Mu opioid receptor mRNA expression, binding, and functional coupling to G-proteins in human epileptic hippocampus

• Published in: Hippocampus Vol. 22; no. 2; pp. 122 - 127
• Main Authors: Cuellar-Herrera, Manola, Velasco, Ana Luisa, Velasco, Francisco, Chavez, Laura, Orozco-Suarez, Sandra, Armagan, Guliz, Turunc, Ezgi, Bojnik, Engin, Yalcin, Ayfer, Benyhe, Sandor, Borsodi, Anna, Alonso-Vanegas, Mario, Rocha, Luisa
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.02.2012
• Subjects: Adolescent; Adult; binding; Epilepsy, Temporal Lobe - metabolism; Female; G-protein; GTP-Binding Proteins - metabolism; hippocampus; Hippocampus - metabolism; Humans; Male; mesial temporal lobe epilepsy; Middle Aged; mRNA; mu opiod receptor; Receptors, Opioid, mu - metabolism; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - analysis; Young Adult
• ISSN: 1050-9631; 1098-1063
• DOI: 10.1002/hipo.20891

Mu opioid receptors (MOR) are known to be involved in seizure activity. The main goal of the present study was to characterize the MOR mRNA expression, binding, as well as G protein activation mediated by these receptors in epileptic hippocampus of patients with pharmacoresistant mesial temporal lobe epilepsy (TLE). In contrast with autopsy samples, hippocampus obtained from patients with mesial TLE demonstrated enhanced MOR mRNA expression (116%). Saturation binding experiments revealed significantly higher (60%) Bmax values for the mesial TLE group, whereas the Kd values were not statistically different. Although mesial TLE group demonstrated high levels of basal binding for the G proteins (136%), DAMGO‐stimulated [35S]GTPγS binding did not demonstrate significant alterations. In conclusion, our present data provide strong evidence that the epileptic hippocampus of patients with pharmacoresistant mesial TLE presents significant alterations in MOR. Such changes may represent adaptive mechanisms to compensate for other as yet unknown alterations. © 2010 Wiley Periodicals, Inc.