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Related Experiment Videos

Presynaptic mechanism underlying cAMP-dependent synaptic potentiation.

Masahiro Kaneko1, Tomoyuki Takahashi

  • 1Department of Neurophysiology, University of Tokyo Graduate School of Medicine, Tokyo 113-0033, Japan.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|June 4, 2004
PubMed
Summary

Forskolin enhances synaptic transmission by increasing cAMP levels in nerve terminals. This potentiation occurs via the Epac pathway, boosting both release probability and vesicle availability at the calyx of Held.

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Area of Science:

  • Neuroscience
  • Cellular Neuroscience
  • Synaptic Plasticity

Background:

  • Forskolin, an adenylyl cyclase activator, is known to facilitate synaptic transmission.
  • The precise intracellular mechanisms driving this presynaptic facilitation remain largely unelucidated.
  • The calyx of Held synapse offers a unique model for simultaneous presynaptic and postsynaptic electrophysiological recordings.

Purpose of the Study:

  • To investigate the intracellular mechanisms by which forskolin enhances synaptic transmission at the calyx of Held.
  • To identify the specific downstream targets of cyclic adenosine monophosphate (cAMP) involved in synaptic potentiation.
  • To determine the role of Epac (Exchange protein directly activated by cAMP) in forskolin-mediated synaptic facilitation.

Main Methods:

Related Experiment Videos

  • Simultaneous whole-cell recordings from presynaptic and postsynaptic compartments of the calyx of Held.
  • Application of forskolin and cyclic adenosine monophosphate (cAMP) to modulate intracellular signaling.
  • Intracellular delivery of a selective Epac agonist (8-(4-chlorophenylthio)-2'-O-methyl-cAMP).
  • Measurement of excitatory postsynaptic currents (EPSCs) and presynaptic calcium (Ca2+) and potassium (K+) currents.

    • Main Results:

    • Forskolin and intracellular cAMP application significantly potentiated EPSCs at the calyx of Held.
    • Synaptic potentiation correlated with increased release probability (P) and the number of releasable synaptic vesicles (N).
    • Forskolin did not alter presynaptic Ca2+ or K+ currents, indicating cAMP acts downstream of Ca2+ influx.
    • Selective activation of Epac mimicked the effects of forskolin, potentiating EPSCs.

    Conclusions:

    • Increased cAMP concentration in presynaptic terminals facilitates transmitter release at the calyx of Held.
    • The Epac pathway is identified as the primary mediator of cAMP-induced synaptic potentiation.
    • Forskolin enhances synaptic transmission by increasing both release probability and vesicle pool size through Epac activation.