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Related Concept Videos

Recycling Endosomes and Transcytosis00:58

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The recycling endosome, also known as the endosomal recycling compartment (ERC), is a part of the slow-recycling process of the endocytic pathway. Molecules internalized through receptor-mediated endocytosis are either degraded in the lysosomes or are recycled to the plasma membrane through the fast- or slow-recycling route.
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In the secretory pathway, vesicles transport proteins from one cellular compartment to another in forward transport to deliver the protein to its correct location. Occasionally, misfolded proteins and incorrect proteins escape their original compartments, and a retrieval pathway is used to return the escaped proteins to their original compartment.
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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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The endoplasmic reticulum or ER makes up for more than half of the membranes in a cell and accounts for 10% of total cell volume. It is also the primary protein and lipid synthesis factory for most cell organelles, such as the Golgi apparatus, lysosomes, secretory vesicles, and the plasma membrane. Despite being the most extensive and functionally complex subcellular organelle, ER was the last to be discovered. After years of deliberation, Keith Porter and George Palade in the year 1954,...
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The early endosome containing internalized molecules matures through transformations in its location, morphology, intraluminal pH, and membrane protein composition. Together, these changes result in a more acidic late endosome that contains multiple intraluminal vesicles; therefore, the late endosome is also called a multivesicular body (MVB).
Changes in location
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Fusion of Secretory Vesicles with the Plasma Membrane01:26

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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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Related Experiment Video

Updated: Jan 11, 2026

Measuring Synaptic Vesicle Endocytosis in Cultured Hippocampal Neurons
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Measuring Synaptic Vesicle Endocytosis in Cultured Hippocampal Neurons

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Dual endomembrane recycling pathways function in parallel to support synapse maintenance and plasticity.

Garrett D Chavis1, Pilar Rivero-Ríos2, Tunahan Uygun2

  • 1Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA; Molecular and Integrative Physiology Graduate Program, University, Ann Arbor, MI 48109, USA; Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI 48109, USA.

Neuroscience
|November 14, 2025
PubMed
Summary
This summary is machine-generated.

The SNX17-Retriever and SNX27-Retromer pathways maintain excitatory synapses in neurons. Both pathways are crucial for synaptic plasticity, with parallel roles in synapse maintenance and function.

Keywords:
Endocytic traffickingProtein recyclingRetrieverRetromerSNX17SNX27SynapseSynaptic plasticity

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Last Updated: Jan 11, 2026

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • The SNX27-Retromer and SNX17-Retriever complexes are vital for recycling cellular components.
  • Their specific roles in neuronal synapse maintenance and plasticity remain largely unknown.

Purpose of the Study:

  • To investigate the distinct and overlapping functions of SNX17-Retriever and SNX27-Retromer pathways in neurons.
  • To determine the contribution of these pathways to excitatory synapse maintenance and plasticity.

Main Methods:

  • In vivo disruption of SNX17 and SNX27 pathways in developing rats.
  • Analysis of excitatory synapse loss in CA1 pyramidal neurons.
  • Experiments using cultured hippocampal neurons to study pathway localization and function.
  • Assessment of synaptic plasticity, including LTP, LTD, and homeostatic synaptic scaling.

Main Results:

  • Disruption of either SNX17-Retriever or SNX27-Retromer pathways caused significant loss of excitatory synapses in vivo and in vitro.
  • SNX17 and SNX27 showed prominent colocalization with Retriever/Retromer in early endosomes.
  • Combined disruption of both pathways resulted in an additive loss of excitatory synapses, indicating parallel functions.
  • Specific cargoes were found to be unique to each pathway.
  • Both pathways were essential for various forms of synaptic plasticity, including LTP, LTD, and homeostatic synaptic scaling.

Conclusions:

  • The SNX17-Retriever and SNX27-Retromer pathways operate in parallel to maintain excitatory synapses in neurons.
  • These pathways play crucial, non-redundant roles in regulating synaptic plasticity.
  • The combined action of these pathways is essential for long-lasting synaptic plasticity.