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Modulation of Ca 2+ signals by phosphatidylinositol‐linked novel D1 dopamine receptor in hippocampal neurons
Author(s) -
Ming Yuling,
Zhang Hai,
Long Lihong,
Wang Fang,
Chen Jianguo,
Zhen Xuechu
Publication year - 2006
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2006.03961.x
Subject(s) - phospholipase c , phosphatidylinositol , endocrinology , medicine , chemistry , calcium in biology , voltage dependent calcium channel , receptor , dopamine , phosphatidylinositol 4,5 bisphosphate , stimulation , calcium , biology , signal transduction , biochemistry
Abstract Recent evidence indicates the existence of a putative novel phosphatidylinositol‐linked D1 dopamine receptor in brain that mediates phosphatidylinositol hydrolysis via activation of phospholipase Cβ. The present work was designed to characterize the Ca 2+ signals regulated by this phosphatidylinositol‐linked D 1 dopamine receptor in primary cultures of hippocampal neurons. The results indicated that stimulation of phosphatidylinositol‐linked D1 dopamine receptor by its newly identified selective agonist SKF83959 induced a long‐lasting increase in basal [Ca 2+ ] i in a time‐ and dose‐dependent manner. Stimulation was observable at 0.1 μ m and reached the maximal effect at 30 μ m . The [Ca 2+ ] i increase induced by 1 μ m SKF83959 reached a plateau in 5 ± 2.13 min, an average 96 ± 5.6% increase over control. The sustained elevation of [Ca 2+ ] i was due to both intracellular calcium release and calcium influx. The initial component of Ca 2+ increase through release from intracellular stores was necessary for triggering the late component of Ca 2+ rise through influx. We further demonstrated that activation of phospholipase Cβ/inositol triphosphate was responsible for SKF83959‐induced Ca 2+ release from intracellular stores. Moreover, inhibition of voltage‐operated calcium channel or NMDA receptor‐gated calcium channel strongly attenuated SKF83959‐induced Ca 2+ influx, indicating that both voltage‐operated calcium channel and NMDA receptor contribute to phosphatidylinositol‐linked D 1 receptor regulation of [Ca 2+ ] i .