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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

Hillary Quansah, Prosper N'Gouemo

CNS Neurosci Ther. 2014 Sep;20(9):860-6.

PMID: 24948133

Abstract:

Aims:
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(+) /Ca(2+) 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(+) /Ca(2+) 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.
Methods:
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).
Results:
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.
Conclusions:
These findings suggest acid-sensing ion channels and the Na(+) /Ca(2+) exchanger may play an important role in the pathophysiology of inherited AGS susceptibility in the GEPR-3s.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP415697084	SN-6		415697-08-4	Price

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