A Single Episode of Cortical Spreading Depolarization Increases mRNA Levels of Proinflammatory Cytokines, Calcitonin Gene-Related Peptide and Pannexin-1 Channels in the Cerebral Cortex

被引:13
作者
Volobueva, Maria N. N. [1 ]
Suleymanova, Elena M. M. [1 ]
Smirnova, Maria P. P. [2 ]
Bolshakov, Alexey P. P. [1 ]
Vinogradova, Lyudmila V. V. [1 ]
机构
[1] Russian Acad Sci, Inst Higher Nervous Act & Neurophysiol, Dept Mol Neurobiol, Butlerova St 5A, Moscow 117485, Russia
[2] Russian Acad Sci, Inst Higher Nervous Act & Neurophysiol, Dept Conditioned Reflexes & Physiol Emot, Butlerova St 5A, Moscow 117485, Russia
基金
俄罗斯科学基金会;
关键词
cortical spreading depolarization; neuroinflammation; interleukin-1beta; tumor necrosis factor; interleukin-6; calcitonin gene-related peptide; pannexin-1; channel; migraine aura; TRAUMATIC BRAIN-INJURY; MENINGEAL NOCICEPTORS; SERUM-LEVELS; DEPRESSION; MIGRAINE; NEUROINFLAMMATION; EXPRESSION; HEADACHE;
D O I
10.3390/ijms24010085
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cortical spreading depolarization (CSD) is the neuronal correlate of migraine aura and the reliable consequence of acute brain injury. The role of CSD in triggering headaches that follow migraine aura and brain injury remains to be uncertain. We examined whether a single CSD occurring in awake animals modified the expression of proinflammatory cytokines (Il1b, TNF, and Il6) and endogenous mediators of nociception/neuroinflammation-pannexin 1 (Panx1) channel and calcitonin gene-related peptide (CGRP), transforming growth factor beta (TGFb) in the cortex. Unilateral microinjury of the somatosensory cortex triggering a single CSD was produced in awake Wistar rats. Three hours later, tissue samples from the lesioned cortex, intact ipsilesional cortex invaded by CSD, and homologous areas of the contralateral sham-treated cortex were harvested and analyzed using qPCR. Three hours post-injury, intact CSD-exposed cortexes increased TNF, Il1b, Panx1, and CGRP mRNA levels. The strongest upregulation of proinflammatory cytokines was observed at the injury site, while CGRP and Panx1 were upregulated more strongly in the intact cortexes invaded by CSD. A single CSD is sufficient to produce low-grade parenchymal neuroinflammation with simultaneous overexpression of Panx1 and CGRP. The CSD-induced molecular changes may contribute to pathogenic mechanisms of migraine pain and post-injury headache.
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页数:10
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