Abstract
Migraine is a disorder characterized by attacks of monolateral headaches, often accompanied by nausea, vomiting, and photophobia. Around 30% of patients also report aura symptoms. The cause of the aura is believed to be related to the cortical spreading depression (CSD), a wave of neuronal and glial depolarization originating in the occipital cortex, followed by temporary neuronal silencing. During a migraine attack, increased expression of inflammatory mediators, along with a decrease in the expression of anti-inflammatory genes, have been observed. The aim of this study was to evaluate the expression of inflammatory genes, in particular that of IL-1 receptor antagonist (IL-1RN), following CSD in a mouse model of familial hemiplegic migraine type 1 (FHM-1). We show here that the expression of IL-1RN was upregulated after the CSD, suggesting a possible attempt to modulate the inflammatory response. This study allows researchers to better understand the development of the disease and aids in the search for new therapeutic strategies in migraine.
Highlights
Migraine is a common neurological disease, representing the fourth cause of years lived with disability (YLDs) for women, and the eighth for men [1,2,3]
No significant differences in IL-1 receptor antagonist (IL-1RN) levels were observed a murine model of FHM1 (Figure 1)
Higherwere levels observed of IL-1RN were observed upon in FHM1animals as WT mice. sham-operated higher of IL-1RN
Summary
Migraine is a common neurological disease, representing the fourth cause of years lived with disability (YLDs) for women, and the eighth for men [1,2,3] It is characterized by attacks of monolateral headaches, associated with nausea as well as phono- and photophobia [4]. The cause of the aura is believed to be related to the cortical spreading depression (CSD), a self-propagating wave of cellular depolarization from the occipital cortex, followed by a transitory neuronal silencing [5,6]. The manifestation of these attacks depends on a genetic predisposition, associated to environmental stimuli such as stress, hormones, meteorological changes, and sleep disorders. Recent evidence suggests that immunoinflammatory events may play a role in the pathogenesis of migraine [7,8]
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