Differential neuroprotection by A(1) receptor activation and A(2A) receptor inhibition following pilocarpine-induced status epilepticus
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2011-10-01
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Rosim, Fernanda Elisa 
Persike, Daniele Suzete
Amorim, Rebeca Padrão
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Aiming at a better understanding of the role of A(2A) in temporal lobe epilepsy (TLE), we characterized the effects of the A(2A) antagonist SCH58261 (7-(2-phenylethyl)-5-amino-2(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c] pyrimidine) on seizures and neuroprotection in the pilocarpine model. the effects of SCH58261 were further analyzed in combination with the A(1) agonist R-Pia (R(-)-N-6-(2)-phenylisopropyl adenosine). Eight groups were studied: pilocarpine (Pilo), SCH + Pilo, R-Pia + Pilo, R-Pia + SCH + Pilo, Saline, SCH + Saline, R-Pia + Saline, and R-Pia + SCH + Saline. the administration of SCH58261, R-Pia, and R-Pia + SCH58261 prior to pilocarpine increased the latency to SE, and decreased either the incidence of or rate of mortality from SE compared with controls. Administration of R-Pia and R-Pia + SCH58261 prior to pilocarpine reduced the number of Fluoro-Jade B-stained cells in the hippocampus and piriform cortex when compared with control. This study showed that pretreatment with R-Pia and SCH58261 reduces seizure occurrence, although only R-Pia has neuroprotective properties. Further studies are needed to clarify the neuroprotective role of A(2A) in TLE. (C) 2011 Elsevier Inc. All rights reserved.
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Epilepsy & Behavior. San Diego: Academic Press Inc Elsevier Science, v. 22, n. 2, p. 207-213, 2011.