Effects of GM1-ganglioside and alpha-sialyl cholesterol on amino acid uptake, protein synthesis, and Na+,K(+)-ATPase activity in superior cervical and nodose ganglia excised from adult rats.
We examined the effect of GM1-ganglioside in combination with cholera toxin B, and synthetic alpha-sialyl cholesterol (alpha-SC) on neutral amino acid (tritiated alpha-aminoisobutyric acid, [3H]AIB) uptake, protein synthesis [( 3H]leucine incorporation), and Na+,K(+)-ATPase activity in isolated superior cervical ganglia (SCG) and nodose ganglia (NG) from adult rats after aerobic incubation, usually for 2 h at 37 degrees C in vitro. Cholera toxin B, that specifically masks the oligosaccharide chain of GM1-ganglioside, antagonized the GM1-induced changes in [3H]AIB uptake, [3H]leucine incorporation, and Na+,K(+)-ATPase activity almost completely in SCG, but partially in NG. Although cholesterol itself had little effect on either [3H]AIB uptake and Na+,K(+)-ATPase activity both in SCG and NG, alpha-SC caused considerable reduction of both amino acid uptake and the transport enzyme activity in each ganglia. However, cholesterol was more effective than alpha-SC in decreasing [3H]leucine incorporation in either ganglia. Whereas addition of EGTA markedly reduced either GM1-induced or alpha-SC-induced change in [3H]leucine incorporation into acid-insoluble fraction in both SCG and NG, application of Ca2+ ionophore produced considerable recovery of the protein synthesis from the inhibited level by Ca2(+)-deprivation. ATP and creatine phosphate contents in SCG were elevated by the presence of GM1 or alpha-SC, whereas [3H]AIB uptake and Na+,K(+)-ATPase activity were inhibited, suggesting that utilization for membrane transport was diminished as a result of GM1- or alpha-SC-induced decrease of ATPase activity.
Ando
M
M
Department of Physiology, Fujita Health University School of Medicine, Aichi, Japan.
Nakashima
Y
Y
Nagata
Y
Y
D000596:Amino Acids / Q000378:metabolism*; D000621:Aminoisobutyric Acids / Q000493:pharmacokinetics*; D000818:Animals; D002772:Cholera Toxin / Q000494:pharmacology; D002788:Cholesterol Esters / Q000494:pharmacology*; D005260:Female; D005677:G(M1) Ganglioside / Q000494:pharmacology*; D005728:Ganglia, Sympathetic / Q000378:metabolism*; D008297:Male; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D009620:Nodose Ganglion / Q000378:metabolism*; D051381:Rats; D012794:Sialic Acids / Q000494:pharmacology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D000596:Amino Acids; D000621:Aminoisobutyric Acids; D002788:Cholesterol Esters; D009419:Nerve Tissue Proteins; D012794:Sialic Acids; C055195:N-acetylneuraminyl cholesterol; C100049:2-aminoisobutyric acid; D005677:G(M1) Ganglioside; D002772:Cholera Toxin; D000254:Sodium-Potassium-Exchanging ATPase