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Related Concept Videos

The Synapse02:47

The Synapse

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.
Fusion of Secretory Vesicles with the Plasma Membrane01:26

Fusion of Secretory Vesicles with the Plasma Membrane

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.
In 1993, Jim Rothman proposed that the antiparallel pairing of vesicular and transmembrane SNAREs, or...
Chemical Synapses01:26

Chemical Synapses

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...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Chemical Synapses01:26

Chemical Synapses

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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Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...

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Updated: Jun 19, 2026

Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient
08:06

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Published on: September 3, 2014

The classical complement cascade mediates CNS synapse elimination.

Beth Stevens1, Nicola J Allen, Luis E Vazquez

  • 1Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA. beths@standfordmedalumni.org

Cell
|December 18, 2007
PubMed
Summary
This summary is machine-generated.

Complement protein C1q tags unwanted synapses for elimination during neural development. Aberrant C1q reactivation in the adult retina suggests a role in neurodegenerative diseases like glaucoma.

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Area of Science:

  • Neuroscience
  • Immunology
  • Developmental Biology

Background:

  • Mature neural circuits require eliminating unnecessary synaptic connections during development.
  • The complement system, initiated by C1q, plays a role in immune responses.

Purpose of the Study:

  • To investigate the role of C1q in synaptic pruning during neural development.
  • To explore the potential involvement of C1q in neurodegenerative diseases.

Main Methods:

  • Studied C1q expression in postnatal neurons and its localization to synapses.
  • Utilized C1q-deficient and C3-deficient mice to assess synapse elimination.
  • Examined C1q expression in an adult mouse model of glaucoma.

Main Results:

  • Postnatal neurons express C1q, which localizes to synapses.
  • Mice lacking C1q or C3 showed significant defects in central nervous system synapse elimination.
  • C1q is upregulated and relocalized to synapses in the adult retina during early glaucoma.

Conclusions:

  • Neuronal C1q tags synapses for elimination during development.
  • Complement-mediated synapse elimination may be reactivated in neurodegenerative conditions such as glaucoma.