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Related Experiment Videos

Synaptic vesicle recycling in synapsin I knock-out mice

T A Ryan1, L Li, L S Chin

  • 1Stanford University Medical School, California 94305, USA. timr@leland.stanford.edu

The Journal of Cell Biology
|September 1, 1996
PubMed
Summary

Synapsin I deficiency in mice reduces the number of exocytosed synaptic vesicles and the recycling pool. However, the processes of endocytosis and vesicle priming remain unaffected, indicating a specific role in vesicle release.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Synapsins are neuron-specific phosphoproteins involved in neurotransmitter release regulation.
  • Previous studies on synapsin I (Ia and Ib) knock-out mice showed limited electrophysiological changes.
  • Synapsin I is a major substrate for cAMP and Ca2+/Calmodulin-dependent protein kinases.

Purpose of the Study:

  • To investigate the detailed synaptic vesicle recycling dynamics in synapsin I-deficient mice.
  • To characterize the role of synapsin I in synaptic vesicle exocytosis and recycling using FM 1-43.
  • To compare synaptic bouton function in synapsin I knock-out and wild-type hippocampal cultures.

Main Methods:

  • Utilized the optical tracer FM 1-43 to monitor synaptic vesicle recycling.

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  • Analyzed individual synaptic boutons in hippocampal cell cultures.
  • Compared synapsin I-deficient mice with wild-type equivalents.

    • Main Results:

    • Synapsin I-deficient mice exhibited a significant reduction in exocytosed vesicles during action potential trains.
    • The total recycling vesicle pool was also significantly reduced in synapsin I-deficient mice.
    • Kinetics of endocytosis and synaptic vesicle repriming were found to be normal.

    Conclusions:

    • Synapsin I plays a crucial role in regulating the size of the readily releasable and recycling vesicle pools.
    • While synapsin I impacts vesicle exocytosis, it does not appear to affect the fundamental processes of endocytosis or vesicle priming.
    • These findings highlight a specific function of synapsin I in controlling the quantity of vesicles available for release at the synapse.