Abstract
Since the discovery of nitric oxide (NO) as gaseous signaling molecule, two other gaseous mediators, carbon monoxide (CO) and hydrogen sulfide (H2S) have been found to be also involved in many physiological and pathophysiological functions. This review will briefly summarize our recent progress in the pathophysiology of NO and H2S. In the photoreceptor cells, the level of intracellular Ca2+ is kept relatively low by H2S. Intraperitoneal injection of H2S donor to mice protected photoreceptor cells from light-induced retinal degeneration caused by oxidative stress and elevation of intracellular Ca2+. Another gaseous mediator NO induces Ca2+ release from the endoplasmic reticulum via S-nitrosylated type 1 ryanodine receptor (RyR1) Ca2+ release channel. NO-induced Ca2+ release (NICR) was abolished in primary cultured neurons from the knock-in mice, in which the S-nitrosylation site Cys-3636 of RyR1 was replaced by Ala (Ryr1C3636A). The neurons in hippocampal CA3 region of Ryr1C3636A mice were protected against seizure-induced neuronal cell death. The result indicates that NICR is critical for status epilepticus-induced neurodegeneration. The developments in the pathophysiology of gaseous mediators in the central nervous system will provide a better pharmacological advances for the treatment of neurodegenerative diseases.
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