| Animal model . | Axon phenotype . | References . |
|---|---|---|
| Shiverer (Mbp null) | Decreased axon caliber/neurofilament phosphorylation, minimal axon degeneration | Rosenbluth, 1980; Brady et al., 1999 |
| Plp1 null | Progressive axon loss, axonal spheroids containing multivesicular bodies, disorganized cytoskeletal components, and membranous organelles, impaired axon transport, and microtubule abnormalities | Klugmann et al., 1997; Griffiths et al., 1998; Garbern et al., 2002; Edgar et al., 2004; Yin et al., 2016 |
| Cnp null | Mislocalization of voltage-gated sodium channels and Caspr, progressive axon loss, axonal spheroids with accumulations of membranous organelles, impaired axon transport, and impaired formation and maintenance of cytoplasmic channels | Lappe-Siefke et al., 2003; Rasband et al., 2005; Snaidero et al., 2017 |
| Mag null | Decreased axon caliber/neurofilament phosphorylation, progressive axon loss, increased susceptibility to EAE/neurotoxic injury, and decreased Cdk5/Erk1/2 kinase activity | Fruttiger et al., 1995; Yin et al., 1998; Dashiell et al., 2002; Pan et al., 2005; Nguyen et al., 2009 |
| EAE | Axon loss, irreversible cytoskeletal fragmentation, impaired mitochondrial morphology and trafficking, impaired axon transport, oxidative damage, and increased axoplasmic calcium | Siffrin et al., 2010; Nikić et al., 2011; Sorbara et al., 2014; Höflich et al., 2016; Mei et al., 2016 |
| Lysolecithin | Impaired axon transport, increased mitochondrial stationary site size and transport rate, and disrupted nodal architecture | Arroyo et al., 2004; Kiryu-Seo et al., 2010; Ohno et al., 2014; Höflich et al., 2016; Schultz et al., 2017 |
| Cuprizone | Axon loss, impaired axon transport, and increased mitochondrial stationary site size | Ohno et al., 2014; Sachs et al., 2014; Höflich et al., 2016; Schultz et al., 2017 |
| DT ablation | Axon loss, impaired axon transport, and neurofilament dephosphorylation | Traka et al., 2010, 2016; Pohl et al., 2011; Oluich et al., 2012 |
| Animal model . | Axon phenotype . | References . |
|---|---|---|
| Shiverer (Mbp null) | Decreased axon caliber/neurofilament phosphorylation, minimal axon degeneration | Rosenbluth, 1980; Brady et al., 1999 |
| Plp1 null | Progressive axon loss, axonal spheroids containing multivesicular bodies, disorganized cytoskeletal components, and membranous organelles, impaired axon transport, and microtubule abnormalities | Klugmann et al., 1997; Griffiths et al., 1998; Garbern et al., 2002; Edgar et al., 2004; Yin et al., 2016 |
| Cnp null | Mislocalization of voltage-gated sodium channels and Caspr, progressive axon loss, axonal spheroids with accumulations of membranous organelles, impaired axon transport, and impaired formation and maintenance of cytoplasmic channels | Lappe-Siefke et al., 2003; Rasband et al., 2005; Snaidero et al., 2017 |
| Mag null | Decreased axon caliber/neurofilament phosphorylation, progressive axon loss, increased susceptibility to EAE/neurotoxic injury, and decreased Cdk5/Erk1/2 kinase activity | Fruttiger et al., 1995; Yin et al., 1998; Dashiell et al., 2002; Pan et al., 2005; Nguyen et al., 2009 |
| EAE | Axon loss, irreversible cytoskeletal fragmentation, impaired mitochondrial morphology and trafficking, impaired axon transport, oxidative damage, and increased axoplasmic calcium | Siffrin et al., 2010; Nikić et al., 2011; Sorbara et al., 2014; Höflich et al., 2016; Mei et al., 2016 |
| Lysolecithin | Impaired axon transport, increased mitochondrial stationary site size and transport rate, and disrupted nodal architecture | Arroyo et al., 2004; Kiryu-Seo et al., 2010; Ohno et al., 2014; Höflich et al., 2016; Schultz et al., 2017 |
| Cuprizone | Axon loss, impaired axon transport, and increased mitochondrial stationary site size | Ohno et al., 2014; Sachs et al., 2014; Höflich et al., 2016; Schultz et al., 2017 |
| DT ablation | Axon loss, impaired axon transport, and neurofilament dephosphorylation | Traka et al., 2010, 2016; Pohl et al., 2011; Oluich et al., 2012 |