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 (H2 S) is a gas transmitter that may mediate cerebral ischemic injury. But the role of H2 S in seizures has not been understood yet. We examined the effect of H2 S on seizure-like events (SLEs) 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 NaHS aggravated both PTZ- and pilocarpine-induced SLEs in rats, while both low-Mg(2+) /high-K(+) - and 4-AP-induced SLEs were also exacerbated by NaHS 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 H2 S level in SLEs in vivo and in vitro. Enzymes that control H2 S biosynthesis could be interesting targets for antiepileptic strategies in poststroke epilepsy treatment.
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 (H2 S) is a gas transmitter that may mediate cerebral ischemic injury. But the role of H2 S in seizures has not been understood yet. We examined the effect of H2 S on seizure-like events (SLEs) and underlying mechanisms. METHODS AND RESULTS:Pentylenetetrazole (PTZ)- and pilocarpine-induced ratepilepticseizure models were tested. Low-Mg(2+) /high-K(+) - and 4-aminopyridine (4-AP)-induced epilepticseizure models were examined using patch-clamp recordings in brain slices. It was found that NaHS aggravated both PTZ- and pilocarpine-induced SLEs in rats, while both low-Mg(2+) /high-K(+) - and 4-AP-induced SLEs were also exacerbated by NaHS 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 H2 S level in SLEs in vivo and in vitro. Enzymes that control H2 S biosynthesis could be interesting targets for antiepileptic strategies in poststroke epilepsy treatment.
Authors: Poojya Anantharam; Elizabeth M Whitley; Belinda Mahama; Dong-Suk Kim; Souvarish Sarkar; Cristina Santana; Adriano Chan; Anumantha G Kanthasamy; Arthi Kanthasamy; Gerry R Boss; Wilson K Rumbeiha Journal: Ann N Y Acad Sci Date: 2017-11 Impact factor: 5.691
Authors: Maria Eduarda T Oliveira; Gustavo V B Paulino; Erivaldo D Dos Santos Júnior; Francisca A da Silva Oliveira; Vânia M M Melo; Jeferson S Ursulino; Thiago M de Aquino; Ashok K Shetty; Melissa Fontes Landell; Daniel Leite Góes Gitaí Journal: Mol Neurobiol Date: 2022-08-13 Impact factor: 5.682
Authors: Wilson Rumbeiha; Elizabeth Whitley; Poojya Anantharam; Dong-Suk Kim; Arthi Kanthasamy Journal: Ann N Y Acad Sci Date: 2016-07-21 Impact factor: 5.691