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Changes in synaptosomal glutamate release during postnatal development in the rat hippocampus and cortex
K J Collard1, R Edwards, Y Liu
1Department of Physiology, University of Wales, College of Cardiff, UK.
Insights
Glutamate release from rat brain synaptosomes increases significantly after postnatal day 15. This developmental change in neurotransmitter release may explain why neonatal brains are less vulnerable to ischemic damage.
Area of Science:
- Neuroscience
- Developmental Biology
- Neurochemistry
Background:
- Glutamate is a key excitatory neurotransmitter in the brain.
- Understanding glutamate release during development is crucial for comprehending brain maturation and vulnerability.
- Synaptosomes are essential for studying neurotransmitter release mechanisms.
Purpose of the Study:
- To investigate the developmental changes in potassium-induced glutamate release from rat hippocampal and cortical synaptosomes.
- To correlate these changes with brain maturation and potential neuroprotection during development.
Main Methods:
- Utilized radiolabeled [3H]L-glutamate to quantify release.
- Examined synaptosomes from rats across various developmental stages, from postnatal day 4 (PND 4) to adulthood.
- Stimulated neurotransmitter release using potassium (K+) depolarization.
Main Results:
- Synaptosomes from younger rats (PND 4-PND 15) showed significantly lower [3H]L-glutamate release compared to adults.
- Glutamate release sensitivity increased progressively from PND 15, reaching adult levels.
- Variations in release sensitivity were observed during early development (PND 4-PND 15).
Conclusions:
- The lower glutamate release in neonatal rats may contribute to their relative resistance to ischemic injury.
- Developmental changes in K+-evoked glutamate release are linked to neural plasticity during critical developmental periods.
- This study highlights a key neurochemical maturation process influencing brain development and resilience.
Abstract:
The effectiveness of K+ depolarisation in inducing the release of [3H]L-glutamate from preloaded hippocampal and cortical synaptosomes was examined in rats aged from postnatal day 4 (PND 4) to adult. In the lower age groups studied (PND 4-PND 15), the response to depolarisation was always smaller than that seen in the adult. From PND 15, the sensitivity of the release process increased steadily to a maximum level in the adult. The relatively small amounts of glutamate released in response to K(+)-depolarisation in the younger age groups may be a factor which contributes to the relative insensitivity of neonatal brain to ischaemic damage. Discrete variations in the sensitivity to K+ depolarisation observed in animals aged from PND 4 to PND 15 may be involved in plastic changes in neural activity which are known to occur during this important development period.