Differential regulation of K<sup>+</sup>-Cl<sup>-</sup> cotransporter 2 (KCC2) and Na<sup>+</sup>-K<sup>+</sup>-Cl<sup>-</sup> cotransporter 1 (NKCC1) expression by zolpidem in CA1 and CA3 hippocampal subregions of the lithium-pilocarpine status epilepticus rat model.
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ABSTRACT: Status epilepticus is linked to cognitive decline due to damage to the hippocampus, a key structure involved in cognition. The hippocampus's high vulnerability to epilepsy-related damage is the main reason for this impairment. Convulsive seizures, such as those observed in status epilepticus, can cause various hippocampal pathologies, including inflammation, abnormal neurogenesis, and neuronal death. Interestingly, substantial evidence points to the therapeutic potential of the sedative/hypnotic agent zolpidem for neurorehabilitation in brain injury patients, following the unexpected discovery of its paradoxical awakening effect. In this study, we successfully established an ideal lithium-pilocarpine rat model of status epilepticus, which displayed significant deficits in hippocampal-depen
SUBMITTER: Othman MZ
PROVIDER: S-EPMC12044352 | biostudies-literature | 2025 Apr
REPOSITORIES: biostudies-literature
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