The Antinociceptive Effect of Sigma-1 Receptor Antagonist, BD1047, in a Capsaicin Induced Headache Model in Rats.
10.4196/kjpp.2009.13.6.425
- Author:
Young Bae KWON
1
;
Young Chan JEONG
;
Jung Kee KWON
;
Ji Seon SON
;
Kee Won KIM
Author Information
1. Department of Pharmacology, College of Medicine, Chonbuk National University, Jeonju 561-180, Korea. keewon222@gmail.com
- Publication Type:Original Article
- Keywords:
Fos;
Headache;
N-methyl-D-aspartate receptor;
Sigma-1 receptor;
Trigeminal nucleus caudalis
- MeSH:
Animals;
Capsaicin;
Headache;
Migraine Disorders;
Models, Animal;
N-Methylaspartate;
Neurons;
Phosphorylation;
Rats;
Receptors, sigma;
Trigeminal Nuclei
- From:The Korean Journal of Physiology and Pharmacology
2009;13(6):425-429
- CountryRepublic of Korea
- Language:English
-
Abstract:
Intracranial headaches, including migraines, are mediated by nociceptive activation of the trigeminal nucleus caudalis (TNC), but the precise mechanisms are poorly understood. We previously demonstrated that selective blockage of spinal sigma-1 receptors (Sig-1R) produces a prominent antinociceptive effect in several types of pain models. This study evaluates whether the Sig-1R antagonist (BD1047) has an antinociceptive effect on capsaicin (a potent C-fiber activator) induced headache models in rats. Intracisternal infusion of capsaicin evoked pain behavior (face grooming), which was significantly attenuated by BD1047 pretreatment. BD1047 consistently reduced capsaicin-induced Fos-like immunoreactivity (Fos-LI), a neuronal activator, in the TNC in a dose-dependent manner. Moreover, capsaicin-induced phosphorylation of N-methyl-D-aspartate receptor subunit 1 was reversed by BD1047 pretreatment in the TNC. These results indicate that the Sig-1R antagonist has an inhibitory effect on nociceptive activation of the TNC in the capsaicin-induced headache animal model.
