Rapid desensitization of the thyrotropin-releasing hormone receptor expressed in single human embryonal kidney 293 cells.

摘要: This study uses fluorescence microscopy combined with dynamic video imaging to examine the events associated rapid desensitization of thyrotropin-releasing hormone receptor (TRH-R). In single non-pituitary human embryonic kidney 293 (HEK-293) cells, expressing either rat or TRH-Rs, TRH produced a dose-dependent monophasic rise in [Ca2+]i. Ca2+ transient was completely abolished by pretreatment cells intracellular antagonists thapsigargin cyclopiazonic acid, but not EGTA, voltage-operated channel (VOCC) antagonist nifedipine second-messenger-operated SK&F 96365. These results suggest that causes mobilization from thapsigargin/cyclopiazonic acid-sensitive stores influx extracellular Ca2+. HEK-293 also failed respond KCl slow Ca(2+)-channel activator BAY K 8644, suggesting they lack L-type VOCCs. Rat and TRH-Rs are highly conserved except at C-terminus where sequence differs. The is believed be important desensitization. Despite differences this region, expressed underwent (within 1 min) did involve loss. Similarly bradykinin endogenous displays We conclude TRH-R-expressing mobilizes resulting transient. as well displayed