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Related Concept Videos

Chemical Synapses01:26

Chemical Synapses

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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.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
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Chemical Synapses01:26

Chemical Synapses

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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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The Synapse02:47

The Synapse

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Neurons communicate with one another by passing on their electrical signals to other neurons. A synapse is the location where two neurons meet to exchange signals. At the synapse, the neuron that sends the signal is called the presynaptic cell, while the neuron that receives the message is called the postsynaptic cell. Note that most neurons can be both presynaptic and postsynaptic, as they both transmit and receive information.
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Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

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When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
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Fusion of Secretory Vesicles with the Plasma Membrane01:26

Fusion of Secretory Vesicles with the Plasma Membrane

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Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
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Amyloid Fibrils03:03

Amyloid Fibrils

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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Related Experiment Video

Updated: Mar 9, 2026

Recombinant α- β- and γ-Synucleins Stimulate Protein Phosphatase 2A Catalytic Subunit Activity in Cell Free Assays
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Recombinant α- β- and γ-Synucleins Stimulate Protein Phosphatase 2A Catalytic Subunit Activity in Cell Free Assays

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Synucleins Have Multiple Effects on Presynaptic Architecture.

Karina J Vargas1, Nikolas Schrod2, Taylor Davis1

  • 1Department of Neurology, Yale University, New Haven, CT 06536, USA; Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University, New Haven, CT 06536, USA.

Cell Reports
|January 5, 2017
PubMed
Summary
This summary is machine-generated.

Synucleins regulate presynaptic terminal size and organization. Deleting these proteins alters synaptic vesicle structure and impacts Parkinson

Keywords:
Parkinson’s diseaseamphiphysincalcineurinendocytosisknockout mousepresynapticreserve poolsynaptic vesicletetheringtomography

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Structural Biology

Background:

  • Synucleins (alpha, beta, gamma) are abundant presynaptic proteins.
  • Alpha-synuclein is implicated in Parkinson's disease (PD) pathogenesis.
  • Understanding synuclein function is crucial for neurodegenerative disease research.

Purpose of the Study:

  • To investigate the physiological and pathological roles of synucleins.
  • To determine how synuclein deletion and PD-associated mutations affect synapse architecture.

Main Methods:

  • Utilized mouse models with synuclein gene deletions (αβγ-synuclein-/-).
  • Overexpressed alpha-synuclein Parkinson's disease mutants in mice.
  • Employed electron microscopy (EM) and cryoelectron tomography (cryo-ET) for ultrastructural analysis.
  • Analyzed protein phosphorylation changes in synuclein-deficient neurons.

Main Results:

  • Synucleins regulate presynapse size and synaptic vesicle (SV) pool organization.
  • Synuclein deletion increased SV tethering to the active zone but decreased SV inter-linking.
  • Alpha-synuclein PD mutants affected the presynaptic cytomatrix, correlating with reduced neurotransmission.

Conclusions:

  • Synucleins are key regulators of presynaptic terminal structure and function.
  • Ultrastructural changes observed are linked to protein phosphorylation alterations.
  • Findings provide insights into synuclein's role in synaptic plasticity and Parkinson's disease.