Related Experiment Video
Updated: Dec 15, 2025

10:55
Assessment of Dendritic Arborization in the Dentate Gyrus of the Hippocampal Region in Mice
Published on: March 31, 2015
10.6K
Dendritic Spine Density is Increased in Arcadlin-deleted Mouse Hippocampus
Chiaki Takeuchi1, Miho Ishikawa1, Toshinori Sawano1
1Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, Japan.
Neuroscience
|July 7, 2020
Summary
Arcadlin, a cell adhesion molecule, reduces dendritic spine density in the hippocampus. This molecule is crucial for neural network remodeling in response to antidepressants and electroconvulsive seizures.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Neural network remodeling is influenced by neural activity and interventions like antidepressants.
- Synaptic cell adhesion molecules are key to neural circuitry and synaptic strength modulation.
- Arcadlin (Protocadherin-8) is a unique protocadherin rapidly induced by neural activity.
Purpose of the Study:
- To investigate the function of Arcadlin in hippocampal neuron morphology.
- To determine Arcadlin's role in neural remodeling induced by electroconvulsive seizures (ECS) and fluoxetine.
Main Methods:
- Analysis of dendritic morphology in Arcadlin-deficient (Acad-/-) mice.
- Assessment of spine density changes following ECS in wild-type and Acad-/- mice.
- Evaluation of Arcadlin induction and spine density changes after chronic fluoxetine treatment in wild-type and Acad-/- mice.
Main Results:
- Acad-/- mice exhibited higher dendritic spine density compared to wild-type mice.
- ECS treatment induced Arcadlin and decreased spine density in wild-type mice, an effect absent in Acad-/- mice.
- Chronic fluoxetine treatment induced Arcadlin and reduced spine density in wild-type mice, with this effect diminished in Acad-/- mice.
Conclusions:
- Arcadlin possesses spine-repulsing activity.
- Arcadlin mediates the decrease in hippocampal dendritic spine density induced by fluoxetine.
- Arcadlin plays a significant role in the activity-dependent remodeling of hippocampal neurons.

