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Related Experiment Video

Updated: Dec 15, 2025

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

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Published on: February 5, 2018

The endogenous neuronal complement inhibitor SRPX2 protects against complement-mediated synapse elimination during

Qifei Cong¹, Breeanne M Soteros¹, Mackenna Wollet²

¹Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.

Nature Neuroscience

|July 15, 2020

Summary

The sushi domain protein SRPX2 acts as a complement inhibitor in neurons, protecting synapses from elimination. SRPX2 deficiency leads to increased synapse loss and altered brain development, highlighting its crucial role in neural circuit maintenance.

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Published on: November 14, 2014

Area of Science:

Neuroscience
Immunology
Molecular Biology

Background:

Complement-mediated synapse elimination is vital for brain development and implicated in neurological disorders.
The role of neuronal complement inhibitors in regulating synapse elimination remains largely unexplored.

Purpose of the Study:

To investigate whether neurons express complement inhibitors that safeguard synapses from complement-mediated elimination.
To elucidate the function of the sushi domain protein SRPX2 in synapse regulation and complement pathways.

Main Methods:

Direct binding assays of SRPX2 to C1q.
Analysis of SRPX2 knockout (SRPX2^-/Y) mice for complement deposition and microglial activity.
Assessment of synapse numbers, axon segregation, and spine pruning in specific brain regions (lateral geniculate nucleus and somatosensory cortex).
Generation and analysis of C3^-/-;SRPX2^-/Y double-knockout mice.

Main Results:

SRPX2 directly binds to C1q, inhibiting its activity.
SRPX2^-/Y mice exhibit elevated C3 deposition and increased microglial synapse engulfment.
These mice show transient synapse loss and altered retinogeniculate axon segregation, along with reduced thalamocortical synapses and increased spine pruning in the cortex.
Double-knockout mice lacking both C3 and SRPX2 display C3^-/- phenotypes, confirming C3's necessity for SRPX2's effects.

Conclusions:

SRPX2 functions as a neuronal complement inhibitor, protecting synapses from complement-mediated elimination.
SRPX2 plays a critical role in maintaining synapse stability in both the thalamus and the cortex.
The findings establish SRPX2 as a key regulator of synapse elimination via the complement system.