Abstract
The inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) acts as a Ca2+ release channel on internal Ca2+ stores. Type 1 IP3R (IP3R1) is enriched in growth cones of neurons in chick dorsal root ganglia. Depletion of internal Ca2+ stores and inhibition of IP3 signaling with drugs inhibited neurite extension. Microinjection of heparin, a competitive IP3R blocker, induced neurite retraction. Acute localized loss of function of IP3R1 in the growth cone induced by chromophore-assisted laser inactivation resulted in growth arrest and neurite retraction. IP3-induced Ca2+ release in growth cones appears to have a crucial role in control of nerve growth.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcium / metabolism
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Calcium Channels / metabolism*
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Calcium Signaling
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Cells, Cultured
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Cerebellum / metabolism
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Chick Embryo
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Ganglia, Spinal / cytology
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Growth Cones / metabolism*
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Heparin / pharmacology
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Inositol 1,4,5-Trisphosphate / metabolism*
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Inositol 1,4,5-Trisphosphate Receptors
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Lasers
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Lithium Chloride / pharmacology
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Mice
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Microscopy, Video
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Microsomes / metabolism
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Microtubules / metabolism
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Neurites / drug effects
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Neurites / physiology*
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Pseudopodia / drug effects
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Pseudopodia / physiology
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Receptors, Cytoplasmic and Nuclear / metabolism*
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Signal Transduction
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Thapsigargin / pharmacology
Substances
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Calcium Channels
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Inositol 1,4,5-Trisphosphate Receptors
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Receptors, Cytoplasmic and Nuclear
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Thapsigargin
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Inositol 1,4,5-Trisphosphate
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Heparin
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Lithium Chloride
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Calcium