MicroRNA-23a contributes to hippocampal neuronal injuries and spatial memory impairment in an experimental model of temporal lobe epilepsy.

Temporal lobe epilepsy (TLE) is the most common form of epilepsy characterized by spontaneous recurrent seizures. It has been widely accepted that individuals with TLE tend to have neuronal injuries and memory impairment. However, little is known about the underlying molecular mechanisms. MicroRNAs (miRNAs) are small noncoding RNAs that regulate the expression of target genes at the posttranscriptional level. An increasing body of evidence suggests that miRNAs play pivotal roles in the pathogenesis of epilepsy. Here, we sought to determine the role of miR-23a, one of the most common miRNAs involved in various cancer types, in hippocampal neuronal injuries and spatial memory impairment in an experimental model of TLE. We found that miR-23a is upregulated in the hippocampus after status epilepticus (SE) in kanic acid (KA)-induced TLE mice. Furthermore, the upregulation of miR-23a is accompanied by hippocampal oxidative damage, neuronal injuries and spatial memory impairment in TLE mice. Inhibition of miR-23a expression by miR-23a antagomirs reduced hippocampal oxidative stress, neuronal injuries and improved spatial memory, while an increase in miR-23a expression by miR-23a agomir exacerbated hippocampal oxidative stress, neuronal injuries and spatial memory impairment in TLE mice. Our findings suggest that miR-23a contributes to hippocampal oxidative damage and neuronal injuries, which may consequently contribute to spatial memory impairment in TLE mice. Thus, targeting miR-23a in the epileptic brain may provide a novel strategy for protecting against hippocampal neuronal injuries and improving spatial memory in TLE patients.

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