Abstracts

Rationale: The outcome of surgery in patients with temporal lobe epilepsy (TLE) and normal high-resolution magnetic resonance imaging (MRI) has been significantly worse than in patients with unilateral hippocampal damage upon MRI. As our previous studies have demonstrated that increased adenosine clearance by elevated adenosine kinase (ADK) and deletion of adenosine A1 receptors (A1Rs) both cause spontaneous intrahippocampal electrographic seizures. We hypothesized that the epileptogenic mechanisms underlying MR negative temporal lobe epilepsy is related to changes in ADK and A1Rs expression, and that those changes might be associated with the development of epilepsy in these patients. Methods: Surgically resected human epileptic cortical specimens from MR negative temporal lobe epilepsy patients with mild hippocampus sclerosis (n=16), we use immunohistochemistry approach to examine the expression of ADK and A1Rs, and compared that with control cortical issue.  Results: In control group, ADK displayed weak staining in the pyramidal neurons within the different hippocampal subfields and cortex, while A1Rs showed mediate staining in the different hippocampal subfields and cortex. In the mild hippocampus sclerosis group, neuronal ADK and A1Rs were markedly reduced in subfields showing neuron loss, while in the peripheral area of lesion in hippocampus and cortex, neuronal ADK increased in the a revertant fetal expression pattern. Conclusions: A1Rs is downregulated in MR negative temporal lobe epilepsy patients with mild hippocampus sclerosis in areas with mild neuron loss, while ADK is upregulated in the peripheral area of lesion in hippocampus and cortex. The alteration may be part of the mechanism underlying impaired adenosine signaling found in MR negative temporal lobe epilepsy patients with mild hippocampus sclerosis Funding: BIBD-PXM2013_014226_07_000084,National Natural Science Foundation of China (81571275), Scientific Research Common Program of Beijing Commission of Education (KM201410025027).