Identification of the Avulsion-Injured Spinal Motoneurons.

J Mol Neurosci

Zhongshan School of Medicine, Sun Yat-sen University, No. 74 Zhongshan Road 2, Guangzhou, 510080, People's Republic of China.

Published: September 2015

In laboratory studies, counting the spinal motoneurons that survived axonal injury is a major method to estimate the severity and regenerative capacity of the injured motoneurons after the axonal injury and rehabilitation surgery. However, the typical motoneuron marker, the choline acetyltransferase (ChAT), could not be detected in the injured motoneurons within the first 3-4 weeks postinjury. It is necessary to explore the useful and reliable specific phenotypic markers to assess the fate of injured motoneurons in axonal injury. Here, we used the fluorogold to retrograde trace the injured motoneurons in the spinal cord and studied the expression patterns of the alpha-motoneuron marker, the neuronal nuclei DNA-binding protein (NeuN) and the peripheral nerve injury marker, the activating transcriptional factor (ATF-3), and the oxidative stress marker, the neuronal nitric oxide synthase (nNOS) within the first 4 weeks of the root avulsion of the right brachial plexus (BPRA) in the adult male Sprague-Dawley rats. Our results showed that ATF-3 was rapidly induced and sustained to express only in the nuclei of the fluorogold-labeled injured motoneurons but none in the unaffected motoneurons from the 24 h of the injury; meanwhile, the NeuN almost disappeared in the avulsion-affected motoneurons within the first 4 weeks. The nNOS was not detected in the motoneurons until the second week of the injury. On the basis of the present data, we suggest that ATF-3 labels avulsion-injured motoneurons while NeuN and nNOS are poor markers within the first 4 weeks of BPRA.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4543425PMC
http://dx.doi.org/10.1007/s12031-015-0588-4DOI Listing

Publication Analysis

Top Keywords

injured motoneurons
20
axonal injury
12
motoneurons
11
spinal motoneurons
8
motoneurons axonal
8
marker neuronal
8
injury
6
injured
5
identification avulsion-injured
4
avulsion-injured spinal
4

Similar Publications

Shh Protects the Injured Spinal Cord in Mice by Promoting the Proliferation and Inhibiting the Apoptosis of Nerve Cells via the Gli1-TGF-β1/ERK Axis.

Cell Biochem Funct

January 2025

Stem Cells & Biotherapy Engineering Research Center of Henan, College of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.

Spinal cord injury (SCI) is a common neurological trauma that cannot be completely cured with surgical techniques and medications. In this study, we established a mouse SCI model and used an adeno-associated virus (AAV) to achieve the high expression of sonic hedgehog (Shh) at the injury site to further investigate the therapeutic effect and mechanism of Shh on SCI. The results of the present study show that Shh may promote motor function recovery.

View Article and Find Full Text PDF

Functional recovery from brain damage, such as stroke, is a plastic process in the brain. The excitatory glutamate -amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) plays a crucial role in neuronal functions, and the synaptic trafficking of AMPAR is a fundamental mechanism underlying synaptic plasticity. We recently identified a collapsin response mediator protein 2 (CRMP2)-binding compound, edonerpic maleate, which augments rehabilitative training-dependent functional recovery from brain damage by facilitating experience-driven synaptic delivery of AMPARs.

View Article and Find Full Text PDF

Acute neuroinflammation, which is notably characterized by a significant elevation in pro-inflammatory cytokines and chemokines, often rapidly develops following a traumatic spinal cord injury and exacerbates damage in the lesion area. This study addresses the limitations inherent in strategies that regulate only a single or a few cytokines, which are often insufficient to counteract the progression of secondary injuries. We explore the use of polydopamine nanoparticles as a broad-spectrum immunomodulator, capable of capturing by adsorption a wide range of cytokines and thereby effectively suppressing neuroinflammation.

View Article and Find Full Text PDF
Article Synopsis
  • The disruption of nerve tissues from spinal cord injury (SCI) can lead to further damage due to immune inflammatory responses involving Toll-like receptors, particularly TLR3, although its specific role in secondary neuronal injury is not fully clear.
  • Researchers created a model using rat motor neurons to apply pressure, discovering that this pressure leads to neuronal damage, cell death, and decreased cell growth, all tied to increased TLR3 expression and its signaling molecules.
  • Targeting TLR3 helped reduce injury and cell death in the neurons, promoting healthier cell processes like autophagy and reducing mitochondrial problems through specific signaling pathways (TLR3/IRF3 and TLR3/NF-κB).
View Article and Find Full Text PDF

Introduction: Spinal cord injury (SCI) can result in sensory and locomotor function loss below the injured segment. Hyperbaric oxygen therapy (HBOT) has been proven to alleviate SCI. This study aims to establish a reproducible rat model of SCI and investigate the impact of HBOT on alterations in brain neuronal activity and neuromotor function in this experimental rat SCI model using resting-state functional magnetic resonance imaging (rs-fMRI).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!