The effect of CA1 administration of orexin-A on hippocampal expression of COX-2 and BDNF in a rat model of orofacial pain

• Published in: Arquivos de neuro-psiquiatria 2018-09, Vol.76 (9), p.603-608
• Main Authors: Kooshki, Razieh, Abbasnejad, Mehdi, Esmaeili-Mahani, Saeed, Raoof, Maryam
• Format: Article
• Language: English
• Subjects: Animals; Benzoxazoles - pharmacology; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - metabolism; Capsaicin; Cyclooxygenase 2 - metabolism; Cyclooxygenase-2; Disease Models, Animal; Facial Pain - metabolism; Hippocampus; Hippocampus - drug effects; Hippocampus - metabolism; Male; Neurons - drug effects; Neurons - metabolism; NEUROSCIENCES; Orexin Receptors - metabolism; Orexins; Orexins - pharmacology; Orofacial pain; Pain; Polymerase chain reaction; PSYCHIATRY; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction; Reverse transcription; Urea - analogs & derivatives; Urea - pharmacology
• ISSN: 0004-282X; 1678-4227; 1678-4227
• DOI: 10.1590/0004-282X20180099

ABSTRACT The neuropeptide orexin-A and its receptors are widely distributed in both hippocampal circuitry and pain transmission pathways. Objective: Involvement of the CA1 orexin 1 receptor (OX1R) on the modulation of orofacial pain and pain-induced changes in hippocampal expression of cyclooxygenase-2 (COX-2) and brain-derived neurotrophic factor (BDNF) was investigated. Methods: Orofacial pain was induced by an intra-lip injection of capsaicin (100 μg). Reverse transcription polymerase chain reaction and immunoblot analysis were used to indicate changes in hippocampal BDNF and COX-2 expression, respectively. Results: Capsaicin induces a significant pain response, which is not affected by either orexin-A or SB-334867-A, an OX1R antagonist. However, an increased expression of COX-2 and decreased expression of BDNF was observed in the hippocampus of animals that received capsaicin or SB-334867-A (80 nM) plus capsaicin. Meanwhile, orexin-A (40 pM) attenuated the effects of capsaicin on the expression of COX-2 and BDNF. Conclusions: CA1 OX1R activation moderates capsaicin-induced neuronal inflammation and neurotrophic deficiency.