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Regulated plasmalemmal expansion in nerve growth cones
R O Lockerbie1, V E Miller, K H Pfenninger
1Department of Cellular and Structural Biology, University of Colorado School of Medicine, Denver.
The Journal of Cell Biology
|March 1, 1991
Summary
Nerve growth cone membrane expansion is regulated, involving an internal precursor membrane pool. Calcium influx and depolarization trigger this process, distinct from neurotransmitter release.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- The nerve growth cone directs neuronal development through dynamic membrane remodeling.
- Understanding plasmalemmal expansion mechanisms is crucial for nerve regeneration research.
Purpose of the Study:
- To investigate the molecular mechanisms driving plasmalemmal expansion in nerve growth cones.
- To identify the source of new membrane material during growth cone advance.
Main Methods:
- Development of a cell-free assay using isolated growth cone particles from fetal rat brain.
- Quantification of membrane addition via 125I-wheat germ agglutinin (WGA) ligand binding.
- Morphometric analysis of cytoplasmic membrane compartments and assessment of neurotransmitter uptake/release.
Main Results:
- Calcium ionophore A23187 and high potassium (K+) or veratridine induced plasmalemmal expansion by increasing WGA binding sites (Bmax).
- This expansion was calcium-dependent and linked to the reduction of a specific cytoplasmic membrane compartment.
- Neurotransmitter (GABA, serotonin) uptake occurred, but Ca2+-dependent release was not observed, dissociating exocytosis from membrane expansion.
Conclusions:
- Plasmalemmal expansion in nerve growth cones is a regulated process.
- An internal pool of precursor membrane is mobilized during growth cone expansion.
- Membrane addition is independent of Ca2+-dependent neurotransmitter exocytosis.