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Related Experiment Video

Updated: Nov 25, 2025

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

Published on: October 27, 2019

Microglial G_i-dependent dynamics regulate brain network hyperexcitability.

Mario Merlini¹, Victoria A Rafalski¹, Keran Ma¹

¹Gladstone Institutes, San Francisco, CA, USA.

Nature Neuroscience

|December 15, 2020

Summary

This summary is machine-generated.

Microglial dynamics regulated by G_i signaling are crucial for brain health. Inhibiting G_i in microglia disrupts brain surveillance, leading to seizures and neuronal network hyperexcitability.

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Last Updated: Nov 25, 2025

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

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Published on: February 16, 2018

Area of Science:

Neuroscience
Cell Biology
Neuroimmunology

Background:

Microglia, the brain's resident immune cells, constantly survey their environment.
Microglial dynamics are essential for maintaining brain homeostasis and function.
Dysfunctional microglial surveillance is implicated in various neurological disorders.

Purpose of the Study:

To investigate the role of G_i-dependent microglial dynamics in preventing neuronal network hyperexcitability.
To determine the consequences of inhibiting G_i signaling in microglia on brain function.

Main Methods:

Generation of G_i-inhibited (Mg^PTX) mice.
Assessment of microglial brain surveillance and process motility.
Electrophysiological recordings in awake adult mice to measure neuronal activity and hypersynchrony.

Main Results:

Genetic inhibition of G_i in microglia led to reduced brain surveillance and directed process motility.
Mg^PTX mice exhibited spontaneous seizures.
Physiologically evoked neuronal activity resulted in increased hypersynchrony in Mg^PTX mice.

Conclusions:

G_i-dependent microglial dynamics are critical for preventing neuronal network hyperexcitability.
Disruption of microglial surveillance contributes to seizure generation and network dysfunction.
Targeting G_i signaling in microglia may offer therapeutic strategies for neurological diseases characterized by hyperexcitability.