Journal ArticleDOI
Spreading Depression Triggers Headache by Activating Neuronal Panx1 Channels
Hulya Karatas,Sefik Evren Erdener,Yasemin Gursoy-Ozdemir,Sevda Lule,Emine Eren-Koçak,Zumrut Duygu Sen,Turgay Dalkara +6 more
TLDR
A previously unknown signaling pathway between stressed neurons and trigeminal afferents during cortical spreading depression (CSD), the putative cause of migraine aura and headache, is described.Abstract:
The initial phase in the development of a migraine is still poorly understood. Here, we describe a previously unknown signaling pathway between stressed neurons and trigeminal afferents during cortical spreading depression (CSD), the putative cause of migraine aura and headache. CSD caused neuronal Pannexin1 (Panx1) megachannel opening and caspase-1 activation followed by high-mobility group box 1 (HMGB1) release from neurons and nuclear factor κB activation in astrocytes. Suppression of this cascade abolished CSD-induced trigeminovascular activation, dural mast cell degranulation, and headache. CSD-induced neuronal megachannel opening may promote sustained activation of trigeminal afferents via parenchymal inflammatory cascades reaching glia limitans. This pathway may function to alarm an organism with headache when neurons are stressed.read more
Citations
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Pathophysiology of Migraine: A Disorder of Sensory Processing
Peter J. Goadsby,Philip R. Holland,Margarida Martins-Oliveira,Jan Hoffmann,Christoph J. Schankin,Simon Akerman +5 more
TL;DR: Investment in understanding migraine leaves us at a new dawn, able to transform its impact on a global scale, as well as understand fundamental aspects of human biology.
Journal ArticleDOI
HMGB1 in Health and Disease
Rui Kang,Ruochan Chen,Qiuhong Zhang,Wen Hou,Sha Wu,Lizhi Cao,Jin Huang,Yan Yu,Xue Gong Fan,Zhengwen Yan,Zhengwen Yan,Xiaofang Sun,Haichao Wang,Qingde Wang,Allan Tsung,Timothy R. Billiar,Herbert J. Zeh,Michael T. Lotze,Daolin Tang +18 more
TL;DR: High-mobility group box 1 (HMGB1), the most abundant and well-studied HMG protein, senses and coordinates the cellular stress response and plays a critical role not only inside of the cell as a DNA chaperone, chromosome guardian, autophagy sustainer, and protector from apoptotic cell death, but also outside thecell as the prototypic damage associated molecular pattern molecule (DAMP).
Journal ArticleDOI
Migraine pathophysiology: Anatomy of the trigeminovascular pathway and associated neurological symptoms, cortical spreading depression, sensitization, and modulation of pain
Rodrigo Noseda,Rami Burstein +1 more
TL;DR: Scientific evidence supports the notion that migraine pathophysiology involves inherited alteration of brain excitability, intracranial arterial dilatation, recurrent activation, and sensitization of the trigeminovascular pathway, and consequential structural and functional changes in genetically susceptible individuals.
Journal ArticleDOI
Migraine: multiple processes, complex pathophysiology.
TL;DR: Attempts to understand the headache pain itself point to activation of the trigeminovascular pathway as a prerequisite for explaining why the pain is restricted to the head, often affecting the periorbital area and the eye, and intensifies when intracranial pressure increases.
Journal ArticleDOI
Inflammasomes in the CNS
TL;DR: The current understanding of the functions of different inflammasomes in the CNS and their roles in neurological diseases is reviewed.
References
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Journal ArticleDOI
Mechanisms of migraine aura revealed by functional MRI in human visual cortex
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Journal ArticleDOI
Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model
TL;DR: This work establishes a link between migraine aura and headache by demonstrating that cortical spreading depression activates trigeminovascular afferents and evokes a series of cortical meningeal and brainstem events consistent with the development of headache.
Journal ArticleDOI
Pathophysiology of the migraine aura. The spreading depression theory.
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