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Related Experiment Videos

Anti-B-50 (GAP-43) antibodies decrease exocytosis of glutamate in permeated synaptosomes

J J Hens1, W E Ghijsen, U Weller

  • 1Department of Medical Pharmacology, Rudolf Magnus Institute for Neurosciences, Utrecht University, The Netherlands.

European Journal of Pharmacology
|January 9, 1999
PubMed
Summary

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Protein kinase C substrate B-50 (GAP-43) plays a role in glutamate release from synaptic vesicles. Anti-B-50 antibodies partially inhibited Ca(2+)-induced glutamate release, suggesting involvement in vesicle recycling.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Protein kinase C substrate B-50 (also known as GAP-43) is involved in neuronal plasticity.
  • Neurotransmitter release from synaptic vesicles is a critical process in neuronal communication.

Purpose of the Study:

  • To investigate the role of B-50 (GAP-43) in glutamate release from synaptosomes.
  • To compare the effect of anti-B-50 antibodies on glutamate and noradrenaline release.

Main Methods:

  • Streptolysin-O-permeated synaptosomes were used to study neurotransmitter release.
  • Anti-B-50 antibodies were employed to assess the function of B-50 (GAP-43).
  • Calcium-dependent and ATP-dependent release mechanisms were analyzed.

Main Results:

Related Experiment Videos

  • Ca(2+)-induced glutamate release was partially inhibited by anti-B-50 antibodies.
  • Ca(2+)-induced noradrenaline release was almost completely inhibited by anti-B-50 antibodies.
  • Basal glutamate release was reduced by anti-B-50 antibodies, while basal noradrenaline release was unaffected.

Conclusions:

  • B-50 (GAP-43) is important for the regulation of exocytosis of both glutamate and noradrenaline.
  • B-50's role appears to be in vesicle recycling and/or recruitment, not the Ca(2+)-induced fusion step.