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Related Experiment Video

Updated: Oct 26, 2025

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

Protocol for interfering peptide injection into adult mouse hippocampus and spatial memory testing.

Shanshan Cheng¹, Yuqian Shen¹, Zi Chao Zhang^1,2

¹School of Life Science and Technology, Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.

|August 2, 2021

Summary

This study details a method to disrupt hippocampal metabotropic glutamate receptor-dependent long-term depression (mGluR-LTD) in mice. The technique impairs mGluR-LTD and associated learning and memory behaviors.

Keywords:

Behavior Model Organisms Neuroscience

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Published on: April 15, 2016

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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

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$Combined Optogenetic and Freeze-fracture Replica Immunolabeling to Examine Input-specific Arrangement of Glutamate Receptors in the Mouse Amygdala$

Combined Optogenetic and Freeze-fracture Replica Immunolabeling to Examine Input-specific Arrangement of Glutamate Receptors in the Mouse Amygdala

Published on: April 15, 2016

Area of Science:

Neuroscience
Molecular Biology

Background:

Metabotropic glutamate receptor-dependent long-term depression (mGluR-LTD) is crucial for neural plasticity, behavior, learning, and memory.
mGluR-LTD requires rapid, local protein synthesis within minutes.

Purpose of the Study:

To present a protocol for disrupting mGluR-LTD in the adult mouse hippocampus.
To investigate the role of specific protein interactions in mGluR-LTD.

Main Methods:

A protocol for delivering an interfering peptide into the adult mouse hippocampus was developed.
The peptide was designed to disrupt the interaction between polyglutamine binding protein 1 and eukaryotic elongation factor 2.

Main Results:

The delivered peptide successfully impaired hippocampal mGluR-LTD.
Disruption of mGluR-LTD led to deficits in associated behaviors.

Conclusions:

The described method effectively inhibits mGluR-LTD in adult mice.
Targeting the polyglutamine binding protein 1 and eukaryotic elongation factor 2 interaction is a viable strategy to modulate synaptic plasticity and behavior.