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Sequential changes in glutamate transporter mRNA levels during Fe(3+)-induced epileptogenesis
1Department of Psychiatry, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki, Japan.
Brain Research. Molecular Brain Research
|January 29, 2000
Summary
Severe head injury can trigger epilepsy by affecting glutamate transporters. Impaired glial glutamate transport in rats led to seizures, suggesting a mechanism for chronic epileptogenesis after brain injury.
Area of Science:
- Neuroscience
- Epilepsy Research
- Neurochemistry
Background:
- Severe head injury is linked to recurrent seizures and epilepsy.
- Parenchymal hemorrhage, a consequence of head injury, correlates with post-traumatic epilepsy.
- Ferric cation injection into rat amygdala induces lipid peroxidation and seizures, modeling aspects of head injury.
Purpose of the Study:
- To investigate if glutamate regulation is perturbed following severe head injury.
- To explore the role of glutamate transporters in chronic epileptogenesis after brain injury.
- To examine changes in glutamate transporter mRNA levels post-injury.
Main Methods:
- Rats received ferric chloride (FeCl3) microinjection into the amygdaloid body.
- mRNA levels of glutamate transporters GLAST, GLT-1, and EAAC-1 were measured.
- Measurements were taken in hippocampi and cerebral cortex at various time points post-injection.
Main Results:
- Neuronal transporter EAAC-1 mRNA increased bilaterally for up to 30 days.
- Glial transporter GLT-1 mRNA returned to basal levels.
- Glial transporter GLAST mRNA was downregulated at 15 and 30 days, coinciding with spontaneous seizures.
Conclusions:
- Epileptogenesis following severe head injury may involve impaired glial glutamate transport.
- Downregulation of GLAST suggests a disruption in glutamate homeostasis.
- This disruption can lead to neuronal excitation and an imbalance of neurotransmitters, contributing to chronic epilepsy.