Abstract: Neurons are energy-demanding cells. Disruptions in energy metabolism can quickly interrupt neuronal function, leading to cell death and neurodegeneration. For instance, ischemia rapidly depletes adenosine triphosphate (ATP) thereby disrupting energy-dependent cellular processes crucial for homeostasis, and axon degeneration is preceded by a collapse of axonal ATP levels. The initial extension and regeneration of axons are also considered to require significant bioenergetic utilization. Therefore, understanding neuronal bioenergetics and the regulation of intracellular ATP levels is crucial for both our basic understanding of neuronal function and ultimately developing new therapies to facilitate neuronal regeneration after injuries. Work performed over 20 years ago, using available approaches, lead to the hypothesis that actin filament dynamics are a major “sink” of ATP utilization in embryonic ciliary ganglion neurons (Bernstein and Bamburg, 2003) and platelets (Daniel et al., 1986). However, neither of these studies directly measured ATP and relied on indirect measurements or quantitative estimation of ATP. Our recent work (Holland and Gallo, 2023) revisited this hypothesis using modern live imaging ratiometric intra-cellular reporters of ATP and the ATP/ADP ratio and failed to obtain data consistent with the hypothesis that actin filament dynamics are a sink of ATP utilization in embryonic sensory neurons. Thus, these recent data indicate that the contribution of cytoskeletal dynamics and other bioenergetic sinks would benefit from additional scrutiny.