RGD Reference Report - Calcitonin gene-related peptide facilitates sensitization of the vestibular nucleus in a rat model of chronic migraine. - Rat Genome Database

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

Authors: Zhang, Yun  Zhang, Yixin  Tian, Ke  Wang, Yunfeng  Fan, Xiaoping  Pan, Qi  Qin, Guangcheng  Zhang, Dunke  Chen, Lixue  Zhou, Jiying 
Citation: Zhang Y, etal., J Headache Pain. 2020 Jun 10;21(1):72. doi: 10.1186/s10194-020-01145-y.
RGD ID: 405650618
Pubmed: PMID:32522232   (View Abstract at PubMed)
PMCID: PMC7288551   (View Article at PubMed Central)
DOI: DOI:10.1186/s10194-020-01145-y   (Journal Full-text)


BACKGROUND: Vestibular migraine has recently been recognized as a novel subtype of migraine. However, the mechanism that relate vestibular symptoms to migraine had not been well elucidated. Thus, the present study investigated vestibular dysfunction in a rat model of chronic migraine (CM), and to dissect potential mechanisms between migraine and vertigo.
METHODS: Rats subjected to recurrent intermittent administration of nitroglycerin (NTG) were used as the CM model. Migraine- and vestibular-related behaviors were analyzed. Immunofluorescent analyses and quantitative real-time polymerase chain reaction were employed to detect expressions of c-fos and calcitonin gene-related peptide (CGRP) in the trigeminal nucleus caudalis (TNC) and vestibular nucleus (VN). Morphological changes of vestibular afferent terminals was determined under transmission electron microscopy. FluoroGold (FG) and CTB-555 were selected as retrograde tracers and injected into the VN and TNC, respectively. Lentiviral vectors comprising CGRP short hairpin RNA (LV-CGRP) was injected into the trigeminal ganglion.
RESULTS: CM led to persistent thermal hyperalgesia, spontaneous facial pain, and prominent vestibular dysfunction, accompanied by the upregulation of c-fos labeling neurons and CGRP immunoreactivity in the TNC (c-fos: vehicle vs. CM = 2.9 ± 0.6 vs. 45.5 ± 3.4; CGRP OD: vehicle vs. CM = 0.1 ± 0.0 vs. 0.2 ± 0.0) and VN (c-fos: vehicle vs. CM = 2.3 ± 0.8 vs. 54.0 ± 2.1; CGRP mRNA: vehicle vs. CM = 1.0 ± 0.1 vs. 2.4 ± 0.1). Furthermore, FG-positive neurons was accumulated in the superficial layer of the TNC, and the number of c-fos+/FG+ neurons were significantly increased in rats with CM compared to the vehicle group (vehicle vs. CM = 25.3 ± 2.2 vs. 83.9 ± 3.0). Meanwhile, CTB-555+ neurons dispersed throughout the VN. The structure of vestibular afferent terminals was less pronounced after CM compared with the peripheral vestibular dysfunction model. In vivo knockdown of CGRP in the trigeminal ganglion significantly reduced the number of c-fos labeling neurons (LV-CGRP vs. LV-NC = 9.9 ± 3.0 vs. 60.0 ± 4.5) and CGRP mRNA (LV-CGRP vs. LV-NC = 1.0 ± 0.1 vs. 2.1 ± 0.2) in the VN, further attenuating vestibular dysfunction after CM.
CONCLUSIONS: These data demonstrates the possibility of sensitization of vestibular nucleus neurons to impair vestibular function after CM, and anti-CGRP treatment to restore vestibular dysfunction in patients with CM.



RGD Manual Disease Annotations    Click to see Annotation Detail View
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CALCAHumanmigraine treatmentISOCalca (Rattus norvegicus) RGD 
CalcaRatmigraine treatmentIEP  RGD 
CalcaMousemigraine treatmentISOCalca (Rattus norvegicus) RGD 
FOSHumanmigraine treatmentISOFos (Rattus norvegicus) RGD 
FosRatmigraine treatmentIEP  RGD 
FosMousemigraine treatmentISOFos (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Calca  (calcitonin-related polypeptide alpha)
Fos  (Fos proto-oncogene, AP-1 transcription factor subunit)

Genes (Mus musculus)
Calca  (calcitonin/calcitonin-related polypeptide, alpha)
Fos  (FBJ osteosarcoma oncogene)

Genes (Homo sapiens)
CALCA  (calcitonin related polypeptide alpha)
FOS  (Fos proto-oncogene, AP-1 transcription factor subunit)


Additional Information