Effect of low-dose dexmethasone on the expression of NR_2A and NR_2B in hippocampus in temporal lobe epileptic rat
Wang Mei-n
Abstract
Wang Mei-n
Abstract
Objective To explore the effect of dexmethasone on the expressions of the subunits NR 2 A and NR 2 B of NMDA receptors in hippocampus in temporal lobe epileptic rats after kindling. Methods Male Wistar rats were randomly divided into normal group,sham group,natrium saline pretreatment group before kindling( TLE group) and Dex pretreatment group prior to be kindled( Dex group). Typical temporal lobe epileptic model was kindled by Kainic acid( KA) microinjected into right Nucleus amygdalae. In situ hybridization was used to spatio-temporally observe the expression of NR 2 AmRNA and NR 2 BmRNA in hippocampus after kindling or sham operating in rats. Results There was no difference of positive cell count( PCC) of NR 2 AmRNA expression in hippocampus between Sham group and normal group both in total and in each hippocampal subarea( P 0. 05). Compared to Sham group,NR 2 AmRNA expressed higher at 24h,7d,14d,21d after kindling( P 0. 05),and enhanced in CA 1 and DG regions both in total and on 21d after kindling( P 0. 05). While,compared to TLE group,NR 2 AmRNA increased at 6h in Dex group( P 0. 05),and decreased on 7d,14d,21d after kindling( P 0. 05),especially declined in CA 1 and DG regions both in total and on 21d in Dex group than that of TLE group after kindling( P 0. 05). In general,NR 2 BmRNA expressed higher in CA 3 region than that in CA 1 and DG regions in Sham and normal groups( P 0. 05). However,in TLE and Dex groups,its expression was increased in DG than that in CA 1 and CA 3 regions( P 0. 05),and it was enhanced in each subareas in hippocampus in Dex group than that of TLE group( P 0. 05). Conclusion There are temporal and spatial changes of NR 2 A and NR 2 B expressions in hippocampus in TLE rats. Low-dose dex may play its antiepileptic and protective role via alleviating temporospatial unbalance of the expression of NR 2 A and NR 2 B in hippocampus in temporal lobe epilepsy.
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Objective To explore the effect of dexmethasone on the expressions of the subunits NR 2 A and NR 2 B of NMDA receptors in hippocampus in temporal lobe epileptic rats after kindling. Methods Male Wistar rats were randomly divided into normal group,sham group,natrium saline pretreatment group before kindling( TLE group) and Dex pretreatment group prior to be kindled( Dex group). Typical temporal lobe epileptic model was kindled by Kainic acid( KA) microinjected into right Nucleus amygdalae. In situ hybridization was used to spatio-temporally observe the expression of NR 2 AmRNA and NR 2 BmRNA in hippocampus after kindling or sham operating in rats. Results There was no difference of positive cell count( PCC) of NR 2 AmRNA expression in hippocampus between Sham group and normal group both in total and in each hippocampal subarea( P 0. 05). Compared to Sham group,NR 2 AmRNA expressed higher at 24h,7d,14d,21d after kindling( P 0. 05),and enhanced in CA 1 and DG regions both in total and on 21d after kindling( P 0. 05). While,compared to TLE group,NR 2 AmRNA increased at 6h in Dex group( P 0. 05),and decreased on 7d,14d,21d after kindling( P 0. 05),especially declined in CA 1 and DG regions both in total and on 21d in Dex group than that of TLE group after kindling( P 0. 05). In general,NR 2 BmRNA expressed higher in CA 3 region than that in CA 1 and DG regions in Sham and normal groups( P 0. 05). However,in TLE and Dex groups,its expression was increased in DG than that in CA 1 and CA 3 regions( P 0. 05),and it was enhanced in each subareas in hippocampus in Dex group than that of TLE group( P 0. 05). Conclusion There are temporal and spatial changes of NR 2 A and NR 2 B expressions in hippocampus in TLE rats. Low-dose dex may play its antiepileptic and protective role via alleviating temporospatial unbalance of the expression of NR 2 A and NR 2 B in hippocampus in temporal lobe epilepsy.
Key concepts: Kindling, Hippocampus, Kainic acid, Kindling model, Temporal lobe, Hippocampal formation, Epilepsy, Internal medicine