Abstract
Studies suggest that microRNA (miR)‑34c may serve a role in cognitive function in rodent and primate groups. A previous study demonstrated an increase in miR‑34c expression in chronic epileptic rats with memory disorders, induced by pentylenetetrazol (PTZ). However, the mechanism underlying the effects of miR‑34c on cognitive function in epileptic rats remains unclear. Therefore, the present study investigated alterations in cognitive function in temporal lobe epileptic rats, induced by repeated injections of PTZ, following treatment with an miR‑34c agomir compared with a scramble group. Increased expression of miR‑34c was observed in the agomir group, in addition to an increased deficit in learning and memory function in the Morris water maze test. Glutamate receptor ionotropic N‑methyl‑D‑aspartate (NMDA) 2B (NR2B), phosphorylated (p)‑reduced nicotinamide‑adenine dinucleotide phosphate‑dependent diflavin oxidoreductase 1 (NR1) and p‑glutamate receptor 1 (GluR1) protein expression was detected in the hippocampus using western blotting. Additionally, the downregulation of NR2B, p‑NR1 and p‑GluR1 in the miR‑34c agomir group demonstrated that miR‑34c may serve a negative role in cognitive function in epileptic seizures, by dysregulating NMDA and α-amino-3-hydroxy-5‑methyl‑4‑isoxazolepropionic acid receptors, which are associated with long‑term potentiation.