Abstract
Sarm1 is an evolutionary conserved protein that is essential for Wallerian axon degeneration. Sarm1 has emerged as a therapeutic target to treat neuropathies derived from metabolic or chemical stress and physical injury of axons. Yet, the full repertoire of consequences of inhibiting Sarm1 remains unknown. Here we show that loss of Sarm1 in zebrafish does not affect the sensorimotor transformations that underlie rheotaxis. In addition, Sarm1 deficit accelerates the re-growth of regenerating axons. These data indicate that systemic inhibition of Sarm1 is a viable therapeutic option compatible with sustained nervous system function.