Effects of Cholera Toxin on Thyroid Cyclic Amp-Dependent Protein Kinase and Ornithine Decarboxylase Activities

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Abstract
Cholera toxin activated beef thyroid cyclic AMP-dependent protein kinase in a dose (0.2 to 8 μug/ml)-related fashion. Thus, when beef thyroid slices were incubated with toxin (8 pg/ml) for 90 minutes and then assayed for protein kinase, the activity ratio (i.e. -cyclic AMP/+cyclic AMP) increased from 0.32 ± 0.02 to 0.77 ± 0.06. The toxin (5 μug/ml)-induced increase was abolished by inclusion of ganglioside GH1 in the incubation medium (I50, 0.7 μpg/ml), whereas, gangliosides Gdla and GT1 were without effect. In contrast, TSH-activated protein kinase was unaffected by ganglioside addition. Cholera toxin increased rat thyroid ornithine decarboxylase (ODC) activity in-vitro in a dose (0.1 to 10 μug/ml)-related fashion [basal, 100 of cholera toxin (10 μug/ml), 1500 pmol 14CO2/g tissue/30 min]. The toxin (1 μug/ml)- (but not TSH-) induced increase in ODC was abolished by inclusion of ganglioside Gm1 in the incubation medium (I50” 0.07 μug/ml), whereas gangliosides GDla and GT1 were without effect. Cholera toxin stimulation of ODC was inhibited by indomethacin or iodide as are the stimulatory effects of TSH or dibutyryl cyclic AMP. These results demonstrate that although there are differences in the TSH and cholera toxin responses with respect to receptor (ganglioside) interaction, they nevertheless elicit similar intracellular responses in thyroid.