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Related Concept Videos

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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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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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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Complex microtubule structures are present in resting cells and in dividing cells. In resting cells, they are responsible for maintaining the cellular architecture, tracks for intracellular transport, positioning of organelles, assembly of cilia and flagella. They mediate the bipolar spindle assembly for chromosomal segregation and positioning of the cell division plate in dividing cells. The formation of microtubule complex structures depends on the cell type, cell stage, and cell function.
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Related Experiment Video

Updated: Oct 30, 2025

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species
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Fractionation for Resolution of Soluble and Insoluble Huntingtin Species

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Huntingtin and the Synapse.

Jessica C Barron1, Emily P Hurley1, Matthew P Parsons1

  • 1Division of Biomedical Sciences, Faculty of Medicine, Memorial University, St. John's, NL, Canada.

Frontiers in Cellular Neuroscience
|July 2, 2021
PubMed
Summary
This summary is machine-generated.

Huntington disease (HD) therapies targeting mutant huntingtin (mHTT) may lower essential wild-type huntingtin (wtHTT). This review argues that wtHTT loss impairs synaptic function, preceding neurodegeneration in HD.

Keywords:
HuntingtinHuntington diseaseautophagyendocytosisexcitotoxicityexocytosisintracellular tranportsynaptic plastcity

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Efficient and Scalable Production of Full-length Human Huntingtin Variants in Mammalian Cells using a Transient Expression System
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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Huntington disease (HD) is a genetic disorder caused by a CAG repeat expansion in the huntingtin (HTT) gene, leading to mutant HTT (mHTT) protein production.
  • Current RNA-targeting therapies for HD, such as antisense oligonucleotides (ASOs) and RNA interference (RNAi), aim to reduce mHTT levels.
  • These therapies often lack selectivity, potentially lowering beneficial wild-type HTT (wtHTT) levels, which are already reduced in HD patients.

Purpose of the Study:

  • To review the critical role of wtHTT at the synapse.
  • To discuss the consequences of wtHTT reduction on synaptic function in the context of HD.
  • To argue that wtHTT loss is detrimental to synaptic health and may precede neurodegeneration.

Main Methods:

  • Literature review focusing on the function of wtHTT in synaptic transmission.
  • Analysis of the impact of reduced wtHTT levels on pre- and postsynaptic mechanisms.
  • Synthesis of evidence linking synaptic dysfunction to neurodegenerative processes in HD.

Main Results:

  • Wild-type HTT (wtHTT) plays a crucial role in multiple aspects of synaptic neurotransmission.
  • wtHTT is implicated in protein transport, neurotransmitter release, and vesicle recycling at synapses.
  • Reduced wtHTT levels negatively impact both pre- and postsynaptic functions, leading to synaptic dysfunction.

Conclusions:

  • Wild-type HTT (wtHTT) is essential for maintaining normal synaptic function.
  • Synaptic dysfunction resulting from wtHTT loss is a sensitive indicator of neuronal health and precedes neurodegeneration in HD.
  • Non-selective therapies that deplete wtHTT may exacerbate HD pathology by compromising synaptic integrity.