Involvement of phosphatidylinositol 4,5-bisphosphate in the desensitization of canonical transient receptor potential 5open access
- Authors
- Kim, Byung Joo; Kim, Min Tae; Jeon, Ju-Hong; Kim, Seon Jeong; So, Insuk
- Issue Date
- Sep-2008
- Publisher
- PHARMACEUTICAL SOC JAPAN
- Keywords
- canonical transient receptor potential 5; muscarinic stimulation; phosphatidylinositol 4,5-bisphosphate
- Citation
- BIOLOGICAL & PHARMACEUTICAL BULLETIN, v.31, no.9, pp.1733 - 1738
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOLOGICAL & PHARMACEUTICAL BULLETIN
- Volume
- 31
- Number
- 9
- Start Page
- 1733
- End Page
- 1738
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/171876
- DOI
- 10.1248/bpb.31.1733
- ISSN
- 0918-6158
- Abstract
- The classic transient receptor potential channel (TRPC) is a candidate for Ca2+-permeable cation channel in mammalian cells. TRPC5 is desensitized rapidly after activation by G protein-coupled receptor. Here we investigate the mechanisms of desensitization of TRPC5 using patch-clamp recording. TRPC5 was initially activated by muscarinic stimulation using 50 mu M carbachol (CCh) and decayed rapidly in the presence of CCh (desensitization). Intracellularly-applied phosphatidylinositol 4,5-bisphosphate (PIP2) slowed the rate of desensitization. In contrast, several other phosphoinositides, including PI(3,4)P-2, PI(3,5)P-2, PI(3,4,5)P-3 and PI(4)P, had no effect on the desensitization of the TRPC5 current. This indicates that PIP2 attenuates the desensitization of the TRPC5 current in a highly selective manner. Neither wortmannin, an inhibitor of phosphatidylinositol 4-kinase, or poly-L-lysine (PLL), a scavenger of PIP2, had any effect on desensitization of the TRPC5 current. PIP2 breakdown appears to he a required step in the desensitization of TRPC5 current, but PIP2 depletion alone was insufficient for channel desensitization. TRPC5 was inhibited by cytochalasin D treatment. In mouse ileal myocytes, the desensitization of CCh-activated inward current (I-CCh) also slowed in the presence of PIP2 in recording pipettes. These results indicate that PIP2 is involved in the desensitization of TRPC5 currents.
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