Abstracts

RATIONALE:Epilepsy is a disorder in which abnormal neuronal firing is associated with increased extracellular glutamate concentration. Recent findings indicate that the cytosolic proteins commplexin I and II interact with the SNAP receptor complex and may modulate neurotransmitter release in inhibitory and excitatory neurons respectively (Lancet 353, 154, 1998). Since abnormal expression of these regulatory proteins may influence glutamate release, we have therefore examined the expression of both complexins in the hippocampus from patients with temporal lobe epilepsy. METHODS:Surgically removed tissue was dissected and the CA1 region subjected to RT-PCR. RESULTS: Following normalization to the reporter gene b-actin, a 54% decrease in complexin II gene expression was detected in epilepsy patients (n=5)(p T0.01). Expression of synaptophysin, a neuronal marker, was reduced by 36% in epilepsy patients. No change in the expression of the inhibitory complexin I was observed. These results were confirmed by immunochemistry. CONCLUSIONS:It is suggested that in temporal lobe epilepsy, CA1 pathology involves excitatory (glutamatergic) neurons. Such an imbalance between excitatory and inhibitory circuitry may contribute to the pathophysiology of this disorder. (Supported by the Medical Research Council of Canada/Glaxo Wellcome/Savoy Foundation).