Related Experiment Video
Updated: Aug 13, 2025

Lipidomics and Transcriptomics in Neurological Diseases
Published on: March 18, 2022
Kainic acid induced hyperexcitability in thalamic reticular nucleus that initiates an inflammatory response through
Dongbin Li1, Xiaosi Zhang2, Ruoshi Liu3
1Department of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China; First Department of Neurology and Neuroscience Center, Heilongjiang Provincial Hospital, Harbin, China.
Objective:
To explore the relationship between the proinflammatory factor high-mobility group box 1 (HMGB1) and glutamatergic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the development of epilepsy.
Methods:
Thalamic reticular nucleus (TRN) slices were treated with kainic acid (KA) to simulate seizures. Action potentials and spontaneous inhibitory postsynaptic currents (sIPSCs) were recorded within TRN slices using whole-cell patch clamp techniques. The translocation of HMGB1 was detected by immunofluorescence. The HMGB1/TLR4 signaling pathway and its downstream inflammatory factors (IL-1β and NF-κB) were detected by RTPCR, Western blot and ELISA.
Results:
KA-evoked spikings were observed in TRN slices and blocked by perampanel. sIPSCs in the TRN were enhanced by KA and reduced by perampanel. The translocation of HMGB1 in the TRN was promoted by KA and inhibited by perampanel. The expression of the HMGB1/TLR4 signaling pathway was promoted by KA and suppressed by perampanel.
Conclusion:
KA induced hyperexcitability activates the HMGB1/TLR4 pathway, which potentially leading to neuroinflammation in epilepsy.
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