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Assessment of Dendritic Arborization in the Dentate Gyrus of the Hippocampal Region in Mice
Published on: March 31, 2015
Hippocampal dendritic spines modifications induced by perinatal asphyxia.
G E Saraceno1, R Castilla, G E Barreto
1Laboratorio de Citoarquitectura y Plasticidad Neuronal, Instituto de Investigaciones Cardiológicas "Prof. Dr. Alberto C. Taquini", UBA-CONICET, Buenos Aires, Argentina.
Neural Plasticity
|May 31, 2012
Summary
Perinatal asphyxia (PA) alters brain synapses, reducing F-actin in hippocampal spines. This suggests long-term changes in the actin cytoskeleton contribute to synaptic damage after birth asphyxia.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Neuroscience
Background:
- Perinatal asphyxia (PA) impacts synaptic function and neuronal structure.
- Previous research linked hypoxia to long-term ubi-protein accumulation in rat neostriatum.
- F-actin's concentration in dendritic spines suggests its role in CNS alterations due to hypoxia.
Purpose of the Study:
- To investigate the effects of PA on the actin cytoskeleton in hippocampal postsynaptic densities (PSD).
- To assess long-term changes in synaptic structure and F-actin organization following PA.
Main Methods:
- Utilized correlative fluorescence-electron microscopy photooxidation in 4-month-old rats.
- Analyzed hippocampal postsynaptic densities (PSD) for F-actin and ubiquitination levels.
- Performed western blot analysis for β-actin expression in PSD.
Main Results:
- Postsynaptic densities (PSD) exhibited increased thickness and ubiquitination.
- A significant decrease in F-actin-stained spines was observed in hippocampal excitatory synapses post-PA.
- Western blot showed a non-significant trend towards decreased β-actin in PSD of PA animals.
Conclusions:
- Long-term alterations in the actin cytoskeleton may play a role in postsynaptic density (PSD) changes induced by perinatal asphyxia.
- Synaptic damage following PA appears to be a widespread phenomenon affecting actin organization.

