ArticleCerebral cortex (New York, N.Y. : 1991)2019
Determinants of Optogenetic Cortical Spreading Depolarizations.
Article in Cerebral cortex (New York, N.Y. : 1991), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- Behavioral Deficits and Cortical Network Dysfunction Following Repeated Mild Traumatic Brain Injuries.Journal of neurotrauma · 2026Article
- From bench to bedside: relevant animal models across the migraine attack phases.The journal of headache and pain · 2026Review
- Cortical spreading depolarizations in stroke: Mechanisms, neuroprotective interventions, and monitoring techniques.GeroScience · 2026Review
- Choosing a skull clearing technique for chronic mesoscopic optical imaging in awake mice.Neurophotonics · 2026Article
- Review
- Spreading depolarization activates the cGAS-STING pathway and drives cranial nociception: therapeutic potential of STING modulation.The journal of headache and pain · 2026Article
- Spreading depolarization as a therapeutic target in migraine.Nature reviews. Neurology · 2025Review
- Olfactory Bulb Pinprick Induction of Cortical Spreading Depolarizations.bioRxiv : the preprint server for biology · 2025Article
- State-of-the-art preclinical techniques to study the impact of spreading depolarizations in awake rodents.The journal of headache and pain · 2025Review
- Possible Role of Novel Mitochondrial Subsets in Migraine.Life (Basel, Switzerland) · 2025Review
- Article
- Progesterone receptors regulate susceptibility to spreading depression.Experimental neurology · 2025Article
- Optogenetic cortical spreading depression originating from the primary visual cortex induces migraine-like pain and anxiety behaviors in freely moving C57BL/6 J mice.The journal of headache and pain · 2025Article
- Mechanisms underlying CSD initiation implicated by genetic mouse models of migraine.The journal of headache and pain · 2025Review
- Behavioral and Cognitive Consequences of Spreading Depolarizations: A Translational Scoping Review.Journal of neurotrauma · 2025Article
- Article
- Article
- The effect of P2X7 antagonism on subcortical spread of optogenetically-triggered cortical spreading depression and neuroinflammation.The journal of headache and pain · 2024Article
- Synaptic-like transmission between neural axons and arteriolar smooth muscle cells drives cerebral neurovascular coupling.Nature neuroscience · 2024Article
- Spreading Depolarizations Contribute to the Acute Behavior Deficits Associated With a Mild Traumatic Brain Injury in Mice.Journal of neurotrauma · 2024Article
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Authors and funding
15 authors.
Funding
Abstract
Cortical spreading depolarization (SD) is the electrophysiological event underlying migraine aura, and a critical contributor to secondary damage after brain injury. Experimental models of SD have been used for decades in migraine and brain injury research; however, they are highly invasive and often cause primary tissue injury, diminishing their translational value. Here we present a non-invasive method to trigger SDs using light-induced depolarization in transgenic mice expressing channelrhodopsin-2 in neurons (Thy1-ChR2-YFP). Focal illumination (470 nm, 1-10 mW) through intact skull using an optical fiber evokes power-dependent steady extracellular potential shifts and local elevations of extracellular [K+] that culminate in an SD when power exceeds a threshold. Using the model, we show that homozygous mice are significantly more susceptible to SD (i.e., lower light thresholds) than heterozygous ChR2 mice. Moreover, we show SD susceptibility differs significantly among cortical divisions (motor, whisker barrel, sensory, visual, in decreasing order of susceptibility), which correlates with relative channelrhodopsin-2 expression. Furthermore, the NMDA receptor antagonist MK-801 blocks the transition to SD without diminishing extracellular potential shifts. Altogether, our data show that the optogenetic SD model is highly suitable for examining physiological or pharmacological modulation of SD in acute and longitudinal studies.
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