Amiloride and SN-6 suppress audiogenic seizure susceptibility in genetically epilepsy-prone rats.
Amiloride and SN-6 suppress audiogenic seizure susceptibility in genetically epilepsy-prone rats.
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DOI：
10.1111/cns.12296
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发表时间：
2014-09
影响因子：
5.5
通讯作者：
N'Gouemo P
中科院分区：
文献类型：
--
作者：
Quansah H;N'Gouemo P
We have recently reported that amiloride, a potent and nonselective blocker of acid-sensing ion channels, prevents the development of pilocarpine-induced seizures and status epilepticus. Amiloride is also known to suppress the activity of Na+/Ca2+ and Na+/H+ exchangers that have been implicated in the pathophysiology of seizures. Here, we evaluated the effects of amiloride, SN-6 (a potent blocker of Na+/Ca2+ exchangers) and zoniporide (a potent blocker of Na+/H+ exchangers) on acoustically evoked seizures (audiogenic seizures, AGS) in genetically epilepsy-prone rats (GEPR-3s), a model of inherited generalized epilepsy. Male, six-week-old GEPR-3s were used. The GEPR-3s were tested for AGS susceptibility before and after treatment with various doses of amiloride, SN-6, and zoniporide (1, 3, 10, and 30 mg/kg; per os). We found that pretreatment with amiloride and SN-6 markedly reduced the incidence and severity of AGS in the GEPR-3s. In contrast, administration of zoniporide only minimally reduced the incidence and severity of AGS in the GEPR-3s. A combination of noneffective doses of SN-6 and zoniporide also suppressed AGS susceptibility in the GEPR-3s. These findings suggest acid-sensing ion channels and the Na+/Ca2+ exchanger may play an important role in the pathophysiology of inherited AGS susceptibility in the GEPR-3s.
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影响因子：
11.2
作者：
COULTER, DA;HUGUENARD, JR;PRINCE, DA
通讯作者：
PRINCE, DA
DOI：
10.1152/ajpcell.1999.276.4.c788
发表时间：
1999-04-01
影响因子：
5.5
作者：
Bell, SM;Schreiner, CM;Scott, WJ
通讯作者：
Scott, WJ
DOI：
10.1152/ajpcell.1997.272.4.c1250
发表时间：
1997-04-01
影响因子：
5.5
作者：
Quednau, BD;Nicoll, DA;Philipson, KD
通讯作者：
Philipson, KD
影响因子：
3.3
作者：
Bolshakov, KV;Essin, KV;Magazanik, LG
通讯作者：
Magazanik, LG
影响因子：
2.9
作者：
Lin, CW;Kalaria, RN;LaManna, JC
通讯作者：
LaManna, JC