Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Integration of Synaptic Events01:28

Integration of Synaptic Events

Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
Synaptic Signaling01:09

Synaptic Signaling

Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...
Synaptic Signaling01:12

Synaptic Signaling

Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
Long-term Depression01:03

Long-term Depression

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.
Calcium Ion Concentration Mechanism
If over time, all...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

iAstrocytes model cytokine influences on complement expression and neuronal network synchronization.

bioRxiv : the preprint server for biology·2026
Same author

Protein-guided RNA barcoding links transcriptomes to synaptic architecture.

bioRxiv : the preprint server for biology·2026
Same author

Engulfment by brain macrophages in a short-lived vertebrate.

bioRxiv : the preprint server for biology·2026
Same author

Biomarkers.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2025
Same author

Basic Science and Pathogenesis.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2025
Same author

Basic Science and Pathogenesis.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2025
Same journal

Body-Brain Integration: The Lower Brainstem in Sleep-Wake Regulation.

Annual review of neuroscience·2026
Same journal

Planning in the Brain: It's Not What You Think It Is.

Annual review of neuroscience·2026
Same journal

The Emerging Neurobiology of Psychedelics: Critical Periods, Metaplasticity, and Extracellular Matrix Remodeling.

Annual review of neuroscience·2026
Same journal

Rethinking Predictive Processing.

Annual review of neuroscience·2026
Same journal

Path Integration in Alzheimer's Disease: Orientation, Movement, and Theta Rhythmicity.

Annual review of neuroscience·2026
Same journal

The Cellular and Circuit Basis of Temperature Sensation in <i>Drosophila</i>.

Annual review of neuroscience·2026
See all related articles

Related Experiment Video

Updated: May 21, 2026

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes
06:43

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

Published on: February 5, 2018

The complement system: an unexpected role in synaptic pruning during development and disease.

Alexander H Stephan1, Ben A Barres, Beth Stevens

  • 1Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305-5125, USA. astephan@stanford.edu

Annual Review of Neuroscience
|June 22, 2012
PubMed
Summary
This summary is machine-generated.

The classical complement cascade unexpectedly eliminates central nervous system (CNS) synapses during development. This pathway may be reactivated in neurodegenerative diseases, driving synapse loss.

More Related Videos

An Engulfment Assay: A Protocol to Assess Interactions Between CNS Phagocytes and Neurons
07:38

An Engulfment Assay: A Protocol to Assess Interactions Between CNS Phagocytes and Neurons

Published on: June 8, 2014

Experience-Dependent Remodeling of Juvenile Brain Olfactory Sensory Neuron Synaptic Connectivity in an Early-Life Critical Period
07:13

Experience-Dependent Remodeling of Juvenile Brain Olfactory Sensory Neuron Synaptic Connectivity in an Early-Life Critical Period

Published on: March 1, 2024

Related Experiment Videos

Last Updated: May 21, 2026

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes
06:43

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

Published on: February 5, 2018

An Engulfment Assay: A Protocol to Assess Interactions Between CNS Phagocytes and Neurons
07:38

An Engulfment Assay: A Protocol to Assess Interactions Between CNS Phagocytes and Neurons

Published on: June 8, 2014

Experience-Dependent Remodeling of Juvenile Brain Olfactory Sensory Neuron Synaptic Connectivity in an Early-Life Critical Period
07:13

Experience-Dependent Remodeling of Juvenile Brain Olfactory Sensory Neuron Synaptic Connectivity in an Early-Life Critical Period

Published on: March 1, 2024

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • The classical complement cascade, typically involved in immune responses, has an unknown role in the central nervous system (CNS).
  • Synapse elimination is crucial for proper brain wiring during development.

Purpose of the Study:

  • To investigate the role of the classical complement cascade in CNS synapse elimination.
  • To explore the potential involvement of complement-mediated synapse elimination in neurodegenerative diseases.

Main Methods:

  • Localization of complement proteins to developing CNS synapses.
  • Assessment of complement protein function in synapse elimination.
  • Investigation of astrocyte-derived signals inducing complement expression.
  • Analysis of complement protein upregulation in neurodegenerative disease models.

Main Results:

  • Complement proteins are found at developing CNS synapses during active elimination phases.
  • These proteins are essential for normal brain wiring.
  • Astrocytes induce complement component expression in the CNS.
  • Complement proteins are upregulated in the mature brain during neurodegenerative diseases, preceding neuron loss.

Conclusions:

  • The classical complement cascade plays a critical role in developmental synapse elimination in the CNS.
  • This developmental mechanism may be reactivated in neurodegenerative conditions, contributing to synapse loss and disease progression.