Alteration of neurofilament (NF) proteins is considered a critical component and a causative factor for a number of neuropathologies, especially certain neurotoxicities. Correlative observations have supported this hypothesis; the current study tests this relationship by exposure of neurotoxicants to crayfish, a species lacking NFs. Morphological and immunological tests verified the absence of NFs in crayfish peripheral nerve axons. Tail injections of acrylamide (ACR), 2,5-hexanedione (2,5-HD), or 3,4-dimethyl-2,5-HD (3,4-DMHD) produced ataxia and paralysis. Morphological expression of axonal degeneration in a spatial and temporal pattern of progression comparable to mammalian species possessing NFs was observed. With gamma-diketones, time to onset was slower than observed in mammals but relative potency between neurotoxic analogues was maintained. Non-neurotoxic analogues failed to produce any functional signs of neurotoxicity. These data are consistent with the conclusion that NF accumulations are not cause-effect related to axonal degeneration in these models of neurotoxicity and raise questions as to the relationship between accumulation of NF proteins and axonal degeneration in other neuropathological conditions.
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