Highly differentiated cultures of rat and mouse sensory ganglia were treated for varying periods (up to 6 hr) with selected doses (1 x 10-3 M to 5 x 10-5 M) of the cardiac glycoside, ouabain (Strophanthin G). This inhibitor of active Na and K transport produced a selective and progressive swelling of elements of the Golgi complex in many, but not all, neurons. After 6 hr of treatment, virtually all Golgi complexes in affected neurons were either altered or absent; large cytoplasmic vacuoles limited by agranular membrane were prominent in these neurons. This response was not observed in satellite cells and Schwann cells. Within a few hours of ouabain withdrawal, the neuronal vacuoles disappeared and normal Golgi areas were again observed. These observations suggest that there is a site for active transport of Na and K on the Golgi membrane of these neurons. In discussing the possible significance of this observation, it is suggested that if this site were directed so that cation was actively pumped from Golgi cisternae into cytoplasm (and if there were differential water and ion permeabilities in various parts of the endoplasmic reticulum-Golgi system), then such a pumping mechanism could provide an explanation for the concentrating function of the Golgi apparatus.
REVERSIBLE ALTERATIONS IN THE GOLGI COMPLEX OF CULTURED NEURONS TREATED WITH AN INHIBITOR OF ACTIVE NA AND K TRANSPORT
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William O. Whetsell, Richard P. Bunge; REVERSIBLE ALTERATIONS IN THE GOLGI COMPLEX OF CULTURED NEURONS TREATED WITH AN INHIBITOR OF ACTIVE NA AND K TRANSPORT . J Cell Biol 1 August 1969; 42 (2): 490–500. doi: https://doi.org/10.1083/jcb.42.2.490
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