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Related Experiment Videos

Signalling synapse formation between identified neurons

P Drapeau1, S Catarsi, D C Merz

  • 1Centre for Research in Neuroscience, McGill University, Montreal, Quebec, Canada.

Journal of Physiology, Paris
|January 1, 1995
PubMed
Summary

Presynaptic neurons selectively alter postsynaptic 5-HT responses during synapse formation. Cell surface glycoproteins and cytoplasmic signals mediate this crucial change in neuronal communication.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Synaptic Plasticity

Background:

  • Investigating neuronal communication during synapse formation in leech neurons.
  • Identifying activity-dependent modulation via extrasynaptic 5-hydroxytryptamine (5-HT) responses.
  • Understanding how presynaptic neurons select 5-HT responses at synapses.

Purpose of the Study:

  • To elucidate the mechanism of selective 5-HT response modulation during synapse formation.
  • To identify cell surface molecules and intracellular signals involved in this process.
  • To investigate the role of protein kinase C (PKC) and tyrosine phosphorylation.

Main Methods:

  • In vitro culture of identified leech neurons.
  • Electrophysiological recordings (single channel recording).

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  • Immunocytochemistry for tyrosine phosphorylation.
  • Treatment with fixation, trypsin, wheat germ agglutinin, and tyrosine kinase inhibitors.

    • Main Results:

    • Presynaptic contact induces a loss of extrasynaptic 5-HT response in postsynaptic neurons.
    • This modulation is mediated by cell-surface glycoproteins and a cytoplasmic signal.
    • Protein kinase C (PKC) modulation of cation channels is uncoupled at contacted sites.
    • Tyrosine phosphorylation in the postsynaptic cytoplasm correlates with synapse formation.

    Conclusions:

    • Synapse formation involves presynaptic induction of specific changes in postsynaptic 5-HT sensitivity.
    • A cytoplasmic signal, involving tyrosine phosphorylation, uncouples cation channel modulation by PKC.
    • These findings reveal a novel mechanism for activity-dependent synaptic modulation.