• Neuroscience · Oct 2016

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

    • Aleksey V Yakovlev, Evgeniya D Kurmasheva, Rashid Giniatullin, Ilgam Khalilov, and Guzel F Sitdikova.
    • Department of Human and Animal Physiology, Institute of Fundamental Medicine and Biology, Kazan Federal University, 420008 Kazan, Russia. Electronic address: alv.yakovlev@gmail.com.
    • Neuroscience. 2016 Oct 27.

    AbstractHydrogen sulfide (H2S) is an endogenous gasotransmitter with neuroprotective properties that participates in the regulation of transmitter release and neuronal excitability in various brain structures. The role of H2S in the growth and maturation of neural networks however remains unclear. The aim of the present study is to reveal the effects of H2S on neuronal spontaneous activity relevant to neuronal maturation in hippocampal slices of neonatal rats. Sodium hydrosulfide (NaHS) (100 μM), a classical donor of H2S 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 H2S synthesis L-cysteine (1 mM) induced an initial increase followed by an inhibition of GDPs and spiking activity. Our experiments indicate that the increase of 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 H2S appears to be due to the rightward shift of activation and inactivation of voltage-gated Na(+) currents, thus preventing network activity. NaHS also reduced NMDA-mediated currents, without essential effect on AMPA/kainate or GABAA-mediated currents Finally, H2S 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, H2S prevents the enhanced neuronal excitability typical to early hippocampal networks.Copyright © 2016. Published by Elsevier Ltd.

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