Abstract
Functional connectivity (FC) has been used to investigate the pathophysiology of migraine. We aimed to identify atypical FC between the periaqueductal gray (PAG) and other brain areas in rats induced by repeated meningeal nociception. The rat model was established by infusing an inflammatory soup (IS) through supradural catheters in conscious rats. Quiescent and face-grooming behaviors were observed to assess nociceptive behavior. FC analysis seeded on the PAG was performed on rats 21 days after IS infusion. The rats exhibited nociceptive behavior correlates of human behaviors associated with migraine after IS infusion. The PAG showed increased FC with the prefrontal cortex, cingulate gyrus, and motor cortex but decreased FC with the basal ganglia, dorsal lateral thalamus, internal capsule and prelimbic cortex in the rat model. The atypical FC of the PAG with brain regions in the rat model that are involved in nociception, somatosensory processing, emotional processing, and pain modulation are consistent with the clinical data from migraineurs, indicate that resting-state FC changes in migraine patients may be a consequence of headache attacks, and further validate this rat model of chronic migraine.
Highlights
Primary headache is one of the most common disorders of the nervous system, with a 1-year prevalence rate of 47% among the global population[1]
The validity and reliability of this model of chronic migraine has been proven by mimicking the chronic migraine phenotype[28, 29], an increase in extracellular glutamate in the trigeminal nucleus caudalis (TNC)[30], increased expression of calcitonin gene-related peptide (CGRP) in the medulla[31] and a response to triptans[29]
We sought to test the hypothesis that there is atypical Functional connectivity (FC) of the periaqueductal gray (PAG) with brain areas related to nociception, emotion processing, and pain modulation which may be consistent with clinical studies in migraineurs
Summary
Primary headache is one of the most common disorders of the nervous system, with a 1-year prevalence rate of 47% among the global population[1]. Preclinical research has revealed that afferent trigeminal nociceptive traffic is inhibited by stimulation of the PAG18, and molecules related to inflammation and pain, such as calcitonin gene-related peptide (CGRP), act in the PAG19. All of these findings indicate that the PAG plays an important role in the pathogenesis of migraine. If there are changes concordant with those in rs-FC studies of migraineurs, such findings may further validate the applicability of this as a rat model of chronic migraine and could provide a new approach for future research using MRI to study migraine
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