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Related Concept Videos

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Nonequivalent release sites govern synaptic depression.

Hua Wen1, Matthew J McGinley1, Gail Mandel2

  • 1Vollum Institute, Oregon Health and Sciences University, Portland, OR 97239;

Proceedings of the National Academy of Sciences of the United States of America
|December 31, 2015
PubMed
Summary

Synaptic depression mechanisms were clarified using zebrafish neuromuscular junctions. Findings reveal distinct release site properties, not vesicle availability, dictate steady-state transmission during high-frequency stimulation.

Keywords:
multinomial analysisneuromuscularsynaptic plasticitysynaptic vesiclezebrafish

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Area of Science:

  • Neuroscience
  • Cellular Biology
  • Synaptic Transmission

Background:

  • Synaptic depression is a common phenomenon, but its precise mechanisms are not fully understood.
  • Understanding synaptic function is crucial for comprehending neural circuit behavior.

Purpose of the Study:

  • To investigate the mechanisms underlying short-term synaptic depression.
  • To elucidate the parameters controlling steady-state transmission at the zebrafish neuromuscular junction.

Main Methods:

  • Paired patch clamp recording in zebrafish.
  • Variance analysis to determine release parameters.
  • Studying neuromuscular transmission between motor neurons and skeletal muscle.

Main Results:

  • Identified two distinct subclasses of release sites with differing vesicle reloading rates.
  • A slow-reloading class contributes to depression onset, while a fast-reloading class sustains steady-state transmission.
  • Steady-state transmission is primarily determined by nonuniform release site kinetics, not vesicle availability.

Conclusions:

  • Nonuniform release site kinetics, specifically fast-reloading sites, are solely responsible for maintaining steady-state synaptic transmission.
  • This finding challenges existing models that emphasize vesicle availability for steady-state depression.
  • The duality of release site properties explains the nonlinear frequency dependence of synaptic depression.