| Abstract: | The initial rate of radioactive choline (Ch) uptake in the endplate-rich area (EPA) of both stimulated and unstimulated hemidiaphragms is significantly increased by 0.2 microM dexamethasone (Dex) in the presence of 10 microM Ch. In autoradiographs, the mean grain densities above the muscle fibres are not altered by Dex. The mean grain densities above the nerve endings are significantly increased in the presence of Dex in stimulated tissue, and slightly but not significantly increased in unstimulated tissue. There is a positive correlation between the initial rate of Ch uptake in the EPA and the amount of isotope in the nerve terminals, in the absence and presence of Dex. Without correcting for the large amount of diffusion which occurs, the ratio of the grain densities above the nerve terminals to that above the muscle fibres in the presence of Dex is 2.12 in stimulated tissue, and 1.40 in unstimulated tissue. The ratio in the stimulated tissue is significantly greater than the control ratio in the absence of Dex (1.66). Therefore, Dex affects radioactive Ch uptake in nerve endings and not in muscle fibres in the rat diaphragm. The stimulation-induced increase in the uptake of isotope into the nerve endings is abolished in a Na+-depleted medium, and in the absence of Ca2+. Dex has no effect on this abolition. We conclude that relatively low concentrations of Dex affect Ch transport in rat diaphragm nerve endings by a mechanism as yet to be defined. |
