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Related Experiment Videos

Diffusion, not uptake, limits glycine concentration in the synaptic cleft

M J Titmus1, H Korn, D S Faber

  • 1Department of Physiology, University at Buffalo, New York 14214, USA.

Journal of Neurophysiology
|April 1, 1996
PubMed
Summary
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Active glycine uptake does not limit the duration of inhibitory postsynaptic currents (IPSCs) in goldfish Mauthner cells. Diffusion, not uptake, clears the inhibitory transmitter glycine from synapses.

Area of Science:

  • Neuroscience
  • Synaptic Transmission
  • Neuropharmacology

Background:

  • The duration of neurotransmitter action is crucial for synaptic signaling.
  • Active uptake mechanisms are hypothesized to limit neurotransmitter action duration.
  • Glycine is a major inhibitory neurotransmitter in the central nervous system.

Purpose of the Study:

  • To investigate whether active glycine uptake limits the duration of inhibitory postsynaptic currents (IPSCs).
  • To determine the role of glycine uptake and diffusion in shaping synaptic responses at the goldfish Mauthner cell.
  • To explore potential spillover of glycine to activate other receptors.

Main Methods:

  • Recording of inhibitory postsynaptic potentials and currents (IPSCs) in goldfish Mauthner cells.

Related Experiment Videos

  • Pharmacological manipulation to block Na+-dependent glycine uptake using Li+, Ch+, or N-methyl-D-glucamine.
  • Assessment of temperature dependence of IPSC decay to infer rate-limiting steps.
  • Application of glutamate receptor antagonists (CNQX, APV) to test for glycine spillover effects.

    • Main Results:

    • Temperature coefficients suggest diffusion, not uptake, is the rate-limiting step for IPSC decay.
    • Blocking Na+-dependent glycine uptake did not alter the decay time constants of recurrent collateral or eighth-nerve-evoked IPSCs.
    • Glycine iontophoresis showed uptake may buffer transmitter concentration, but this did not affect IPSC kinetics.
    • Glutamate receptor antagonists applied locally did not affect the prolonged IPSC tail, indicating network-level effects.

    Conclusions:

    • Active glycine uptake does not shape glycinergic IPSCs at the Mauthner cell.
    • Diffusion is sufficiently rapid to clear glycine from the synaptic cleft faster than channel unbinding.
    • Glycine spillover to activate glutamate receptors is unlikely to contribute to prolonged synaptic responses.