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Role of Hippocampus in Memory

Role of Hippocampus in Memory

The hippocampus, a critical brain structure, plays an essential role in memory processing, particularly in the formation and retrieval of memory. This small, seahorse-shaped region is located within the medial temporal lobe, with one hippocampus in each brain hemisphere. Experimental studies involving lesions in the hippocampi of rats have demonstrated significant impairments in tasks such as object recognition and maze navigation, indicating the hippocampus involvement in both recognition and...

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Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

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BAI1 regulates spatial learning and synaptic plasticity in the hippocampus.

Dan Zhu, Chenchen Li, Andrew M Swanson

The Journal of Clinical Investigation

|March 10, 2015

Summary

Brain-specific angiogenesis inhibitor 1 (BAI1) regulates synaptic plasticity by stabilizing PSD-95 protein levels. Loss of BAI1 impairs memory and synaptic function, but restoring PSD-95 rescues these deficits.

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Last Updated: Apr 16, 2026

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Published on: August 11, 2019

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Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

Published on: January 1, 2018

Area of Science:

Neuroscience
Molecular Biology
Synaptic Plasticity

Background:

Synaptic plasticity is crucial for learning and memory.
Molecular regulators of synaptic plasticity are not fully understood.
Brain-specific angiogenesis inhibitor 1 (BAI1) role in synaptic function is unclear.

Purpose of the Study:

Investigate the role of BAI1 in synaptic plasticity and hippocampus-dependent memory.
Elucidate the molecular mechanisms by which BAI1 regulates synaptic function.

Main Methods:

Generated and analyzed mice lacking brain-specific angiogenesis inhibitor 1 (BAI1).
Assessed hippocampus-dependent spatial learning and memory.
Measured long-term potentiation (LTP) and long-term depression (LTD).
Quantified postsynaptic density (PSD) and PSD-95 protein levels.
Investigated BAI1 interaction with MDM2 and its effect on PSD-95 stability.
Utilized viral gene therapy to restore PSD-95 expression in BAI1-deficient mice.

Main Results:

BAI1-deficient mice exhibit deficits in spatial learning and memory.
Enhanced LTP and impaired LTD were observed in BAI1-deficient mice.
Thinning of the postsynaptic density (PSD) and reduced PSD-95 protein levels were found.
BAI1 interacts with MDM2 to prevent PSD-95 polyubiquitination and degradation.
Restoration of PSD-95 expression rescued synaptic plasticity deficits in BAI1-deficient mice.

Conclusions:

BAI1 regulates synaptic plasticity by modulating PSD-95 stability through interaction with MDM2.
BAI1 deficiency leads to impaired synaptic plasticity and memory deficits.
Targeting the BAI1-MDM2-PSD-95 pathway offers therapeutic potential for neurological disorders.