Premium
Nociceptin/orphanin FQ stimulates extracellular acidification and desensitization of the response involves protein kinase C
Author(s) -
Pei Gang,
Ling Kun,
Pu Lu,
Cunningham Martin D,
Ma Lan
Publication year - 1997
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(97)00790-4
Subject(s) - nociceptin receptor , chinese hamster ovary cell , homologous desensitization , desensitization (medicine) , pertussis toxin , extracellular , protein kinase c , protein kinase a , receptor , chemistry , endocrinology , pharmacology , agonist , medicine , g protein , biology , kinase , biochemistry , opioid , opioid peptide
A Chinese hamster ovary (CHO) cell line, CHO‐ORL 1 , stably expressing human opioid receptor‐like receptor 1 (ORL 1 ) has been used to determine ORL 1 ‐mediated signaling events using microphysiometry. Nociceptin/orphanin FQ (N/OFQ), a specific endogenous agonist of ORL 1 , induced an increase in extracellular acidification rate (ECAR) in CHO‐ORL 1 cells. The ECAR response stimulated by N/OFQ was concentration‐dependent and pertussis toxin‐sensitive. Repeated exposures of the cells to N/OFQ caused desensitization of ORL 1 . The ECAR response was recovered at the half‐life of approximately 12 min after the initial challenge. Pretreatment with inhibitor of cAMP‐dependent kinase did not affect desensitization of ORL 1 . However, specific inhibitors for protein kinase C almost abolished N/OFQ‐induced desensitization of extracellular acidification responsiveness, indicating the involvement of protein kinase C in the process.