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Synaptic proteins after electroconvulsive seizures in immature rats
Journal of Neurochemistry
|November 1, 1980
Summary
Electroconvulsive seizures in immature rats reduced synaptic proteins and glial cells in the forebrain. Enolase 14-3-2 levels remained unchanged, except for an increase during later seizures, suggesting metabolic demands.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Biochemistry
Background:
- Electroconvulsive seizures (ECS) are used therapeutically but can impact brain development.
- The immature brain's response to ECS is not fully understood, particularly regarding synaptic and glial components.
Purpose of the Study:
- To investigate the effects of ECS administered during different developmental periods on forebrain synaptic proteins and glial markers in young rats.
- To determine if ECS impacts overall forebrain growth and specific neuronal or glial enzyme concentrations.
Main Methods:
- Rats received ECS during specific early postnatal days (2-11, 9-18, or 19-28).
- Forebrain synaptic proteins (synaptin, D1, D2, D3), total protein, forebrain weight, glial enzyme (glutamine synthetase), and neuronal enzyme (enolase 14-3-2) were quantified at 30 days of age.
Main Results:
- ECS led to reduced levels of synaptic proteins and forebrain weight.
- Glutamine synthetase, a glial marker, was also decreased, indicating a reduction in glial cells.
- Neuronal enolase 14-3-2 remained unchanged, except for an increase in rats seized later (days 19-28).
Conclusions:
- ECS during immaturity causes a parallel decrease in synaptic material and glial cell content in the rat forebrain.
- The elevated enolase 14-3-2 in later seizure groups suggests increased glycolytic activity to meet energy demands during seizures in the developing brain.