Inflammation induced by LPS enhances epileptogenesis in immature rat and may be partially reversed by IL1RA.
Inflammation induced by LPS enhances epileptogenesis in immature rat and may be partially reversed by IL1RA.
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DOI:
10.1111/j.1528-1167.2010.02606.x
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发表时间:
2010-07
期刊:
影响因子:
5.6
通讯作者:
Sankar R
中科院分区:
文献类型:
--
作者:
Auvin S;Shin D;Mazarati A;Sankar R
Inflammatory signaling in the CNS has been shown to exacerbate both seizure activity and seizure-induced neuronal injury. However, it has not been firmly established whether neurodegeneration is a prerequisite of proconvulsant effect of neuroinflammation, or whether the latter may facilitate seizures without involving neuronal injury. We examined effects of inflammation in the rapid kindling model, where seizure progression occurs in the absence of neurodegeneration. P14 male Wistar rats were subjected to a rapid kindling procedure –60 electrical stimulations of the hippocampus delivered every five minutes at the current that had been established to induce afterdischarge. LPS was injected (50μg/kg i.p. 2h prior the RKP); IL-1Ra was injected (25mg/kg i.p. 2h prior the RKP). The effects of treatments were examined on baseline hippocampal excitability; on the progression of rapid kindling; and on the retention of rapid kindling. LPS increased baseline hippocampal excitability evident as the decrease of hippocampal ADT. LPS also increased kindling progression. 24 hrs after the completion of kindling procedure, LPS treated animals exhibited increased excitability as compared with saline-treated kindling controls. The kindling progression was blocked by IL1RA when given combination with LPS. IL1RA was able to reverse the effect of LPS on ADD while IL1RA alone decrease ADT. We showed that inflammation provoked by LPS enhanced rapid kindling epileptogenesis in immature rat brains. IL1RA was also able to mitigate this augmentation of epileptogenesis enhanced by LPS.
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影响因子:
5.6
作者:
Mazarati, Andrey;Wu, Jim;Sankar, Raman
通讯作者:
Sankar, Raman
影响因子:
6.1
作者:
Ravizza, Teresa;Noe, Francesco;Vezzani, Annamaria
通讯作者:
Vezzani, Annamaria
影响因子:
2.4
作者:
Hu, SX;Sheng, WS;Chao, SC
通讯作者:
Chao, SC
影响因子:
5.6
作者:
Heida, JG;Boiss, L;Pittman, QJ
通讯作者:
Pittman, QJ
DOI:
10.1016/0165-3806(91)90116-z
发表时间:
1991-07-16
期刊:
DEVELOPMENTAL BRAIN RESEARCH
影响因子:
--
作者:
MICHELSON, HB;LOTHMAN, EW
通讯作者:
LOTHMAN, EW