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NMDA-induced apoptosis in the developing rat brain
Hirotake Takai1, Kei-Ichi Katayama, Akira Yasoshima
1Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Summary
Excessive N-methyl-D-aspartate receptor (NMDAR) stimulation induces apoptosis in the fetal rat brain cortex. Neonatal exposure to NMDAR agonists did not trigger neuronal cell death, suggesting developmental sensitivity.
Area of Science:
- Neuroscience
- Developmental Biology
- Neuropharmacology
Background:
- N-methyl-D-aspartate receptors (NMDARs) are crucial for synaptic plasticity in the developing brain.
- Overstimulation of NMDARs is implicated in triggering neuronal apoptosis.
Purpose of the Study:
- To investigate the effects of N-methyl-D-aspartate (NMDA) administration on neuronal apoptosis in the developing rat brain.
- To determine if NMDA-induced apoptosis differs between fetal and neonatal exposure.
Main Methods:
- NMDA was administered to pregnant dams and neonates (embryonal day 18 to postnatal day 14).
- Apoptotic neuronal cell nuclei were quantified in specific brain regions.
- Dose-dependent effects and time course of apoptosis were analyzed.
Main Results:
- NMDA administration significantly increased apoptotic neuronal cells in the fetal cerebral cortex in a dose-dependent manner.
- Apoptosis peaked 24 hours post-treatment in the fetal group.
- No induction of apoptosis was observed in the neonatal rat brain following NMDA administration.
Conclusions:
- The developing fetal brain, particularly the cerebral cortex, is highly susceptible to NMDA-induced apoptosis.
- Neonatal NMDARs appear resistant to excitotoxic neuronal death within the studied period.
- These findings highlight critical developmental windows for NMDAR-mediated neurotoxicity.