Painful Neuron-Microglia Interactions in the Trigeminal Sensory System~!2009-09-09~!2009-11-23~!2010-05-07~!

Davies, Alexander J.; Kim, Yong Ho; Oh, Seunghee

doi:10.2174/1876386301003020014

Cited by 4 publications

(2 citation statements)

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“…Interestingly, GSE is able to repress the stimulatory effects of CFA in both astrocytes and microglia as demonstrated by reduced levels of GFAP, a structural protein and a marker of astrocyte activation, and OX-42, a marker of activated microglia [57,58]. Enhanced cellular activity of both astrocytes and microglia in the trigeminal system have been implicated in the development of persistent pain states [59]. Thus, it appears that GSE functions to modulate cellular responses to inflammatory stimuli by inhibiting glial cell activation, which in turn, would decrease the excitability state of nociceptive neurons in the TNC.…”

Section: Discussionmentioning

confidence: 99%

Dietary Grape Seed Polyphenols Repress Neuron and Glia Activation in Trigeminal Ganglion and Trigeminal Nucleus Caudalis

2010

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BackgroundInflammation and pain associated with temporomandibular joint disorder, a chronic disease that affects 15% of the adult population, involves activation of trigeminal ganglion nerves and development of peripheral and central sensitization. Natural products represent an underutilized resource in the pursuit of safe and effective ways to treat chronic inflammatory diseases. The goal of this study was to investigate effects of grape seed extract on neurons and glia in trigeminal ganglia and trigeminal nucleus caudalis in response to persistent temporomandibular joint inflammation. Sprague Dawley rats were pretreated with 200 mg/kg/d MegaNatural-BP grape seed extract for 14 days prior to bilateral injections of complete Freund's adjuvant into the temporomandibular joint capsule.ResultsIn response to grape seed extract, basal expression of mitogen-activated protein kinase phosphatase 1 was elevated in neurons and glia in trigeminal ganglia and trigeminal nucleus caudalis, and expression of the glutamate aspartate transporter was increased in spinal glia. Rats on a normal diet injected with adjuvant exhibited greater basal levels of phosphorylated-p38 in trigeminal ganglia neurons and spinal neurons and microglia. Similarly, immunoreactive levels of OX-42 in microglia and glial fibrillary acidic protein in astrocytes were greatly increased in response to adjuvant. However, adjuvant-stimulated levels of phosphorylated-p38, OX-42, and glial fibrillary acidic protein were significantly repressed in extract treated animals. Furthermore, grape seed extract suppressed basal expression of the neuropeptide calcitonin gene-related peptide in spinal neurons.ConclusionsResults from our study provide evidence that grape seed extract may be beneficial as a natural therapeutic option for temporomandibular joint disorders by suppressing development of peripheral and central sensitization.

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Section: Discussionmentioning

confidence: 99%

Dietary Grape Seed Polyphenols Repress Neuron and Glia Activation in Trigeminal Ganglion and Trigeminal Nucleus Caudalis

2010

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“…Nociceptive neurons within the trigeminal ganglion (TG) acquire TN cues and convey them to the TNC [ 4 ]. The pathophysiology of trigeminal pain involves a complex interplay of biological interactions among central nervous system (CNS) resident cells such as neurons, astrocytes, and microglia, like mechanisms observed in spinal neuropathic pain [ 5 ]. The most prevalent glial cells in the CNS, astrocytes, are crucial for maintaining processes notably homeostasis and synapse development [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

GFAP-NpHR mediated optogenetic inhibition of trigeminal nucleus caudalis attenuates hypersensitive behaviors and thalamic discharge attributed to infraorbital nerve constriction injury

KC,

Islam,

Kim

et al. 2023

J Headache Pain

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The significance of hyperactive astrocytes in neuropathic pain is crucial. However, the association between medullary astrocytes and trigeminal neuralgia (TN)-related pain processing is unclear. Here, we examined how optogenetic inhibition of medullary astrocytes in the trigeminal nucleus caudalis (TNC) regulates pain hypersensitivity in an infraorbital nerve (ION) constricted TN model. We used adult Sprague Dawley rats subjected to infraorbital nerve (ION) constriction to mimic TN symptoms, with naive and sham rats serving as controls. For in vivo optogenetic manipulations, rats stereotaxically received AAV8-GFAP-eNpHR3.0-mCherry or AAV8-GFAP-mCherry at the trigeminal nucleus caudalis (TNC). Open field, von Frey, air puff, and acetone tests measured pain behavioral flexibility. In vivo thalamic recordings were obtained simultaneously with optogenetic manipulation in the TNC. Orofacial hyperalgesia and thalamic hyperexcitability were both accompanied by medullary astrocyte hyperactivity, marked by upregulated GFAP. The yellow laser-driven inhibition of TNC astrocytes markedly improved behavioral responses and regulated thalamic neuronal responses. Halorhodopsin-mediated inhibition in medullary astrocytes may modify the nociceptive input transmitted through the trigeminothalamic tract and pain perception. Taken together, these findings imply that this subpopulation in the TNC and its thalamic connections play a significant role in regulating the trigeminal pain circuitry, which might aid in the identification of new therapeutic measures in TN management. Graphical Abstract

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Blockage of the fractalkine pathway reduces hyperalgesia and prevents morphological glial alterations—Comparison between inflammatory and neuropathic orofacial pain in male rats

Lisboa,

Pereira,

Alves

et al. 2023

J of Neuroscience Research

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This study aimed to evaluate the effects of inhibitors of the fractalkine pathway in hyperalgesia in inflammatory and neuropathic orofacial pain in male rats and the morphological changes in microglia and satellite glial cells (SGCs). Rats were submitted to zymosan‐induced arthritis of the temporomandibular joint or infraorbital nerve constriction, and treated intrathecally with a P2X7 antagonist, a cathepsin S inhibitor or a p‐38 mitogen‐activated protein kinase (MAPK) inhibitor. Mechanical hyperalgesia was evaluated 4 and 6 h following arthritis induction or 7 and 14 days following nerve ligation. The expression of the receptor CX3CR1, phospho‐p‐38 MAPK, ionized calcium‐binding adapter molecule‐1 (Iba‐1), and glutamine synthetase and the morphological changes in microglia and SGCs were evaluated by confocal microscopy. In both inflammatory and neuropathic models, untreated animals presented a higher expression of CX3CR1 and developed hyperalgesia and up‐regulation of phospho‐p‐38 MAPK, which was prevented by all drugs (p < .05). The number of microglial processes endpoints and the total branch length were lower in the untreated animals, but the overall immunolabeling of Iba‐1 was altered only in neuropathic rats (p < .05). The mean area of SGCs per neuron was significantly altered only in the inflammatory model (p < .05). All morphological alterations were reverted by modulating the fractalkine pathway (p < .05). In conclusion, the blockage of the fractalkine pathway seemed to be a possible therapeutic strategy for inflammatory and neuropathic orofacial pain, reducing mechanical hyperalgesia by impairing the phosphorylation of p‐38 MAPK and reverting morphological alterations in microglia and SGCs.

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Painful Neuron-Microglia Interactions in the Trigeminal Sensory System~!2009-09-09~!2009-11-23~!2010-05-07~!

Cited by 4 publications

References 0 publications

Dietary Grape Seed Polyphenols Repress Neuron and Glia Activation in Trigeminal Ganglion and Trigeminal Nucleus Caudalis

Dietary Grape Seed Polyphenols Repress Neuron and Glia Activation in Trigeminal Ganglion and Trigeminal Nucleus Caudalis

GFAP-NpHR mediated optogenetic inhibition of trigeminal nucleus caudalis attenuates hypersensitive behaviors and thalamic discharge attributed to infraorbital nerve constriction injury

Blockage of the fractalkine pathway reduces hyperalgesia and prevents morphological glial alterations—Comparison between inflammatory and neuropathic orofacial pain in male rats

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