Convulsive status epilepticus (CSE) is a neurological disease with contraction and extension of limbs, leading to damage of hippocampus and cognition. This study aimed to explore the effects of dexmedetomidine (DEX) on the cognitive function and neuroinflammation in CSE rats. All rats were divided into control group, CSE group and DEX group. Morris water maze test was used to measure cognitive function. Acute hippocampal slices were made to detect long-term potentiation (LTP). Immunohistochemistry was used to determine the expression of alpha 7-nicotinic acetylcholine receptor (alpha 7-nAChR) and interleulcin-1 beta (IL-1 beta). Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of IL-1 beta, tumor necrosis factor-alpha (TNF-alpha), S-100 beta and brain-derived neurotrophic factor (BDNF). Our results showed that DEX improved the memory damage caused by CSE. DEX reduced seizure severity and increased the amplitudes and sustainable time of LTP, and also inhibited the hippocampal expression of alpha 7-nAChR and IL-1 beta in CSE rats. DEX treatment decreased serum IL-1 beta, TNF-alpha and S-100 beta levels and increased BDNF levels. The effects of DEX on seizure severity and LTP could be simulated by nicotine or attenuated by concurrent a-bungarotoxin (alpha-BGT) treatment. In conclusions, DEX significantly improved spatial cognitive dysfunction, reduced seizure severity and increased LTP in CSE rats. Improvements by DEX were closely related to enhancement of cholinergic anti-inflammatory pathway. (C) 2017 Elsevier Inc. All rights reserved.