established risk factor for several neurodegenerative disorders including Alzheimer’s disease and Parkinson’s disease, however, a link between TBI and amyotrophic lateral sclerosis (ALS) has not been clearly elucidated. Using the SOD1G93A rat model known to recapitulate the human ALS condition, we found that exposure to mild, repetitive TBI lead ALS rats to experience earlier disease onset and shortened survival relative to their sham counterparts. Importantly, increased severity of early injury symptoms prior to the onset of ALS disease symptoms was linked to poor health of corticospinal motor neurons and predicted worsened outcome later in life. Whereas ALS rats with only mild behavioral injury deficits exhibited no observable changes in corticospinal motor neuron health and did not present with early onset or shortened survival, those with more severe injury-related deficits exhibited alterations in corticospinal motor neuron health and presented with significantly earlier onset and shortened lifespan. While these studies do not imply that TBI causes ALS, we provide experimental evidence that head injury is a risk factor for earlier disease onset in a genetically predisposed ALS population and is associated with poor health of corticospinal motor neurons.

scholarly journals Corticospinal Motor Neurons Are Susceptible to Increased ER Stress and Display Profound Degeneration in the Absence of UCHL1 Function

2015 ◽  
Vol 25 (11) ◽  
pp. 4259-4272 ◽  
Author(s):  
Javier H. Jara ◽  
Barış Genç ◽  
Gregory A. Cox ◽  
Martha C. Bohn ◽  
Raymond P. Roos ◽  
...  
Keyword(s):  
Er Stress ◽  
Motor Neurons ◽  
Corticospinal Motor Neurons

Free insulin-like growth factor (IGF)-I and IGF binding proteins 2, 5, and 6 in spinal motor neurons in amyotrophic lateral sclerosis

The Lancet ◽  
2003 ◽  
Vol 361 (9362) ◽  
pp. 1007-1011 ◽  
Author(s):  
Nadine Wilczak ◽  
Rob AI de Vos ◽  
Jacques De Keyser
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Growth Factor ◽  
Motor Neurons ◽  
Igf Binding Proteins ◽  
Spinal Motor Neurons ◽  
Spinal Motor ◽  
Free Insulin ◽  
Igf I ◽  
Igf Binding ◽  
Lateral Sclerosis

Delayed application of IGF-I and GDNF can rescue already injured postnatal motor neurons

Neuroreport ◽  
2001 ◽  
Vol 12 (11) ◽  
pp. 2531-2535 ◽  
Author(s):  
Masako M. Bilak ◽  
Ralph W. Kuncl
Keyword(s):  
Motor Neurons ◽  
Igf I

scholarly journals Neurogenesis of corticospinal motor neurons extending spinal projections in adult mice

2004 ◽  
Vol 101 (46) ◽  
pp. 16357-16362 ◽  
Author(s):  
J. Chen ◽  
S. S. P. Magavi ◽  
J. D. Macklis
Keyword(s):  
Motor Neurons ◽  
Adult Mice ◽  
Corticospinal Motor Neurons

scholarly journals Harmonization of L1CAM Expression Facilitates Axon Outgrowth and Guidance of a Motor Neuron

2020 ◽  
Author(s):  
Tessa Sherry ◽  
Hannah R. Nicholas ◽  
Roger Pocock
Keyword(s):  
Motor Neurons ◽  
Single Neuron ◽  
Early Adulthood ◽  
Axon Outgrowth ◽  
Axonal Development ◽  
Axon Development ◽  
Axonal Defects ◽  
Multiple Signaling ◽  
L1 Cell Adhesion Molecule ◽  
L1cam Expression

ABSTRACTBrain development requires precise regulation of axon outgrowth, guidance and termination by multiple signaling and adhesion molecules. How the expression of these neurodevelopmental regulators is transcriptionally controlled is poorly understood. The Caenorhabditis elegans SMD motor neurons terminate axon outgrowth upon sexual maturity and partially retract their axons during early adulthood. Here we show that C-Terminal Binding Protein-1 (CTBP-1), a transcriptional corepressor, is required for correct SMD axonal development. Loss of CTBP-1 causes multiple defects in SMD axon development: premature outgrowth, defective guidance, delayed termination and absence of retraction. CTBP-1 controls SMD axon development by repressing the expression of SAX-7 – a L1 cell adhesion molecule (L1CAM). CTBP-1-regulated repression is crucial as deregulated SAX-7/L1CAM causes aberrant SMD axons. We found that axonal defects caused by SAX-7/L1CAM misexpression are dependent on a distinct L1CAM, called LAD-2, which itself plays a parallel role in SMD axon guidance. Our results reveal that harmonization of L1CAM expression controls the development and maturation of a single neuron.

Purification and Culture of Corticospinal Motor Neurons

2014 ◽  
Vol 2014 (4) ◽  
pp. pdb.top070938 ◽  
Author(s):  
Wim Mandemakers
Keyword(s):  
Motor Neurons ◽  
Corticospinal Motor Neurons
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