ArticleThe journal of headache and pain2025
Mechanisms underlying the increased susceptibility to initiation of cortical spreading depression in a genetic mouse model of migraine.
Article in The journal of headache and pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- β-Hydroxybutyrate Maintains Energetically Demanding Neural Functions During Exogenous Glucose Deprivation.Cellular and molecular neurobiology · 2026Article
- Hemiplegic migraine: genetics and pathophysiology.The Journal of clinical investigation · 2026Review
- Review
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4 authors.
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Abstract
backgroundThere is evidence from human and animal studies that cortical spreading depression (CSD) is the neurophysiological correlate of migraine aura and a trigger of migraine pain mechanisms. The mechanisms of CSD initiation in the brain of migraineurs remain unknown. Insights into this question can be obtained by studying the mechanisms underlying the facilitation of CSD initiation in genetic mouse models of migraine. Here, we investigated these mechanisms in knock-in mice carrying a mutation in the Ca
methodsBrief high-KCl puffs of increasing duration up to the threshold duration eliciting a CSD were applied on layer 2/3 whilst the membrane potential of a pyramidal neuron located very close to the site of KCl application and the intrinsic optic signal were simultaneously recorded in cortical slices from FHM1 mice. This was done before and after application of MK-801. After blocking the glutamate NMDA receptors (NMDARs), stimuli up to 21 times the control CSD threshold were applied.
resultsA delayed activation of NMDARs above a critical threshold level is necessary for CSD initiation in FHM1 mice. This threshold level of NMDAR activation is quantitatively similar in FHM1 and WT mice, but is reached with a stimulus of much lower intensity and more rapidly in FHM1 mice, thus accounting for the facilitation of CSD initiation in these migraine mouse models. While, no matter the intensity of stimulation, Ca
conclusionsFHM1 mice are more susceptible to CSD initiation than WT mice because the critical threshold level of NMDAR activation, necessary for CSD initiation in both genotypes, is attained with stimuli of much lower intensity and more rapidly in FHM1 mice. Our findings give insights into potential mechanisms of CSD initiation in migraine.
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