The brain works like a network of Christmas lights, with circuits communicating through electrical signals. If one light goes out, it’s easy to find and fix. But in the brain, when circuits malfunction—like during migraine—it’s much harder to pinpoint the problem. Migraine is characterized by not just headache pain but also symptoms like nausea, sensitivity to light, and trouble thinking, both during and between attacks. My research focused on understanding how brain circuits involved in migraine behave to better understand the disorder. I used a mouse model of migraine triggered by CGRP, a chemical that induces migraines in both humans and rodents. I found that CGRP causes certain brain regions—like the anterior cingulate cortex, amygdala, parabrachial nuclei, and thalamus—to become less active, especially in the first 10 minutes when pain is at its worst. CGRP also disrupted how these areas "talk" to each other, particularly connections involving the amygdala, which is linked to emotions and pain. When I treated the mice with the migraine drug sumatriptan, it partially restored normal brain activity. However, mice that experienced early life stress had worse migraine-like behavior and attenuated brain responses to CGRP. Finally, I discovered that eye squinting could be used as a sign of spontaneous pain. By linking squinting to brain activity, it may be possible to use it as a biomarker for migraine pain. This research brings us closer to understanding migraines and finding better ways to treat them.