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001-es BibID:	BIBFORM058174
Első szerző:	Tóth Attila (biológus)
Cím:	Different vanilloid agonists cause different patterns of calcium response in CHO cells heterologously expressing rat TRPV1 / Attila Tóth, Yun Wang, Noémi Kedei, Richard Tran, Larry V. Pearce, Sang-Uk Kang, Mi-Kyung Jin, Hyun-Kyung Choi, Jeewoo Lee, Peter M. Blumberg
Dátum:	2005
ISSN:	0024-3205
Megjegyzések:	The vanilloid receptor subtype 1 (TRPV1 or VR1) is expressed in nociceptive primary afferents of the C-fiber 'pain' pathway and has attracted considerable attention as a therapeutic target. Here, using rat TRPV1 heterologously expressed in Chinese hamster ovary cells, we show that different agonists show different patterns of modulation of the intracellular Ca2+ concentration, monitored in individual cells by fura-2 Ca2+ imaging. We identified 5 parameters (potency, maximal response, latency of response, variability of latency of response among individual cells, and desensitization) which behaved differently for different compounds. The potencies of the compounds examined ranged from EC50 values of 80 pM to 9 microM. Peak levels of induced [Ca2+]i were observed either higher (RTX) or lower (anandamide) than for capsaicin. Significant latencies of response were observed for some (e.g. RTX) but not other derivatives, with great variation among individual cells in this latency. Marked desensitization after stimulation was detected in some cases (e.g. anandamide, capsaicin); for others, no desensitization was observed. We conclude that structurally diverse vanilloid agonists induce marked diversity in the patterns of Ca2+ response. This diversity of response may provide opportunities for pharmacological exploitation.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Life Sciences. - 76 : 25 (2005), p. 2921-2932. -
További szerzők:	Wang, Yun Kedei Noémi Tran, Richard Pearce, Larry V. Kang, Sang-Uk Jin, Mi-Kyung Choi, Hyun-Kyung Lee, Jeewoo Blumberg, Peter M.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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