Nociceptin/orphanin FQ stimulates extracellular acidification and desensitization of the response involves protein kinase C

FEBS Letters

Ma, Lan³  Ling, Kun²  Pei, Gang²  Pu, Lu²  Cunningham, Martin D¹ 

[1] Molecular Devices Corporation, Sunnyvale, CA 94089, USA;Shanghai Institute of Cell Biology, Chinese Academy of Sciences, Shanghai 200031, People's Republic of China;National Laboratory of Medical Neurobiology and Department of Neurobiology, Shanghai Medical University, Shanghai 200032, People's Republic of China

关键词: Opioid receptor-like receptor 1 (ORL1);    Nociceptin/orphanin FQ;    Extracellular acidification;    Opioid receptor;    Receptor desensitization;    Protein kinase C;    N/OFQ;    nociceptin/orphanin FQ;    ORL1;    opioid receptor-like receptor 1;    PTX;    pertussis toxin;    ECAR;    extracellular acidification rate;    PKC;    protein kinase C;    PKA;    cAMP-dependent protein kinase;    BSA;    bovine serum albumin;    LPA;    lysophosphatidic acid;   

DOI  :  10.1016/S0014-5793(97)00790-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

A Chinese hamster ovary (CHO) cell line, CHO-ORL₁, stably expressing human opioid receptor-like receptor 1 (ORL₁) has been used to determine ORL₁-mediated signaling events using microphysiometry. Nociceptin/orphanin FQ (N/OFQ), a specific endogenous agonist of ORL₁, induced an increase in extracellular acidification rate (ECAR) in CHO-ORL₁ 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 ORL₁. 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 ORL₁. 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.

【 授权许可】

Unknown