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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Intracellular sodium changes during the speract response and the acrosome reaction in sea urchin sperm.

The sperm-activating peptide speract and fucose-sulphate glycoconjugate (FSG) are sea urchin egg-envelope components that modulate sperm ion permeability. They influence motility and induce acrosomal reaction (AR), respectively. A fluorescent Na(+)-sensitive dye (Na(+)-binding benzofuran isophthalate, SBFI) was used to determine how these egg envelope components influence sperm Na(+) permeability. [Ca(2+)](i) and pH(i) were also measured to correlate their changes in response to speract and FSG with those observed in [Na(+)](i). SBFI determinations indicate that the resting [Na(+)](i) is 20 +/- 8 mM in sea urchin sperm. Saturating levels of speract increased [Na(+)](i) by approximately 15 mM, while similar levels of FSG caused a further elevation of approximately 30 mM. The kinetics of the [Na(+)](i), [Ca(2+)](i) and pH(i) changes induced by saturating levels of speract were faster than those induced by FSG. Both egg ligands appeared to activate more than one Na(+) transport system. Nifedipine, Ni(2+) and TEA(+) inhibited the ionic changes and the AR induced by FSG but, importantly, did not alter those caused by speract. Thus, there are differences in some of the ionic transport mechanisms that operate in the speract and FSG responses. ZD2788, a blocker of hyperpolarization and cyclic-nucleotide-gated (HCN) channels such as SpHCN present in sea urchin sperm, did not decrease the speract-induced [Na(+)](i) increase, but slowed its kinetics. Therefore, SpHCN does not play a major role in the uptake of Na(+) triggered by this decapeptide. KB-R7943, an inhibitor of Na(+)/Ca(2+) exchangers, decreased the resting [Na(+)](i) and did not change significantly the speract-induced [Ca(2+)](i) increase, but slowed its recovery.[1]


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