Tetramethylpyrazine attenuates periorbital allodynia and neuroinflammation in a model of traumatic brain injury

Wang, Zhijing; Wang, Qi; Wang, Cuijie; Xu, Xiuzhen; Yu, Hongmei

doi:10.1186/s12950-017-0161-8

Cited by 24 publications

(13 citation statements)

References 25 publications

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“…Third, although minimally invasive, the model does require a skin incision a couple of days prior to testing. A review of literature suggests that studies with a scalp incision, such as the one used to implant the coverslip a few days prior to testing in our study, generally yield lower thresholds than those without an incision 25,63–68 . In addition, lower absolute thresholds in our study may also be related to the ascending rather than up‐down method of allodynia assessment that we used to reduce testing times and avoid sensitization 26,37,69 .…”

Section: Discussionmentioning

confidence: 69%

Optogenetic Spreading Depression Elicits Trigeminal Pain and Anxiety Behavior

Harriott

Chung

Uner

et al. 2020

Annals of Neurology

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Objective Cortical spreading depression (SD) is an intense depolarization underlying migraine aura. Despite the weight of evidence linking SD to the pain phase of migraine, controversy remains over a causal role of SD in cephalgia because of the invasive nature of previous SD induction methods. To overcome this problem, we used a novel minimally invasive optogenetic SD induction method and examined the effect of SD on behavior. Methods Optogenetic SD was induced as a single event or repeatedly every other day for 2 weeks. End points, including periorbital and hindpaw mechanical allodynia, mouse grimace, anxiety, and working memory, were examined in male and female mice. Results A single SD produced bilateral periorbital mechanical allodynia that developed within 1 hour and resolved within 2 days. Sumatriptan prevented periorbital allodynia when administered immediately after SD. Repeated SDs also produced bilateral periorbital allodynia that lasted 4 days and resolved within 2 weeks after the last SD. In contrast, the hindpaw withdrawal thresholds did not change after repeated SDs suggesting that SD‐induced allodynia was limited to the trigeminal region. Moreover, repeated SDs increased mouse grimace scores 2 days after the last SD, whereas a single SD did not. Repeated SDs also increased thigmotaxis scores as a measure of anxiety. In contrast, neither single nor repeated SDs affected visuospatial working memory. We did not detect sexual dimorphism in any end point. Interpretation Altogether, these data show a clinically congruent causal relationship among SD, trigeminal pain, and anxiety behavior, possibly reflecting SD modulation of hypothalamic, thalamic, and limbic mechanisms. ANN NEUROL 2021;89:99–110

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Section: Discussionmentioning

confidence: 69%

Optogenetic Spreading Depression Elicits Trigeminal Pain and Anxiety Behavior

Harriott

Chung

Uner

et al. 2020

Annals of Neurology

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“…CGRP has been implicated to be involved in the response to brain tissue damage [ 146 ] and various alterations in CGRP levels have been reported following trauma [ 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 ]. Following focal TBI in newborn piglets, a decrease in CGRP production was observed [ 147 , 148 ], a finding corroborated in focal murine TBI reporting decreased CGRP levels from 3 to 14 days post-trauma [ 153 ]. However, in direct contrast, focal rodent trauma lead to elevated plasma CGRP levels following trauma that peaked at 3 days and remained elevated at 7 days post-TBI [ 150 ].…”

Section: Neurogenic Inflammation In the Cnsmentioning

confidence: 99%

The Role of Neurogenic Inflammation in Blood-Brain Barrier Disruption and Development of Cerebral Oedema Following Acute Central Nervous System (CNS) Injury

Sorby-Adams

Marcoionni

Dempsey

et al. 2017

IJMS

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Acute central nervous system (CNS) injury, encompassing traumatic brain injury (TBI) and stroke, accounts for a significant burden of morbidity and mortality worldwide, largely attributable to the development of cerebral oedema and elevated intracranial pressure (ICP). Despite this, clinical treatments are limited and new therapies are urgently required to improve patient outcomes and survival. Originally characterised in peripheral tissues, such as the skin and lungs as a neurally-elicited inflammatory process that contributes to increased microvascular permeability and tissue swelling, neurogenic inflammation has now been described in acute injury to the brain where it may play a key role in the secondary injury cascades that evolve following both TBI and stroke. In particular, release of the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) appear to be critically involved. In particular, increased SP expression is observed in perivascular tissue following acute CNS injury, with the magnitude of SP release being related to both the frequency and degree of the insult. SP release is associated with profound blood-brain barrier disruption and the subsequent development of vasogenic oedema, as well as neuronal injury and poor functional outcomes. Inhibition of SP through use of a neurokinin 1 (NK1) antagonist is highly beneficial following both TBI and ischaemic stroke in pre-clinical models. The role of CGRP is more unclear, especially with respect to TBI, with both elevations and reductions in CGRP levels reported following trauma. However, a beneficial role has been delineated in stroke, given its potent vasodilatory effects. Thus, modulating neuropeptides represents a novel therapeutic target in the treatment of cerebral oedema following acute CNS injury.

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“…For example, Fu et al (13) found an antidepressant effect of TMP in a chronic unpredictable mild stress mouse model via the suppression of the Toll-like receptor 4 inflammatory signaling pathway. In addition, Wang et al (14) demonstrated that TMP exerts a protective role against traumatic brain injury by attenuating neuroinflammation. Thus, it was hypothesized that TMP may regulate the inflammatory reaction in isoflurane-induced cognitive dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Tetramethylpyrazine ameliorates isoflurane‑induced cognitive dysfunction by inhibiting neuroinflammation via miR‑150 in rats

Cui¹,

Zhang²,

Qu³

2020

Exp Ther Med

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Tetramethylpyrazine (TMP) has neuroprotective effects in the pathogenesis of some human diseases, such as Parkinson's disease. The present study aimed to investigate the role of TMP in isoflurane-induced cognitive dysfunction in rats, and further identify the mechanisms involved in the protective effects of TMP. The Morris water maze test was used to evaluate the cognitive function of rats exposed to isoflurane or treated with TMP. ELISA was conducted to evaluate the effects of isoflurane or TMP on neuroinflammation. The expression of microRNA-150 (miR-150) was measured using reverse transcription-quantitative PCR, and the potential target genes of miR-150 were predicted and verified. The impaired cognitive function induced by isoflurane in the rats was significantly ameliorated by treatment with TMP. In addition, TMP treatment in rats attenuated neuroinflammation caused by isoflurane. The expression of miR-150 was inhibited by isoflurane exposure, but was enhanced by TMP treatment in rats. Furthermore, the overexpression of miR-150 alleviated the isoflurane-induced cognitive dysfunction and neuroinflammation, while the neuroprotective effects of TMP were significantly abrogated by the knockdown of miR-150. AKT3 was a direct target of miR-150, and its mRNA expression was significantly decreased by the overexpression of miR-150 in isoflurane-and TMP-treated rats. These results demonstrated the protective effects of TMP against isoflurane-induced cognitive dysfunction, which were achieved by attenuating neuroinflammation via the regulation of the miR-150/AKT3 pathway. In addition, miR-150 may serve as a novel therapeutic target for the alleviation of cognitive dysfunction induced by anesthetics.

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Tetramethylpyrazine attenuates periorbital allodynia and neuroinflammation in a model of traumatic brain injury

Cited by 24 publications

References 25 publications

Optogenetic Spreading Depression Elicits Trigeminal Pain and Anxiety Behavior

Optogenetic Spreading Depression Elicits Trigeminal Pain and Anxiety Behavior

The Role of Neurogenic Inflammation in Blood-Brain Barrier Disruption and Development of Cerebral Oedema Following Acute Central Nervous System (CNS) Injury

Tetramethylpyrazine ameliorates isoflurane‑induced cognitive dysfunction by inhibiting neuroinflammation via miR‑150 in rats

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