Open AccessAggravation of Seizure‐like Events by Hydrogen Sulfide: Involvement of Multiple Targets that Control Neuronal Excitability
Author(s) -
Luo Yi,
Wu PengFei,
Zhou Jun,
Xiao Wen,
He JinGang,
Guan XinLei,
Zhang JieTing,
Hu ZhuangLi,
Wang Fang,
Chen JianGuo
Publication year - 2014
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12228
Subject(s) - epilepsy , ampa receptor , nmda receptor , pilocarpine , sodium channel , neuroscience , stroke (engine) , glutamate receptor , convulsant , medicine , neuropathic pain , pharmacology , anesthesia , chemistry , receptor , psychology , sodium , engineering , mechanical engineering , organic chemistry
Summary Aims Epileptic seizures are well‐known neurological complications following stroke, occurring in 3% of patients. However, the intrinsic correlation of seizures with stroke remains largely unknown. Hydrogen sulfide (H 2 S) is a gas transmitter that may mediate cerebral ischemic injury. But the role of H 2 S in seizures has not been understood yet. We examined the effect of H 2 S on seizure‐like events ( SLE s) and underlying mechanisms. Methods and Results Pentylenetetrazole ( PTZ )‐ and pilocarpine‐induced rat epileptic seizure models were tested. Low‐Mg 2+ /high‐K + ‐ and 4‐aminopyridine (4‐ AP )‐induced epileptic seizure models were examined using patch‐clamp recordings in brain slices. It was found that Na HS aggravated both PTZ ‐ and pilocarpine‐induced SLE s in rats, while both low‐Mg 2+ /high‐K + ‐ and 4‐ AP ‐induced SLE s were also exacerbated by Na HS in brain slices, which may be due to its regulation on the voltage‐gated sodium channel, N‐methyl‐D‐aspartic acid receptor ( NMDAR ), and α ‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor ( AMPAR ) function. Furthermore, these effects were reversed by blocking voltage‐gated sodium channel, NMDAR , and AMPAR . Conclusions These results suggest a pathological role of increased H 2 S level in SLE s in vivo and in vitro . Enzymes that control H 2 S biosynthesis could be interesting targets for antiepileptic strategies in poststroke epilepsy treatment.