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Related Experiment Video

Updated: Apr 13, 2026

Assessment of Memory Function in Pilocarpine-induced Epileptic Mice

Assessment of Memory Function in Pilocarpine-induced Epileptic Mice

Published on: June 4, 2020

CBP-Dependent memory consolidation in the prefrontal cortex supports object-location learning.

Philip A Vieira¹, Edward Korzus¹

¹Department of Psychology & Neuroscience Program, University of California Riverside, California.

|May 6, 2015

Summary

The cyclic-AMP regulatory element binding protein (CREB) Binding Protein (CBP) histone acetyltransferase (HAT) in the medial prefrontal cortex (mPFC) is crucial for object-location memory. Its hypofunction disrupts long-term spatial memory encoding.

Keywords:

epigenetic regulation histone acetyltransferase mPFC object-location spatial memory

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Related Experiment Videos

Last Updated: Apr 13, 2026

Assessment of Memory Function in Pilocarpine-induced Epileptic Mice

Assessment of Memory Function in Pilocarpine-induced Epileptic Mice

Published on: June 4, 2020

A Within-Subject Experimental Design using an Object Location Task in Rats

A Within-Subject Experimental Design using an Object Location Task in Rats

Published on: May 6, 2021

Place and Response Learning in the Open-field Tower Maze

Place and Response Learning in the Open-field Tower Maze

Published on: October 28, 2015

Area of Science:

Neuroscience
Cognitive Neuroscience
Molecular Neuroscience

Background:

Spatial memory relies on hippocampus-dependent recollection.
The prefrontal cortex-hippocampus interaction is vital for spatial memory.
Prefrontal cortex mechanisms in spatial memory are not fully understood.

Purpose of the Study:

To investigate the role of cyclic-AMP regulatory element binding protein (CREB) Binding Protein (CBP) histone acetyltransferase (HAT) in the medial prefrontal cortex (mPFC) in object-location memory.
To elucidate the molecular mechanisms underlying spatial memory in the mPFC.

Main Methods:

Investigated the effects of acute CBP HAT hypofunction in the mPFC on object-location memory in a delay-dependent manner.
Utilized molecular and genetic approaches to study CBP HAT function in neural circuits.

Main Results:

Acute hypofunction of CBP HAT in the mPFC caused a delay-dependent disruption of object-location memory.
CBP HAT-mediated lysine acetylation of nuclear proteins supports long-term memory encoding in mPFC circuits.

Conclusions:

CBP HAT in the mPFC plays a critical role in long-term object-location memory encoding.
mPFC long-term memory mechanisms complement hippocampus-dependent spatial memory.
mPFC mechanisms are essential for integrating spatial information for behavioral responses.