scholarly journals Peripheral sensory neuron injury contributes to neuropathic pain in experimental autoimmune encephalomyelitis

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
I-Ching Wang ◽  
Chen-Yen Chung ◽  
Fang Liao ◽  
Chih-Cheng Chen ◽  
Cheng-Han Lee
Keyword(s):  
Neuropathic Pain ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Sensory Neuron ◽  
Autoimmune Encephalomyelitis ◽  
Peripheral Sensory ◽  
Neuron Injury ◽  
Experimental Autoimmune

scholarly journals Cathepsin E in neutrophils contributes to the generation of neuropathic pain in experimental autoimmune encephalomyelitis

Pain ◽  
2019 ◽  
Vol 160 (9) ◽  
pp. 2050-2062 ◽  
Author(s):  
Yuka Harada ◽  
Jing Zhang ◽  
Kazuhisa Imari ◽  
Ryo Yamasaki ◽  
Junjun Ni ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Autoimmune Encephalomyelitis ◽  
Cathepsin E ◽  
Experimental Autoimmune

scholarly journals Elevated Expression of Fractalkine (CX3CL1) and Fractalkine Receptor (CX3CR1) in the Dorsal Root Ganglia and Spinal Cord in Experimental Autoimmune Encephalomyelitis: Implications in Multiple Sclerosis-Induced Neuropathic Pain

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Wenjun Zhu ◽  
Crystal Acosta ◽  
Brian MacNeil ◽  
Claudia Cortes ◽  
Howard Intrater ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Neuropathic Pain ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Protein Expression ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Autoimmune Encephalomyelitis ◽  
Receptor Cx3cr1 ◽  
Experimental Autoimmune

Multiple sclerosis (MS) is a central nervous system (CNS) disease resulting from a targeted autoimmune-mediated attack on myelin proteins in the CNS. The release of Th1 inflammatory mediators in the CNS activates macrophages, antibodies, and microglia resulting in myelin damage and the induction of neuropathic pain (NPP). Molecular signaling through fractalkine (CX3CL1), a nociceptive chemokine, via its receptor (CX3CR1) is thought to be associated with MS-induced NPP. An experimental autoimmune encephalomyelitis (EAE) model of MS was utilized to assess time dependent gene and protein expression changes of CX3CL1 and CX3CR1. Results revealed significant increases in mRNA and the protein expression of CX3CL1 and CX3CR1 in the dorsal root ganglia (DRG) and spinal cord (SC) 12 days after EAE induction compared to controls. This increased expression correlated with behavioural thermal sensory abnormalities consistent with NPP. Furthermore, this increased expression correlated with the peak neurological disability caused by EAE induction. This is the first study to identify CX3CL1 signaling through CX3CR1 via the DRG /SC anatomical connection that represents a critical pathway involved in NPP induction in an EAE model of MS.

scholarly journals Involvement of advillin in somatosensory neuron subtype-specific axon regeneration and neuropathic pain

2018 ◽  
Vol 115 (36) ◽  
pp. E8557-E8566 ◽  
Author(s):  
Yu-Chia Chuang ◽  
Cheng-Han Lee ◽  
Wei-Hsin Sun ◽  
Chih-Cheng Chen
Keyword(s):  
Neuropathic Pain ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Focal Adhesion ◽  
Growth Cone ◽  
Axon Regeneration ◽  
Spinal Cord Dorsal Horn ◽  
Drg Neurons ◽  
Autoimmune Encephalomyelitis ◽  
Cone Formation ◽  
Experimental Autoimmune

Advillin is a sensory neuron-specific actin-binding protein expressed at high levels in all types of somatosensory neurons in early development. However, the precise role of advillin in adulthood is largely unknown. Here we reveal advillin expression restricted to isolectin B4-positive (IB4+) neurons in the adult dorsal root ganglia (DRG). Advillin knockout (KO) specifically impaired axonal regeneration in adult IB4+ DRG neurons. During axon regeneration, advillin was expressed at the very tips of filopodia and modulated growth cone formation by interacting with and regulating focal-adhesion–related proteins. The advillin-containing focal-adhesion protein complex was shed from neurite tips during neurite retraction and was detectable in cerebrospinal fluid in experimental autoimmune encephalomyelitis, oxaliplatin-induced peripheral neuropathy, and chronic constriction injury of the sciatic nerve. In addition, advillin KO disturbed experimental autoimmune encephalomyelitis-induced neural plasticity in the spinal-cord dorsal horn and aggravated neuropathic pain. Our study highlights a role for advillin in growth cone formation, axon regeneration, and neuropathic pain associated with IB4+ DRG neurons in adulthood.

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