Control and experimental pups were obtained from the same litter and the injections were always made on the left and right ventricles, respectively, for later identification. Animal protocols were approved by

the Animal Care and Use Committee of UC Berkeley. To decide the statistical test for the comparison between two data sets, we first examined whether the data in each set are normally distributed, using Jarque-Bera test. For data sets with normal distribution, t test was used. For comparison Roxadustat cost involving multiple data sets, one-way ANOVA test was used followed by post-hoc Tukey test. We thank R. Thakar, S. Li, M. Nasir, and D. Liepmann (University of California, Berkeley, CA) for help with PDMS microfluidic molds for making patterned substrates. We thank E. Burstein (University of Michigan Medical School) for providing Myc-tagged ubiquitin constructs, X.B. Yuan (Institute of Neuroscience, Shanghai) for constitutive active RhoA construct, X. Zhang (Institute of Neuroscience, Shanghai) for pCAG-IRES-EGFP, and R. Tsien (University of California,

San Diego, CA) for tdTomato construct. This work was www.selleckchem.com/products/epz-6438.html supported in part by a grant from the National Institutes of Health. “
“The sequestration of ion channels into molecularly distinct axonal domains is vital for nervous system function. Enrichment of voltage-gated sodium (Nav) channels at nodes of Ranvier is of considerable importance, as they function to potentiate the nerve impulse in a saltatory manner along myelinated fibers (Rasband, 2006, Salzer, 2003, Thaxton and Bhat, 2009 and Waxman much and Ritchie, 1993). Recent findings have raised key questions concerning the mechanisms regulating nodal development, such as whether nodes form independently of paranodes, or whether paranodes are sufficient for nodal organization. Neurofascins (Nfascs), a group of cell adhesion molecules with spatio-temporal expression in the nervous system, have been recently implicated in axonal function (Davis and Bennett, 1993,

Tait et al., 2000 and Volkmer et al., 1992). Two major isoforms have been characterized, the glial-specific NfascNF155 (NF155) that localizes to the paranodes (Tait et al., 2000), and the neuron-specific NfascNF186 (NF186) that is enriched at nodes of Ranvier and axon initial segments (Collinson et al., 1998, Davis et al., 1996 and Hassel et al., 1997). Genetic ablation of Nfasc in mice (Nfasc−/−) resulted in paranodal and nodal disorganization due to loss of both NF155 and NF186, and death at postnatal day 7 (P7), further highlighting their importance in myelinated axons ( Sherman et al., 2005). While glial-specific loss of NfascNF155 revealed its specific role in paranodal domain formation and stabilization ( Pillai et al.