KB-R7943 reduces 4-aminopyridine-induced epileptiform activity in adult rats after neuronal damage induced by neonatal monosodium glutamate treatment.

ABSTRACT:

Background

Neonatal monosodium glutamate (MSG) treatment triggers excitotoxicity and induces a degenerative process that affects several brain regions in a way that could lead to epileptogenesis. Na⁺/Ca²⁺ exchangers (NCX1-3) are implicated in Ca²⁺ brain homeostasis; normally, they extrude Ca²⁺ to control cell inflammation, but after damage and in epilepsy, they introduce Ca²⁺ by acting in the reverse mode, amplifying the damage. Changes in NCX3 expression in the hippocampus have been reported immediately after neonatal MSG treatment. In this study, the expression level of NCX1-3 in the entorhinal cortex (EC) and hippocampus (Hp); and the effects of blockade of NCXs on the seizures induced by 4-Aminopyridine (4-AP) were analysed

SUBMITTER: Hernandez-Ojeda M 

PROVIDER: S-EPMC5423021 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature