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Hydrogen sulfide inhibits giant depolarizing potentials and abolishes epileptiform activity of neonatal rat hippocampal slices

Abstract : Hydrogen sulfide (H 2 S) is an endogenous gaso-transmitter with neuroprotective properties that participates in the regulation of transmitter release and neuronal excitability in various brain structures. The role of H 2 S in the growth and maturation of neural networks however remains unclear. The aim of the present study is to reveal the effects of H 2 S on neuronal spontaneous activity relevant to neuronal maturation in hippocampal slices of neonatal rats. Sodium hydrosulfide (NaHS) (100 lM), a classical donor of H 2 S produced a biphasic effect with initial activation and subsequent concentration-dependent suppression of network-driven giant depolarizing potentials (GDPs) and neuronal spiking activity. Likewise, the substrate of H 2 S synthesis L-cysteine (1 mM) induced an initial increase followed by an inhibition of GDPs and spiking activity. Our experiments indicate that the increase in initial discharge activity by NaHS is evoked by neuronal depolarization which is partially mediated by a reduction of outward K + currents. The subsequent decrease in the neuronal activity by H 2 S appears to be due to the rightward shift of activation and inactivation of voltage-gated Na + currents, thus preventing network activity. NaHS also reduced N-methyl-D-aspartate (NMDA)-mediated currents, without essential effect on AMPA/kainate or GABA A-mediated currents. Finally, H 2 S abolished the interictal-like events induced by bicuculline. In summary, our results suggest that through the inhibitory action on voltage-gated Na + channels and NMDA receptors, H 2 S prevents the enhanced neuronal excitability typical to early hippocampal networks. Ó
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Aleksey V yakovlev, Evgeniya D Kurmasheva, Rashid Giniatullin, Ilgam Khalilov, Guzel F Sitdikova. Hydrogen sulfide inhibits giant depolarizing potentials and abolishes epileptiform activity of neonatal rat hippocampal slices. Neuroscience, Elsevier - International Brain Research Organization, 2017, 340, pp.153-165. ⟨10.1016/j.neuroscience.2016.10.051⟩. ⟨hal-01962401⟩



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