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Related Experiment Video

Updated: May 23, 2025

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

Meprin β Modulates Brevican Proteolysis Impairing Neural Plasticity and Memory Formation.

Maximilian Keller¹, Celine Gallagher², Simon Kreiselmaier¹

¹Institute for Pathobiochemistry, University Medical Center, Mainz, Germany.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|May 21, 2025

Summary

Metalloprotease meprin β overexpression in neurons impairs cognitive functions and long-term potentiation (LTP) in mice. Meprin β modulates brevican, a protein linked to learning and memory deficits.

Keywords:

brevican extracellular matrix long‐term potentiation memory consolidation meprin β

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Last Updated: May 23, 2025

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

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Published on: June 17, 2015

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Published on: June 23, 2022

Quantifying Subcellular Ubiquitin-proteasome Activity in the Rodent Brain

Quantifying Subcellular Ubiquitin-proteasome Activity in the Rodent Brain

Published on: May 21, 2019

Area of Science:

Neuroscience
Molecular Biology
Biochemistry

Background:

Meprin β is a metalloprotease involved in various physiological processes, including brain functions.
Its specific roles in the brain beyond amyloid β generation are not fully understood.
Understanding meprin β's broader neurological functions is crucial for comprehending neural circuit dynamics.

Purpose of the Study:

To investigate the broader functions of meprin β in the brain, particularly its impact on cognitive functions and neural plasticity.
To explore the molecular mechanisms underlying meprin β's effects on neuronal function.
To identify potential mediators linking meprin β activity to observed neurological deficits.

Main Methods:

Utilized a mouse model with neuronal overexpression of meprin β in the cortex and hippocampus.
Conducted behavioral assessments using the Morris' Water Maze test.
Performed electrophysiological recordings (long-term potentiation - LTP) in hippocampal slices.
Analyzed protein expression via western blotting and identified proteolytic substrates using N-terminomics.

Main Results:

Meprin β overexpression led to impaired cognitive functions in behavioral tests.
Electrophysiology revealed impaired LTP and increased neuronal excitability in meprin β-overexpressing mice.
No significant changes were observed in NMDA or AMPA receptor expression.
N-terminomics identified brevican as a meprin β substrate, suggesting its role in mediating the observed effects.

Conclusions:

Meprin β plays a significant role in regulating cognitive functions and synaptic plasticity in the brain.
The metalloprotease meprin β influences neuronal excitability and LTP, potentially via modulation of brevican.
These findings highlight meprin β as a key player in neurological processes and suggest its involvement in learning and memory mechanisms.