Repetitive stress in mice causes migraine-like behaviors and calcitonin gene-related peptide-dependent hyperalgesic priming to a migraine trigger.

Repetitive stress in mice causes migraine-like behaviors and calcitonin gene-related peptide-dependent hyperalgesic priming to a migraine trigger.
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DOI:
10.1097/j.pain.0000000000001953
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发表时间:
2020-11
期刊:
影响因子:
7.4
通讯作者:
Dussor G
Dussor G
中科院分区:
医学1区
文献类型:
--
作者:
Avona A;Mason BN;Lackovic J;Wajahat N;Motina M;Quigley L;Burgos-Vega C;Moldovan Loomis C;Garcia-Martinez LF;Akopian AN;Price TJ;Dussor G

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Migraine is the second-most disabling disease worldwide [27], characterized by unilateral throbbing pain, cutaneous allodynia, often accompanied by nausea and sensitivity to light and sound. Attacks can be caused by triggers that include changes in hormones or sleep patterns, skipping meals, consumption of alcohol and certain foods [32]. Susceptibility to attacks following exposure to these common events suggests maladaptive changes have occurred within migraine-related nociceptive pathways. The most commonly-reported trigger for migraine is stress [32], which can increase the duration of headache [57] and may play a role in the development of chronic headache disorders [50]. Attacks often do not occur while stress is ongoing, but rather once the stressful event has passed [53; 54] with greatest susceptibility 6 to 18 hours following resolution of stress [38]. Additionally, multiple days of intense stress are more likely to trigger attacks than a single day [38]. Despite the close correlation between stress and migraine, mechanistic links between the two remain poorly understood.Preclinical migraine studies have used methods of stress including restraint, bright light, unpredictable sounds, wet bedding, exposure to predators, or a combination of stressors. Acute or chronic stress decreases the threshold for cortical-spreading depression (CSD)[6; 58], increases nitric-oxide synthase expression [59], alters immune cell properties in the dura [44; 45], and regulates hypothalamic modulation of the trigeminal nucleus caudalis [48]. Behaviorally, restraint stress increases rat tail-flick responses to high-doses (10 mg/kg) of the nitric oxide (NO) donor nitroglycerin (NTG)[17] and increases eye blinking and shuddering behavior in a mouse model of familial-hemiplegic migraine [15]. Additionally, a 14-day social-defeat stress exposure and 40-day chronic-variable stress protocol caused anxiety-like responses, hindpaw hypersensitivity, and increased responses to high-dose NTG
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