ArticleThe journal of headache and pain2024
Different vulnerability of fast and slow cortical oscillations to suppressive effect of spreading depolarization: state-dependent features potentially relevant to pathogenesis of migraine aura.
Article in The journal of headache and pain, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 10 citations in OpenAlex.
- Heightened Sensitivity of the Hyperexcitable Occipital Cortex to Spreading Depression: Evidence for State-Dependent Mechanisms of Migraine Aura.Neurology international · 2026Article
- Interhemispheric Functional Hypoconnectivity Is an Early Marker of Cortical Epileptogenesis.Biomedicines · 2026Article
- State-of-the-art preclinical techniques to study the impact of spreading depolarizations in awake rodents.The journal of headache and pain · 2025Review
- Inflammatory response of leptomeninges to a single cortical spreading depolarization.The journal of headache and pain · 2024Article
- Transient destabilization of interhemispheric functional connectivity induced by spreading depolarization.Network neuroscience (Cambridge, Mass.) · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
backgroundSpreading depolarization (SD), underlying mechanism of migraine aura and potential activator of pain pathways, is known to elicit transient local silencing cortical activity. Sweeping across the cortex, the electrocorticographic depression is supposed to underlie spreading negative symptoms of migraine aura. Main information about the suppressive effect of SD on cortical oscillations was obtained in anesthetized animals while ictal recordings in conscious patients failed to detect EEG depression during migraine aura. Here, we investigate the suppressive effect of SD on spontaneous cortical activity in awake animals and examine whether the anesthesia modifies the SD effect.
methodsSpectral and spatiotemporal characteristics of spontaneous cortical activity following a single unilateral SD elicited by amygdala pinprick were analyzed in awake freely behaving rats and after induction of urethane anesthesia.
resultsIn wakefulness, SD transiently suppressed cortical oscillations in all frequency bands except delta. Slow delta activity did not decline its power during SD and even increased it afterwards; high-frequency gamma oscillations showed the strongest and longest depression under awake conditions. Unexpectedly, gamma power reduced not only during SD invasion the recording cortical sites but also when SD occupied distant subcortical/cortical areas. Contralateral cortex not invaded by SD also showed transient depression of gamma activity in awake animals. Introduction of general anesthesia modified the pattern of SD-induced depression: SD evoked the strongest cessation of slow delta activity, milder suppression of fast oscillations and no distant changes in gamma activity.
conclusionSlow and fast cortical oscillations differ in their vulnerability to SD influence, especially in wakefulness. In the conscious brain, SD produces stronger and spatially broader depression of fast cortical oscillations than slow ones. The frequency-specific effects of SD on cortical activity of awake brain may underlie some previously unexplained clinical features of migraine aura.
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