scholarly journals Dimethyl Trisulfide Diminishes Traumatic Neuropathic Pain Acting on TRPA1 Receptors in Mice

2021 ◽  
Vol 22 (7) ◽  
pp. 3363
Author(s):  
Ágnes Dombi ◽  
Csenge Sánta ◽  
István Z. Bátai ◽  
Viktória Kormos ◽  
Angéla Kecskés ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Spinal Cord Dorsal Horn ◽  
Nerve Lesion ◽  
Dimethyl Trisulfide ◽  
Macrophage Activity ◽  
Ganglion Neurons

Pharmacotherapy of neuropathic pain is still challenging. Our earlier work indicated an analgesic effect of dimethyl trisulfide (DMTS), which was mediated by somatostatin released from nociceptor nerve endings acting on SST4 receptors. Somatostatin release occurred due to TRPA1 ion channel activation. In the present study, we investigated the effect of DMTS in neuropathic pain evoked by partial ligation of the sciatic nerve in mice. Expression of the mRNA of Trpa1 in murine dorsal-root-ganglion neurons was detected by RNAscope. Involvement of TRPA1 ion channels and SST4 receptors was tested with gene-deleted animals. Macrophage activity at the site of the nerve lesion was determined by lucigenin bioluminescence. Density and activation of microglia in the spinal cord dorsal horn was verified by immunohistochemistry and image analysis. Trpa1 mRNA is expressed in peptidergic and non-peptidergic neurons in the dorsal root ganglion. DMTS ameliorated neuropathic pain in Trpa1 and Sstr4 WT mice, but not in KO ones. DMTS had no effect on macrophage activity around the damaged nerve. Microglial density in the dorsal horn was reduced by DMTS independently from TRPA1. No effect on microglial activation was detected. DMTS might offer a novel therapeutic opportunity in the complementary treatment of neuropathic pain.

scholarly journals An integrated cell isolation and purification method for rat dorsal root ganglion neurons

2019 ◽  
Vol 47 (7) ◽  
pp. 3253-3260
Author(s):  
Huaishuang Shen ◽  
Minfeng Gan ◽  
Huilin Yang ◽  
Jun Zou
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Primary Culture ◽  
Dorsal Root ◽  
Cell Isolation ◽  
Dorsal Root Ganglion Neurons ◽  
Drg Neurons ◽  
Purification Method ◽  
Isolation And Purification ◽  
Ganglion Neurons

Objective Neurobiology studies are increasingly focused on the dorsal root ganglion (DRG), which plays an important role in neuropathic pain. Existing DRG neuron primary culture methods have considerable limitations, including challenging cell isolation and poor cell yield, which cause difficulty in signaling pathway studies. The present study aimed to establish an integrated primary culture method for DRG neurons. Methods DRGs were obtained from fetal rats by microdissection, and then dissociated with trypsin. The dissociated neurons were treated with 5-fluorouracil to promote growth of neurons from the isolated cells. Then, reverse transcription polymerase chain reaction and immunofluorescence assays were used to identify and purify DRG neurons. Results Isolated DRGs were successfully dissociated and showed robust growth as individual DRG neurons in neurobasal medium. Both mRNA and protein assays confirmed that DRG neurons expressed neurofilament-200 and neuron-specific enolase. Conclusions Highly purified, stable DRG neurons could be easily harvested and grown for extended periods by using this integrated cell isolation and purification method, which may help to elucidate the mechanisms underlying neuropathic pain.

Altered tachykinin expression by dorsal root ganglion neurons in a rat model of neuropathic pain

Pain ◽  
1994 ◽  
Vol 58 (2) ◽  
pp. 219-231 ◽  
Author(s):  
James E. Marchand ◽  
Heinrich W. Wurm ◽  
Toshimasa Kato ◽  
Richard M. Kream
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Rat Model ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Ganglion Neurons

scholarly journals The causal role of magnesium deficiency in the neuroinflammation, pain hypersensitivity and memory/emotional deficits in ovariectomized and aging mice

2021 ◽  
Author(s):  
Xian-guo Liu ◽  
Jun Zhang ◽  
Chun-lin Mai ◽  
Ying Xiong ◽  
Zhen-Jia Lin ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Emotional Deficits ◽  
Ganglion Neurons ◽  
Neuronal Disorders

Abstract Background: Postmenopausal women often suffer from chronic pain, memory decline and mood depression. The mechanisms underlying the neuronal disorders are not fully understood and effective treatment is still lacking.Methods: Oral administration of magnesium-L-threonate was tested to treat the neuronal disorders in ovariectomized and aging mice. The pain hypersensitivity, memory function and depression were measured with a set of behavioral tests. Western blots and immunochemistry were used to assess molecular changes.Results: Chronic oral administration of magnesium-L-threonate substantially prevented or reversed the chronic pain, and memory/emotional deficits in both ovariectomized and aging female mice. We found that phospho-p65, an active form of nuclear factor-kappaB, tumor necrosis factor-alpha and interleukin-1beta were significantly upregulated in the neurons of dorsal root ganglion, spinal dorsal horn and hippocampus in ovariectomized and aging mice. The microglia and astrocytes were activated in spinal dorsal horn and hippocampus. The peptidergic C-fibers in dorsal horn were increased, which are associated with potentiation of C-fiber-mediated synaptic transmission in the model mice. In parallel with neuroinflammation and synaptic potentiation, free Mg2+ levels in plasma, cerebrospinal fluid and dorsal root ganglion neurons were significantly reduced. Oral magnesium-L-threonate normalized the neuroinflammation, synaptic potentiation and Mg2+ deficiency, but did not affect the estrogen decline in ovariectomized and aging mice. Furthermore, in cultured dorsal root ganglion neurons estrogen elevated intracellular Mg2+, and depressed the upregulation of phospho-p65, tumor necrosis factor-alpha and interleukin-1beta exclusively in the presence of extracellular Mg2+.Conclusions: Estrogen decline in menopause causes neuroinflammation by reducing intracellular Mg2+ in neurons, leading to chronic pain, memory/emotional deficits. Thus, supplement Mg2+ by oral magnesium-L-threonate may be a novel approach for treating menopause-related neuronal disorders.

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