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Melatonin inhibits cortical spreading depression-evoked trigeminal nociception
Supang M le Grand1, Suthiluk Patumraj, Pansiri Phansuwan-Pujito
1Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Neuroreport
|October 19, 2006
Summary
Melatonin effectively reduces pain signals triggered by cortical spreading depression. This study shows melatonin alleviates neurovascular changes and inflammation associated with this neurological event.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Cortical spreading depression (CSD) is a wave of neural and glial depolarization that can trigger trigeminovascular nociception, a key mechanism in headaches.
- Melatonin, a hormone with antioxidant and anti-inflammatory properties, has shown potential in managing pain conditions.
Purpose of the Study:
- To investigate the efficacy of melatonin in attenuating trigeminovascular nociception evoked by CSD.
- To explore the underlying mechanisms of melatonin's action on neurovascular and cellular responses to CSD.
Main Methods:
- Wistar rats were administered melatonin (20 or 40 mg/kg) or saline prior to CSD induction via cortical KCl application.
- Cortical blood flow and cerebral microvessel ultrastructure were assessed.
- Immunohistochemical analysis for Fos and nitric oxide synthase (NOS) was performed on medulla and cervical cord tissues.
Main Results:
- Melatonin pretreatment significantly reduced CSD-evoked cerebral hyperemia and attenuated microvascular alterations.
- Melatonin administration decreased the number of Fos and NOS-immunoreactive cells in the trigeminal nucleus caudalis.
- These findings indicate a reduction in trigeminovascular activation.
Conclusions:
- Melatonin demonstrates a significant capacity to attenuate trigeminovascular nociception induced by CSD.
- Melatonin's protective effects may involve modulation of neurovascular responses and inflammatory markers within the trigeminal system.
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