Actin-ATP Hydrolysis Is a Major Energy Drain for Neurons

• DOI: 10.1523/jneurosci.23-01-00002.2003
• Publication Date: 2018-04-13T22:30:28Z
• Authors: Barbara W. Bernstein; James R. Bamburg
• Keywords: Neurons; 0301 basic medicine; Hydrolysis; Sodium; Chick Embryo; Bridged Bicyclo Compounds, Heterocyclic; Peptides, Cyclic; Actins; Cell Hypoxia; 3. Good health; Actin Cytoskeleton; Thiazoles; 03 medical and health sciences; Adenosine Triphosphate; Depsipeptides; Animals; Thiazolidines; Calcium; Enzyme Inhibitors; Sodium-Potassium-Exchanging ATPase; Energy Metabolism; Ouabain; Cells, Cultured

In cultured chick ciliary neurons, when ATP synthesis is inhibited, ATP depletion is reduced approximately 50% by slowing actin filament turnover with jasplakinolide or latrunculin A. Jasplakinolide inhibits actin disassembly, and latrunculin A prevents actin assembly by sequestering actin monomers. Cytochalasin D, which allows assembly-disassembly, but only at pointed ends, is less effective in conserving ATP. Ouabain, an Na(+)-K(+)-ATPase inhibitor, and jasplakinolide both prevent approximately 50% of the ATP loss. When applied together, they completely prevent ATP loss over a period of 20 min, suggesting that filament stabilization reduces ATP consumption by decreasing actin-ATP hydrolysis directly rather than indirectly by modulating the activity of Na(+)-K(+)-ATPase, a major energy consumer.