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Salah, A; Dilsiz, P; Frecska-Horvath, L; Ruppe, V; Shoshkes, Reiss C; Carlson, C; Doyle, W; Devinsky, O; Talos, D M
"Altered NMDA and AMPA receptor subunit expression in cortical tissue from autism spectrum disorders and treatment-resistant temporal lobe epilepsy" [Meeting Abstract]
Epilepsy currents 2013 March-April 2013; 13():349-349
Rationale: Autism spectrum disorders (ASDs), characterized by impaired social interactions, impaired communication and stereotyped behaviors, are highly associated with epilepsy (up to 38%). A shift in cortical excitatory/inhibitory balance towards increased excitation and/or decreased inhibition may play a key role in the pathophysiology of both ASDs and epilepsy. We hypothesized that differences in AMPA receptor (AMPAR) and NMDA receptor (NMDAR) subunit expression in ASD and epilepsy patients may represent a basis for distinct clinical neurological manifestations. Identifying specific synaptic mechanisms for autism and epilepsy will allow development of targeted therapies. Methods: Brain specimens from treatment-resistant temporal lobe epilepsy cases were collected prospectively during resective surgery at NYULMC (n=5; ages 21-37 years). Autopsy temporal and frontal lobe samples from ASD patients (n=5; ages 4-22 years) and regionmatched control specimens from cases with normal neurological history (n=10; ages 5-48 years) were obtained from Maryland Brain and Tissue Bank. All ASD cases met the standard diagnostic criteria (Autism Diagnostic Interview-Revised) and had no evidence of epilepsy, while none of the epilepsy patients were diagnosed with autism. The levels of the NMDAR and AMPAR subunits (NR1, NR2A, NR2B, GluR1 and GluR2) were quantified by Western blot and compared among groups (one-way ANOVA and t-tests). Results: Temporal lobe cortex analysis demonstrated a significant increase in NR1 expression in autism patients (288% of control; p<0.0001), but no significant change in epilepsy cases (96% of control; p>0.05). In both groups, NR2A was significantly decreased (ca. 40% of control; p<0.0001), while NR2B demonstrated a significant upregulation (255% of control in autism and 511% of control in epilepsy; p<0.0001). NR2B levels were significantly higher in epilepsy, relative to autism patients (p<0.001). GluR1 expression was increased in both autism (388% of control; p<0.0001) and epilep!

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