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Submitted on July 28, 2005
Accepted on November 17, 2005
Systems Biodynamics NCRC, Division of Molecular and Life Sciences, Pohang University of Science and Technology, Pohang, 790-784, Republic of Korea; Department of Life Science and Food Engineering, Handong Global University, Pohang, 791-708, Republic of Korea
* To whom correspondence should be addressed. E-mail: ktk{at}postech.ac.kr.
Large dense-core vesicles (LDCVs), containing neuropeptides, hormones, and amines, play a crucial role in the activation of the sympathetic nervous system and synaptic modulation. In some secretory cells, LDCVs show activity-dependent potentiation (ADP) which represents enhancement of subsequent exocytosis compared with the previous one. Here we report the signaling mechanism involved in ADP of LDCV release. First, ADP of LDCV release, induced by repetitive stimulation of nicotinic acetylcholine receptors (nAChRs), was augmented by increasing extracellular calcium concentration or calcium influx, showing calcium dependence of ADP. Second, translocation of vesicles was involved in ADP. Electron microscope analysis revealed that nAChR stimulation resulted in LDCV translocation to the plasma membrane, and increase of fused LDCVs in response to repetitive stimulation was observed by amperometry. Third, we provide evidence for involvement of MAPK signaling in ADP. MAPK signaling was activated by nAChR-induced calcium influx, and ADP as well as vesicle translocation was suppressed by inhibition of MAPK signaling with MEK blockers, such as PD 098059 and U0126. Fourth, PD 098059 inhibited nAChR stimulation-induced F-actin disassembly, which has been reported to control vesicle translocation. Taken together, we suggest that ADP of LDCV release is modulated by calcium-dependent activation of MAPK signaling, via regulating F-actin disassembly.
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