Methylprednisolone blocks interleukin 1 beta induced calcitonin gene related peptide release in trigeminal ganglia cells

Neeb, Lars; Hellen, Peter; Hoffmann, J.; Dirnagl, Ulrich; Reuter, Uwe

doi:10.1186/s10194-016-0609-x

Cited by 28 publications

(23 citation statements)

References 38 publications

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“…31 A previous in vivo study suggested that IL-1β can promote powerful activation and mechanical sensitization of meningeal nociceptors and direct application of IL-6 to the dura produced a dose-dependent facial and hind-paw allodynia. 13,33 Another study demonstrated that local administration of TNF-α promoted an increase in the responses of meningeal nociceptors to mechanical stimulation of their dural receptive field and neuronal discharges. 34 In in vitro studies, it has been observed that TNF-α can promote the expression of CGRP and BDNF in trigeminal neurons.…”

Section: Discussionmentioning

confidence: 99%

<p>Electroacupuncture Inhibits Hyperalgesia by Alleviating Inflammatory Factors in a Rat Model of Migraine</p>

Zhao¹,

Liu²,

Xu³

et al. 2020

JPR

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Objective: Acupuncture has a therapeutic effect similar to that of prophylactic drugs and can be considered a treatment option for migraineurs. However, the mechanism of acupuncture treatment's effect on migraine is uncertain. An approach based on anti-inflammatory effects is an important treatment strategy for migraine because non-steroidal anti-inflammatory drugs (NSAIDs) are usually used during migraine attacks. Meningeal inflammation is thought to be responsible for the activation of the trigeminovascular system. Our previous study found that electroacupuncture (EA) decreased neurogenic inflammation mediator expression in the trigeminal ganglion (TG) and alleviated hyperalgesia. The present study examined whether EA would inhibit hyperalgesia by alleviating neurogenic inflammatory factors.Methods: A rat model of migraine was established using dural electrical stimulation (DES). Five groups were analyzed in this study. The Model group received DES three times to mimic migraine attacks, a Control group had sham DES, and three groups received electroacupuncture after DES: a Non-Acu group at a non-acupuncture point, a GB20 group at GB20, and a GB20/34 group at GB20 and GB34 acupuncture points. We evaluated mechanical hyperalgesia using an electronic von Frey esthesiometer in the awake state. After sacrifice, the dura mater was analyzed using immunofluorescence. Serum calcitonin gene-related peptide, cyclooxygenase-2, brainderived neurotrophic factor, IL-1β, IL-6, and TNF levels were determined using enzymelinked immunosorbent assays to evaluate the anti-inflammatory effect of acupuncture. Results: After repeated DES, we observed facial and hind paw mechanical hyperalgesia, which was inhibited by electroacupuncture. Electrical stimulation increased the number of mast cells and macrophages and serum levels of inflammatory factors. GB20 and GB20/34 electroacupuncture significantly decreased the number of mast cells and macrophages and serum levels of inflammatory factors. Moreover, electroacupuncture at GB20/34 was superior to that at GB20 alone in inhibiting hyperalgesia and alleviating inflammatory factors. Conclusion: Electroacupuncture inhibits DES-induced hyperalgesia by alleviating inflammatory factors. Inhibition of dural mast cells, macrophages, and serum inflammatory factors may be one of the mechanisms involved in acupuncture treatment's effect on migraine.

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Section: Discussionmentioning

confidence: 99%

<p>Electroacupuncture Inhibits Hyperalgesia by Alleviating Inflammatory Factors in a Rat Model of Migraine</p>

Zhao¹,

Liu²,

Xu³

et al. 2020

JPR

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“…The release of vasoactive neuropeptides, in particular CGRP from both central and peripheral trigeminal terminals modulates the activity of second order neurons of the trigeminal nucleus caudalis [ 39 ] and increases meningeal blood flow [ 9 , 35 ]. Hence, measurements of the changes in dural blood flow in vivo, and the release of CGRP from meningeal sensory nerves in vitro, are reliable indicators of the activation of trigeminal nociceptive primary sensory neurons [ 9 , 40 – 42 ]. Endovanilloids are defined as endogenous ligands of the TRPV1 receptor and are synthetized or may be taken up by sensory ganglion neurons [ 30 , 43 ].…”

Section: Discussionmentioning

confidence: 99%

Endovanilloids are potential activators of the trigeminovascular nocisensor complex

et al. 2016

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BackgroundIn the dura mater encephali a significant population of trigeminal afferents coexpress the nociceptive ion channel transient receptor potential vanilloid type 1 (TRPV1) receptor and calcitonin gene-related peptide (CGRP). Release of CGRP serves the central transmission of sensory information, initiates local tissue reactions and may also sensitize the nociceptive pathway. To reveal the possible activation of meningeal TRPV1 receptors by endogenously synthetized agonists, the effects of arachidonylethanolamide (anandamide) and N-arachidonoyl-dopamine (NADA) were studied on dural vascular reactions and meningeal CGRP release.MethodsChanges in meningeal blood flow were measured with laser Doppler flowmetry in a rat open cranial window preparation following local dural applications of anandamide and NADA. The release of CGRP evoked by endovanilloids was measured with ELISA in an in vitro dura mater preparation.ResultsTopical application of NADA induced a significant dose-dependent increase in meningeal blood flow that was markedly inhibited by pretreatments with the TRPV1 antagonist capsazepine, the CGRP antagonist CGRP8–37, or by prior systemic capsaicin desensitization. Administration of anandamide resulted in minor increases in meningeal blood flow that was turned into vasoconstriction at the higher concentration. In the in vitro dura mater preparation NADA evoked a significant increase in CGRP release. Cannabinoid CB1 receptors of CGRP releasing nerve fibers seem to counteract the TRPV1 agonistic effect of anandamide in a dose-dependent fashion, a result which is confirmed by the facilitating effect of CB1 receptor inhibition on CGRP release and its reversing effect on the blood flow.ConclusionsThe present findings demonstrate that endovanilloids are potential activators of meningeal TRPV1 receptors and, consequently the trigeminovascular nocisensor complex that may play a significant role in the pathophysiology of headaches. The results also suggest that prejunctional CB1 receptors may modulate meningeal vascular responses.

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“…106 In rat models of abdominal surgery and of parasite infection, significant changes in IL-1β and microglia activation were detected in the brain 3 weeks after insult, but changes in IL-6 were not detected. 107,108 Although we did not observe an IL-6 response, it is intriguing that IL-1β, 99,109 IL-6, 110,111 TNF-α, 112,113 IL-10, and TGF-β 114 have all been linked to pain mechanisms or headaches via calcitonin gene-related peptide. Post-traumatic headaches can increase the amount of time needed for cognitive recovery from TBI, 115 are often part of PCS, 26 and can be associated with sensory hypersensitivity 24 and inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 67%

Selective Reduction of Brain Docosahexaenoic Acid after Experimental Brain Injury and Mitigation of Neuroinflammatory Outcomes with Dietary DHA

Butt¹,

Harrison

Rowe

et al. 2017

Curr Res Concussion

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Background Docosahexaenoic acid (DHA) is an omega-3 fatty acid that is important for brain development and function, but the interactions of dietary DHA with fatty acid profiles, sensory sensitivities, and inflammation that may change after traumatic brain injury (TBI) are poorly understood. It is also unknown whether DHA alters experimental TBI outcomes measured more than 2 weeks after injury. The current study investigated whether dietary DHA, provided before (PreDHA) or after (PostDHA) experimental TBI, would improve outcomes for up to 24 days after injury. Methods Rats consumed predetermined diets for 28 days prior to midline fluid percussion injury (mFPI) or to sham surgery. The effects of PreDHA, TBI, and PostDHA on comprehensive fatty acid profiles, neuroinflammation, sensory sensitivity, and spatial learning were then evaluated. Results The results provided novel evidence that TBI selectively reduced brain DHA content, as injury did not decrease any other fatty acid that was measured. Furthermore, PreDHA and PostDHA attenuated injury-induced increases in sensory sensitivity as well as in tumor necrosis factor-α (TNF-α), interleukin-10, and interleukin-1β in the somatosensory cortex. However, [3 H]PK11195 autoradiography showed that PostDHA

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Methylprednisolone blocks interleukin 1 beta induced calcitonin gene related peptide release in trigeminal ganglia cells

Cited by 28 publications

References 38 publications

<p>Electroacupuncture Inhibits Hyperalgesia by Alleviating Inflammatory Factors in a Rat Model of Migraine</p>

<p>Electroacupuncture Inhibits Hyperalgesia by Alleviating Inflammatory Factors in a Rat Model of Migraine</p>

Endovanilloids are potential activators of the trigeminovascular nocisensor complex

Selective Reduction of Brain Docosahexaenoic Acid after Experimental Brain Injury and Mitigation of Neuroinflammatory Outcomes with Dietary DHA

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