Open AccessExtracellular HMGB1 Modulates Glutamate Metabolism Associated with Kainic Acid-Induced Epilepsy-Like Hyperactivity in Primary Rat Neural Cells
Author(s) -
Yuji Kaneko,
Colleen Pappas,
Teresita Malapira,
Fernando Ĺ. Vale,
Naoki Tajiri,
Cesar V. Borlongan
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000460513
Subject(s) - hmgb1 , glutamate receptor , extracellular , kainic acid , epilepsy , biology , epileptogenesis , microbiology and biotechnology , intracellular , neuroscience , biochemistry , inflammation , immunology , receptor
Neuroinflammatory processes have been implicated in the pathophysiology of seizure/epilepsy. High mobility group box 1 (HMGB1), a non-histone DNA binding protein, behaves like an inflammatory cytokine in response to epileptogenic insults. Kainic acid (KA) is an excitotoxic reagent commonly used to induce epilepsy in rodents. However, the molecular mechanism by which KA-induced HMGB1 affords the initiation of epilepsy, especially the role of extracellular HMGB1 in neurotransmitter expression, remains to be elucidated.