scholarly journals Estrogen improved the regeneration of axons after subcortical axon injury via regulation of PI3K/Akt/CDK5/Tau pathway

2020 ◽  
Vol 10 (9) ◽  
Author(s):  
Xiaohui Xia ◽  
Changlong Zhou ◽  
Xiaochuan Sun ◽  
Xuenong He ◽  
Chang Liu ◽  
...  
Keyword(s):  
Axon Injury

scholarly journals Axon Injury and Regeneration in the Adult Drosophila

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Lorena Soares ◽  
Michael Parisi ◽  
Nancy M. Bonini
Keyword(s):  
Axon Injury ◽  
Adult Drosophila

The Response of Microglia to Axon Injury

1997 ◽  
pp. 549-554
Author(s):  
H. Aldskogius ◽  
L. Liu ◽  
N. P. Eriksson ◽  
J. K. E. Persson ◽  
M. Svensson
Keyword(s):  
Axon Injury

scholarly journals Aberrant information transfer interferes with functional axon regeneration

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Chen Ding ◽  
Marc Hammarlund
Keyword(s):  
Information Transfer ◽  
Synapse Formation ◽  
Axon Regeneration ◽  
Behavioral Recovery ◽  
Axon Injury ◽  
Functional Regeneration ◽  
Key Variables ◽  
And Function ◽  
Circuit Function ◽  
Molecular Components

Functional axon regeneration requires regenerating neurons to restore appropriate synaptic connectivity and circuit function. To model this process, we developed an assay in Caenorhabditis elegans that links axon and synapse regeneration of a single neuron to recovery of behavior. After axon injury and regeneration of the DA9 neuron, synapses reform at their pre-injury location. However, these regenerated synapses often lack key molecular components. Further, synaptic vesicles accumulate in the dendrite in response to axon injury. Dendritic vesicle release results in information misrouting that suppresses behavioral recovery. Dendritic synapse formation depends on dynein and jnk-1. But even when information transfer is corrected, axonal synapses fail to adequately transmit information. Our study reveals unexpected plasticity during functional regeneration. Regeneration of the axon is not sufficient for the reformation of correct neuronal circuits after injury. Rather, synapse reformation and function are also key variables, and manipulation of circuit reformation improves behavioral recovery.

scholarly journals Distal axotomy enhances retrograde presynaptic excitability onto injured pyramidal neurons via trans-synaptic signaling

2016 ◽  
Author(s):  
Tharkika Nagendran ◽  
Rylan S. Larsen ◽  
Rebecca L. Bigler ◽  
Shawn B. Frost ◽  
Benjamin D. Philpot ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Spine Density ◽  
Axon Injury ◽  
Synaptic Remodeling ◽  
Nerve Tracts ◽  
Specific Increase ◽  
Microfluidic Chambers

AbstractInjury of CNS nerve tracts remodels circuitry through dendritic spine loss and hyper-excitability, thus influencing recovery. Due to the complexity of the CNS, a mechanistic understanding of injury-induced synaptic remodeling remains unclear. Using microfluidic chambers to separate and injure distal axons, we show that axotomy causes retrograde dendritic spine loss at directly injured pyramidal neurons followed by retrograde presynaptic hyper-excitability. These remodeling events require activity at the site of injury, axon-to-soma signaling, and transcription. Similarly, directly injured corticospinal neurons in vivo also exhibit a specific increase in spiking following axon injury. Axotomy-induced hyper-excitability of cultured neurons coincides with elimination of inhibitory inputs onto injured neurons, including those formed onto dendritic spines. Netrin-1 downregulation occurs following axon injury and exogenous netrin-1 applied after injury normalizes spine density, presynaptic excitability, and inhibitory inputs at injured neurons. Our findings show that intrinsic signaling within damaged neurons regulates synaptic remodeling and involves netrin-1 signaling.

scholarly journals Differential Effects of Unfolded Protein Response Pathways on Axon Injury-Induced Death of Retinal Ganglion Cells

Neuron ◽  
2012 ◽  
Vol 73 (3) ◽  
pp. 445-452 ◽  
Author(s):  
Yang Hu ◽  
Kevin K. Park ◽  
Liu Yang ◽  
Xin Wei ◽  
Qiang Yang ◽  
...  
Keyword(s):  
Unfolded Protein Response ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Axon Injury ◽  
Differential Effects ◽  
Unfolded Protein ◽  
Protein Response

Engineering a High Throughput Axon Injury System

2011 ◽  
Vol 28 (11) ◽  
pp. 2203-2218 ◽  
Author(s):  
George C. Magou ◽  
Yi Guo ◽  
Mridusmita Choudhury ◽  
Linda Chen ◽  
Nicholae Hususan ◽  
...  
Keyword(s):  
High Throughput ◽  
Axon Injury

Systemic inflammation induces axon injury during brain inflammation

2011 ◽  
Vol 70 (6) ◽  
pp. 932-942 ◽  
Author(s):  
Beatriz Moreno ◽  
John-Paul Jukes ◽  
Nuria Vergara-Irigaray ◽  
Oihana Errea ◽  
Pablo Villoslada ◽  
...  
Keyword(s):  
Systemic Inflammation ◽  
Brain Inflammation ◽  
Axon Injury

scholarly journals HSP90 is a chaperone for DLK and is required for axon injury signaling

2018 ◽  
Vol 115 (42) ◽  
pp. E9899-E9908 ◽  
Author(s):  
Scott Karney-Grobe ◽  
Alexandra Russo ◽  
Erin Frey ◽  
Jeffrey Milbrandt ◽  
Aaron DiAntonio
Keyword(s):  
Leucine Zipper ◽  
Axon Regeneration ◽  
Heat Shock Protein 90 ◽  
Hsp90 Inhibitor ◽  
Loss Of Function ◽  
Hsp90 Inhibition ◽  
Axon Injury ◽  
Evolutionarily Conserved ◽  
The Stability

Peripheral nerve injury induces a robust proregenerative program that drives axon regeneration. While many regeneration-associated genes are known, the mechanisms by which injury activates them are less well-understood. To identify such mechanisms, we performed a loss-of-function pharmacological screen in cultured adult mouse sensory neurons for proteins required to activate this program. Well-characterized inhibitors were present as injury signaling was induced but were removed before axon outgrowth to identify molecules that block induction of the program. Of 480 compounds, 35 prevented injury-induced neurite regrowth. The top hits were inhibitors to heat shock protein 90 (HSP90), a chaperone with no known role in axon injury. HSP90 inhibition blocks injury-induced activation of the proregenerative transcription factor cJun and several regeneration-associated genes. These phenotypes mimic loss of the proregenerative kinase, dual leucine zipper kinase (DLK), a critical neuronal stress sensor that drives axon degeneration, axon regeneration, and cell death. HSP90 is an atypical chaperone that promotes the stability of signaling molecules. HSP90 and DLK show two hallmarks of HSP90–client relationships: (i) HSP90 binds DLK, and (ii) HSP90 inhibition leads to rapid degradation of existing DLK protein. Moreover, HSP90 is required for DLK stability in vivo, where HSP90 inhibitor reduces DLK protein in the sciatic nerve. This phenomenon is evolutionarily conserved in Drosophila. Genetic knockdown of Drosophila HSP90, Hsp83, decreases levels of Drosophila DLK, Wallenda, and blocks Wallenda-dependent synaptic terminal overgrowth and injury signaling. Our findings support the hypothesis that HSP90 chaperones DLK and is required for DLK functions, including proregenerative axon injury signaling.

scholarly journals Experimental Glaucoma Causes Optic Nerve Head Neural Rim Tissue Compression: A Potentially Important Mechanism of Axon Injury

2016 ◽  
Vol 57 (10) ◽  
pp. 4403 ◽  
Author(s):  
Brad Fortune ◽  
Juan Reynaud ◽  
Christy Hardin ◽  
Lin Wang ◽  
Ian A. Sigal ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Optic Nerve Head ◽  
Axon Injury ◽  
Experimental Glaucoma ◽  
Tissue Compression
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