Long-Term Memory Testing
Objective: Assessment of long-term memory enhancement in HDAC3-FLOX mice and RGFP136-treated mice compared to wild-type controls
This is a Long-Term Memory Testing protocol using mouse as the model organism. The procedure involves 6 procedural steps, 1 equipment items, 3 materials. Extracted from a 2011 paper published in Journal of Neuroscience.
Model and subjects
mouse • HDAC3-FLOX genetically modified mice and wild-type controls • Not specified • Not specified • Not specified • Not specified
Study window
Estimated timing pending
Core workflow
Generate focal HDAC3 deletions • Administer RGFP136 pharmacologically • Assess histone acetylation
Primary readouts
- Long-term memory performance in HDAC3-FLOX mice vs wild-type controls
- Long-term memory performance in RGFP136-treated mice vs controls
- Histone acetylation levels following HDAC3 deletion or RGFP136 treatment
- Expression levels of Nr4a2 and c-fos in dorsal hippocampus
Key equipment and reagents
Use this page as an execution guide, then fall back to the source paper whenever you need exact exclusions, dosing details, or assay-specific caveats.
Confirm first
- Verify the animal model, intervention setup, and collection timepoints against the source paper.
- Check that every direct vendor link matches the exact specification your lab plans to run.
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- Work through the protocol steps in order and use the inline vendor chips only when you need to source or verify an item.
- Jump to Experimental Context for readouts, data shape, and analysis flow before planning downstream analysis.
Protocol Steps
Start here. The step list is optimized for running the experiment, with direct vendor links available inline when you need to source a cited item.
Generate focal HDAC3 deletions
Use HDAC3-FLOX genetically modified mice in combination with adeno-associated virus-expressing Cre recombinase to generate focal homozygous deletions of Hdac3 in area CA1 of the dorsal hippocampus
Note: This is a genetic approach to HDAC3 manipulation
View evidence from paper
“We used HDAC3-FLOX genetically modified mice in combination with adeno-associated virus-expressing Cre recombinase to generate focal homozygous deletions of Hdac3 in area CA1 of the dorsal hippocampus”
Administer RGFP136 pharmacologically
Use selective inhibitor of HDAC3, RGFP136, via intrahippocampal delivery as a complementary pharmacologic approach to HDAC3 manipulation
Note: This is a pharmacologic approach complementing the genetic approach
View evidence from paper
“To complement this approach, we also used a selective inhibitor of HDAC3, RGFP136”
Assess histone acetylation
Perform immunohistochemistry to determine if focal deletion or intrahippocampal delivery of RGFP136 resulted in increased histone acetylation
Note: Confirms molecular effects of HDAC3 manipulation
View evidence from paper
“Immunohistochemistry showed that focal deletion or intrahippocampal delivery of RGFP136 resulted in increased histone acetylation”
Test long-term memory
Assess long-term memory in HDAC3-FLOX mice and RGFP136-treated mice compared to wild-type controls to determine if memory is enhanced
Note: Both focal deletion of HDAC3 and HDAC3 inhibition via RGFP136 significantly enhanced long-term memory in a persistent manner
View evidence from paper
“Both the focal deletion of HDAC3 as well as HDAC3 inhibition via RGFP136 significantly enhanced long-term memory in a persistent manner”
Analyze gene expression
Examine expression of genes implicated in long-term memory from dorsal hippocampal punches using quantitative reverse transcription-PCR
Note: Expression of Nr4a2 and c-fos was significantly increased in HDAC3-FLOX mice compared with wild-type controls
View evidence from paper
“Next we examined expression of genes implicated in long-term memory from dorsal hippocampal punches using quantitative reverse transcription-PCR”
Test Nr4a2 mechanism
Deliver Nr4a2 small interfering RNA intrahippocampally to determine if Nr4a2 is required for memory enhancement observed in HDAC3-FLOX mice
Note: Memory enhancements observed in HDAC3-FLOX mice were abolished by intrahippocampal delivery of Nr4a2 siRNA
View evidence from paper
“Memory enhancements observed in HDAC3-FLOX mice were abolished by intrahippocampal delivery of Nr4a2 small interfering RNA”