When neurons in culture are transiently stressed by inhibition of ATP synthesis, they rapidly form within their neurites rod-like actin inclusions that disappear when the insult is removed. Oxidative stress, excitotoxic insults and amyloid beta peptide oligomers also induce rods. Immunostaining of neurites indicates that these rods also contain the majority of the actin filament dynamizing proteins, ADF and cofilin (AC). If the rods reappear within 24 h after the stress is removed, the neurite degenerates distal to the rod but with no increase in neuronal death. Here rods were generated in cultured rat E18 hippocampal cells by overexpression of an AC-GFP fusion protein. Surprisingly, we have found that for a short period (~60 min) immediately after initial rod formation, the loss of mitochondrial membrane potential (_m) and ATP in neurites with rods is slower than in neurites without them. The _m was monitored with the fluorescent dye tetramethylrhodamine methyl ester, and ATP was monitored with the fluorescent ion indicator mag-fura-2. Actin in rods is less dynamic than is filamentous actin in other cytoskeletal structures. Because _m depends on cellular ATP and because ATP hydrolysis associated with actin filament turnover is responsible for a large fraction of neuronal energy consumption (~50%), the formation of rods transiently protects neurites by slowing filament turnover and its associated ATP hydrolysis.