Calcitonin gene-related peptide facilitates sensitization of the vestibular nucleus in a rat model of chronic migraine

Yun, Zhong; Zhang, Yixin; Tian, Kangkai; Wang, Yunfeng; Fan, Xiaoping; Pan, Qi; Qin, Guangcheng; Zhang, Dunke; Chen, Lixue; Zhou, Jiying

doi:10.1186/s10194-020-01145-y

Cited by 39 publications

(51 citation statements)

References 59 publications

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“…Consistent with previous studies (Zhang et al, 2020), we observed that in mice treated with NTG, head grooming time increased as compared with the vehicle control group on days 3, 5, 7, and 9. Moreover, significant change was detected on day 11 (2 days after stopping NTG injection) (Figure 1B and Supplementary Table 2).…”

Section: Repeated Ntg Injection Induced Photophobia and Increased Head Grooming Timesupporting

confidence: 92%

Detecting Abnormal Neuronal Activity in a Chronic Migraine Model by Egr1-EGFP Transgenic Mice

et al. 2021

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Chronic migraine (CM) is a highly disabling neurological disorder characterized by recurrent headache accompanied by a variety of sensory and/or emotional symptoms. However, the mechanisms of migraine onset and its chronicity have not been elucidated. The present study was designed to search for brain regions and neurons that were abnormally activated by CM and might be related to its pathogenesis and different concomitant symptoms. CM models were established here by repeated intraperitoneal injection of nitroglycerin (NTG) every other day for 9 days to early growth response gene 1 (Egr1)-enhanced green fluorescent protein (EGFP) transgenic mice, which allowed monitoring of neuronal activities in the whole brain. CM-related behaviors were recorded through head grooming test and light aversion assay. Elevation of Egr1 expression signals was detected in trigeminal nucleus caudalis (TNC), primary somatosensory cortex (SSp), lateral amygdala nucleus (LA), primary visual area (VISp), and temporal association areas (TEa) 2 h after the last injection of NTG by immunofluorescence and digital slice scanning technology. Meanwhile, no change of Egr1 expression was found in auditory areas (AUD), CA1, ectorhinal area (ECT), piriform (PIR), and anterior cingulate area (ACC). Furthermore, with the strongest support by evidence-based medicine among the current limited oral treatments of CM, topiramate was administrated every day for 11 days from 2 days before the first NTG injection. The results showed that topiramate partially improved the photophobia behavior of CM models in the short-term with gradually weakened efficacy as the course of the disease prolonged. Meanwhile, NTG-induced increase in Egr1 expression was completely reversed in TNC, SSp, and VISp and partially reduced in LA and TEa by topiramate at the same time point mentioned above. In conclusion, the current results suggested that the abnormal hyperactivities in TNC, SSp and VISp were associated with the pathogenesis of CM.

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Section: Repeated Ntg Injection Induced Photophobia and Increased Head Grooming Timesupporting

confidence: 92%

Detecting Abnormal Neuronal Activity in a Chronic Migraine Model by Egr1-EGFP Transgenic Mice

et al. 2021

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“…Our previous animal experiments found behavioral manifestations of vestibular injury in chronic migraine models; the development of vestibular injury was consistent with the trend in the development of allodynia, and we observed that the structure of the vestibular afferent terminal organs in a chronic migraine rat model was preserved (36). In addition, the activation of neurons in the spinal trigeminal nucleus and vestibular nucleus in the animal model of chronic migraine, and further, the activation of the trigeminal nucleus in the chronic migraine model were mainly due to the activation of the vestibular nucleus mediated by the spinal trigeminal nucleus (36). These studies suggested that the vestibular disorders associated with chronic migraine may be due to the activation of the trigeminal neurovascular system caused by the activation of the vestibular nucleus during chronic migraine.…”

Section: Discussionsupporting

confidence: 87%

“…Previous studies suggested that the etiology of vestibular symptoms in migraine patients may be related to the overlap of the trigeminal nerve and the vestibular pathway (35). Our previous animal experiments found behavioral manifestations of vestibular injury in chronic migraine models; the development of vestibular injury was consistent with the trend in the development of allodynia, and we observed that the structure of the vestibular afferent terminal organs in a chronic migraine rat model was preserved (36). In addition, the activation of neurons in the spinal trigeminal nucleus and vestibular nucleus in the animal model of chronic migraine, and further, the activation of the trigeminal nucleus in the chronic migraine model were mainly due to the activation of the vestibular nucleus mediated by the spinal trigeminal nucleus (36).…”

Section: Discussionsupporting

confidence: 75%

Presence and Clinical Value of Vestibular Symptoms in Migraine

Liu

Pan

Fan

et al. 2020

Preprint

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Objective: To evaluate the correlations between the characteristics of vestibular symptoms and migraine, and to explore the clinical value of vestibular symptoms in patients with migraine.Methods: Consecutive patients who visited the outpatient Department of Neurology and presented with a principal complaint of headache were enrolled. Patients with primary headache diagnosed according to International Classification of Headache Disorders (ICHD-3) were divided into the episodic migraine group (EM), chronic migraine group (CM) and tension-type headache group (TTH). Information on clinical symptoms was collected with a semistructured questionnaire, and the characteristics of the vestibular symptoms were recorded.Results: 451 patients were recruited, with 235 EM, 187 CM and 29 TTH. The proportion of patients with vestibular symptoms in the migraine (108/422) was higher than that in the TTH (1/29), and the frequency of vestibular symptoms in the CM was higher. 2-8 days per month was the highest in the EM (131/235), and the migraine features and accompanying symptoms were the most typical. The highest proportion of patients with separate attacks of headache and vestibular symptoms was observed in the low-frequency headache (68.8%) (p<0.05). With an increase in headache frequency, the proportion of concurrent attacks of headache and vestibular symptoms gradually increased, a headache frequency of 8 days per month was a cut-off point for migraine.Conclusion: Vestibular symptoms occur frequently in patients with CM, and the presence of concurrent attacks of vestibular symptoms and headache was significantly related to the headache frequency. A headache frequency of 8 days per month is recommended as a warning sign for CM. Patients with headaches 2-8 days per month have the most typical characteristics and should be selected for clinical trial.

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“…Furthermore, hyperalgesia was ameliorated by knocking down CGRP with short hairpin RNA. 84 In a rat model of migraine (glass micropipette inserted into the visual cortex), a propagating wave of depolarization was induced with a resultant increase in the firing rate of spinal trigeminal nucleus neurons. 85 The increased firing rate was blocked when rats were pretreated with a CGRP-blocking antibody.…”

Section: Dry Eye and Migraine Share Underlying Pathophysiologymentioning

confidence: 99%