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

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Brent, P.J. et al.

Protein phosphorylation and calcium uptake into rat forebrain synaptosomes: modulation by the sigma ligand, 1,3-ditolylguanidine.

The sigma ligand 1,3-di-O-tolylguanidine (DTG) increased basal dynamin and decreased depolarization- stimulated phosphorylation of the synaptosomal protein synapsin Ib without having direct effects on protein kinases or protein phosphatases. DTG dose-dependently decreased the basal cytosolic free Ca2+ concentration ([Ca2+]i) and blocked the depolarization-dependent increases in [Ca2+]i. These effects were inhibited by the sigma antagonists rimcazole and BMY14802. The nitric oxide donors sodium nitroprusside (SNP) and 8-(p-chlorophenylthio)guanosine-3',5'-cyclic monophosphorothioate decreased basal [Ca2+]i and the KCI-evoked rise in [Ca2+]i to an extent similar to DTG. SNP, but not DTG, produced a rise in cyclic GMP levels, suggesting that the effect of DTG on [Ca2+]i was not mediated via downstream regulation of cyclic GMP levels. DTG increased 45Ca2+ uptake and efflux under basal conditions and inhibited the 45Ca2+ uptake induced by depolarization with KCI. The KCI-evoked rise in [Ca2+]i was inhibited by omega-conotoxin (omega-CgTx)-GVIA and -MVIIC but not nifedipine and omega-agatoxin-IVA. The effect of DTG on decreasing the KCI-evoked rise in [Ca2+]i was additive with omega-CgTx-MVIIC but not with omega-CgTx-GVIA. These data suggest that DTG was producing some of its effects on synapsin I and dynamin phosphorylation and intrasynaptosomal Ca2+ levels via inhibition of N-type Ca2+ channels.[1]

References

Protein phosphorylation and calcium uptake into rat forebrain synaptosomes: modulation by the sigma ligand, 1,3-ditolylguanidine. Brent, P.J., Herd, L., Saunders, H., Sim, A.T., Dunkley, P.R. J. Neurochem. (1997) [Pubmed]

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