Mechanisms of nicotine mediated communication between NGF-differentiated PCl2 and HEL cells

被引：3

作者：

Krjukova, J ^{[1
]}

Åkerman, KE ^{[1
]}

机构：

[1] Uppsala Univ, BMC, Dept Physiol, Div Cell Physiol, S-75123 Uppsala, Sweden

来源：

NEUROREPORT | 2002年 / 13卷 / 09期

关键词：

HEL; 92.1.7; cells; nerve growth factor; nicotine; PCl2; transmitter release; voltage-dependent Ca2+ channels;

D O I：

10.1097/00001756-200207020-00017

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

HEL 92.1.7 cells were immobilized among nerve growth factor (NGF)-differentiated PC12 cells. Nicotine caused an immediate Ca2+ mobilisation in the PC12 cells followed by a delayed secondary Ca2+ response in the HEL 92.1.7 cells. The Ca2+ elevation in response to nicotine in PC12 cells was abolished by Na+ removal. The response was diminished by omega-contoxin GVIA (omega-CTx-GVIA) in PC12 cell neurites and by nifedipine in the cell bodies, respectively. The secondary response in HEL 92.1.7 cells was blocked by omega-CTx-GVIA. The results suggest that nicotinic receptor-mediated depolarisation and subsequent activation of voltage dependent Ca2+ channels (VDCC) are sufficient to induce transmitter release from NGF-differentiated PC12 cell varicosities without requirement for additional Ca2+ influx via nicotinic receptor ion channels.

引用

页码：1157 / 1161

页数：5

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