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Calcium Channels in Neuroblastoma Cell Growth Cones
Author(s) -
Zimprich Fritz,
Bolsover Stephen R.
Publication year - 1996
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1996.tb01230.x
Subject(s) - neuroblastoma , calcium , neuroscience , microbiology and biotechnology , biology , chemistry , genetics , cell culture , organic chemistry
The concentration of free calcium ions in the cytosol has been shown to influence many components of growth cone behaviour, including the extension of filopodia and veils, the addition of new membrane to the plasmalemma, the retraction and disappearance of filopodia, and gross collapse and retraction of the growth cone. A spatially localized modulation of these processes by very local calcium changes has been proposed to underlie the steering of growth cones by gradients of neurotransmitters, voltage and cell adhesion molecules. Such local control can be studied in mouse neuroblastoma cells, where depolarization causes calcium to rise in a limited number of spatially restricted hotspots, triggering a localized advance. We have studied the simple, club‐shaped growth cones that are characteristically found on advancing neurites. Depolarization caused calcium to increase most at the distal, leading tip. Agents that disrupt calcium‐induced calcium release do not affect growth cone calcium dynamics, ruling out a local release of calcium at the tip as a cause of the gradient. Using cell‐attached patch recording, we find that L‐type calcium channels are present at a higher density at the distal tip than in the proximal growth cone. Our results show that the calcium gradients seen in depolarized growth cones are a direct consequence of a gradient of calcium channel density.