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Altered transporter-mediated neocortical GABA release in Rasmussen encephalitis
Michael P Rassner1, Vera van Velthoven-Wurster, Georgia Ramantani
1Section of Clinical Neuropharmacology, Department of Neurosurgery, Albert-Ludwigs University, Freiburg, Germany.
Epilepsia
|January 31, 2013
Summary
Epileptic seizures in Rasmussen encephalitis may stem from reduced gamma-aminobutyric acid (GABA) release. This crucial inhibitory neurotransmitter release diminishes with epilepsy duration in RE patients.
Area of Science:
- Neuroscience
- Epileptology
- Neurochemistry
Background:
- Rasmussen encephalitis (RE) is a rare, chronic inflammatory neurological disease characterized by frequent epileptic seizures.
- Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system, crucial for regulating neuronal excitability.
- Dysfunctional GABAergic neurotransmission is implicated in various epilepsy syndromes.
Purpose of the Study:
- To investigate the role of gamma-aminobutyric acid (GABA) release in the pathogenesis of epileptic seizures in Rasmussen encephalitis (RE).
- To determine if insufficient GABA release contributes to seizure generation in RE.
- To explore the relationship between GABA release, extracellular calcium, and epilepsy duration in RE patients.
Main Methods:
- Utilized tritium-labeled GABA ((3)H-GABA) release assays from neocortical synaptosomes.
- Stimulated GABA release via veratridine-induced intrasynaptosomal Na(+) accumulation, mimicking high neuronal activity.
- Compared GABA release in tissues from three RE patients and nine non-RE individuals, manipulating extracellular calcium ([Ca(2+) ]e).
Main Results:
- Markedly reduced (3)H-GABA release was observed in neocortical synaptosomes from RE patients compared to non-RE controls.
- In non-RE tissues, extracellular calcium concentration ([Ca(2+) ]e) showed an inverse relationship with GABA release.
- In RE, the reduction in additional GABA release upon calcium withdrawal correlated with the presurgical duration of epilepsy, indicating a loss of an antiseizure mechanism over time.
Conclusions:
- Insufficient GABA release may promote epileptic seizures in Rasmussen encephalitis.
- The observed reduction in GABA release and its impairment with epilepsy duration suggest a progressive loss of inhibitory control in RE.
- The findings highlight a potential GABAergic deficit contributing to the pathophysiology of RE-associated epilepsy.
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