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Abstract
Methods We used a model of trigeminovascular nociception in Sprague Dawley rats that measures transmission of craniovascular nociception in the trigeminocervical complex (TCC) by the firing of TCC neurons evoked in response to electrical stimulation of afferents from the middle meningeal artery, its branches, and periarterial meninges (MMA). To determine whether GABA receptors in the NRM modulate this nociceptive transmission, and to characterize the modulation, we microinjected GABA, and GABAAand GABAB-receptor agonists and antagonists into the NRM.
Highlights
Nociceptive transmission in the spinal cord is modulated by descending projections from the nucleus raphe magnus (NRM) receiving tonic inhibitory inputs from GABAergic neurons
This study shows that inhibition of NRM neurons by GABAA-receptor activation facilitates transmission of craniovascular nociception in the trigeminocervical complex
Our results suggest that GABAA receptors in the NRM play a role in the pathophysiology of migraine and other primary headache disorders
Summary
Nociceptive transmission in the spinal cord is modulated by descending projections from the nucleus raphe magnus (NRM) receiving tonic inhibitory inputs from GABAergic neurons. The NRM modulates transmission of craniovascular nociception, which is related to head pain, in the trigeminocervical complex
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