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Updated: Dec 17, 2025
Dissection of Hippocampal Dentate Gyrus from Adult Mouse
Published on: November 17, 2009
Morphological and functional abnormalities of hippocampus in APC1638T/1638T mice
Chenguang Li1, Takanori Onouchi2, Masaya Hirayama2,3
1Department of Anatomy, Graduate School of Medicine, Gifu University, 1-1 Yanagido, Gifu, 501-1194, Japan.
Abstract:
In the present study, we examined morphology and function of hippocampus in the APC1638T/1638T mouse. Expression levels of the APC mRNA and protein were both identical in the hippocampus of the APC+/+ and APC1638T/1638T mice. The dentate gyrus of the APC1638T/1638T hippocampus was thicker, and has more densely-populated granule cells in the APC1638T/1638T mouse hippocampus. Immunoelectron microscopy revealed co-localization of APC with alpha-amino-3- hydroxy-5-methyl- isoxazole-4-propionate receptor (AMPA-R) and with PSD-95 at post-synapse in the APC+/+ hippocampus, while APC1638T was co-localized with neither AMPA-R nor PSD-95 in the APC1638T/1638T hippocampus. By immunoprecipitation assay, full-length APC expressed in the APC +/+ mouse was co-immunoprecipitated with AMPA-R and PSD-95. In contrast, APC1638T expressed in the APC1638T/1638T mouse was not co-immunoprecipitated with AMPA-R and PSD-95. In the hippocampal CA1 region of the APC1638T/1638T mouse, c-Fos expression after electric foot shock was decreased compared with the APC+/+ mouse. The present study showed some abnormalities on morphology of the hippocampus caused by a truncated APC (APC1638T). Also, our findings suggest that failure in APC binding to AMPA-R and PSD-95 may bring about less activities of hippocampal neurons in the APC1638T/1638T mouse.
Insights
A truncated APC protein (APC1638T) alters hippocampus morphology and neuron activity in mice. This APC variant fails to bind key synaptic proteins, suggesting a mechanism for reduced hippocampal function.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- The Adenomatous Polyposis Coli (APC) gene plays a crucial role in cellular processes, including neuronal function.
- Mutations in APC are linked to various diseases, but its specific role in hippocampal morphology and synaptic function requires further investigation.
Purpose of the Study:
- To investigate the impact of a specific truncated APC mutation (APC1638T) on hippocampus structure and function.
- To explore the molecular interactions of APC with synaptic proteins in the hippocampus.
Main Methods:
- Comparative analysis of hippocampus morphology in APC(1638T/1638T) and wild-type (APC(+/+)) mice.
- Immunoelectron microscopy to assess co-localization of APC with AMPA-R and PSD-95.
- Immunoprecipitation assays to confirm protein interactions.
- Measurement of c-Fos expression as an indicator of neuronal activity.
Main Results:
- APC(1638T/1638T) mice exhibited a thicker dentate gyrus with more densely-populated granule cells.
- Truncated APC1638T did not co-localize with AMPA-R or PSD-95 at postsynaptic sites, unlike full-length APC.
- APC(1638T/1638T) mice showed decreased c-Fos expression in the CA1 region after stimulation, indicating reduced neuronal activity.
Conclusions:
- A truncated APC protein (APC1638T) causes morphological abnormalities in the hippocampus.
- The failure of APC1638T to bind AMPA-R and PSD-95 may lead to diminished hippocampal neuron activity.
