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Dissection of Hippocampal Dentate Gyrus from Adult Mouse

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Hippocampus undergoes transcriptomic changes and synaptic alterations in a Slc17a5 heterozygous mouse model with

Jiannan Chen¹, Jingkun Zhang², Kunhe Ma³

¹Department of Laboratory Animal Sciences, School of Basic Medical Sciences, Capital Medical University, Beijing, China.

|March 28, 2026

Summary

Haploinsufficiency of the sialic acid transporter gene SLC17A5 causes specific working memory deficits in adult mice. This impairment is linked to molecular disruptions in the brain, including extracellular matrix remodeling and synaptic damage.

Keywords:

Animal model Hippocampus Memory deficit SLC17A5

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Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

Sialin, encoded by Slc17a5, is crucial for lysosomal function.
Complete loss of Sialin causes severe neurological impairment due to sialic acid storage diseases.
The impact of partial Slc17a5 deficiency (haploinsufficiency) on adult brain function is not well understood.

Purpose of the Study:

To investigate the effects of heterozygous Slc17a5 deletion on adult mouse brain function.
To identify molecular mechanisms underlying cognitive deficits in Slc17a5 haploinsufficiency.

Main Methods:

Utilized heterozygous Slc17a5 knockout mice (Slc17a5+/-).
Assessed cognitive function using the Y-maze test.
Performed hippocampal transcriptomic profiling and protein-protein interaction network analysis.
Quantified synaptic protein levels (Synaptophysin).

Main Results:

Slc17a5+/- mice displayed specific working memory deficits.
Transcriptomic analysis revealed dysregulation in extracellular matrix organization and microtubule-based processes.
Identified key hub genes in affected molecular pathways.
Confirmed a significant reduction in the presynaptic protein Synaptophysin, suggesting synaptic damage.

Conclusions:

SLC17A5 haploinsufficiency is sufficient to induce selective cognitive impairment in adult mice.
Molecular disruptions include extracellular matrix remodeling, intracellular transport deficits, and synaptic damage.
Provides mechanistic insights into Slc17a5's role in brain function and neurological disorders.