Abstract
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.
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