Iu, 1993; Pappas and Ritchie, 1998; Sobko et al., 1998) (Figure 1G1). In vitro ES of embryonic DRG neurons, at low frequencies that mimic DRG spontaneous spiking at early Ach esterase Inhibitors Reagents developmental stages, results in activation of purinergic signaling pathways and subsequent inhibition of both SC proliferation and differentiation (Figure 1G2) (Stevens and Fields, 2000; Stevens et al., 2004). Myelination reduction by low-frequency ES has been CP-465022 Data Sheet further attributed to downregulation of the axonal adhesion molecule L1 (Stevens et al., 1998). Glu and GABA also modulate SC maturation (Figure 1G3) (Magnaghi et al., 2006; Saitoh and Araki, 2010; Procacci et al., 2012). However, despite the fact that GABA is identified to be released by SCs (see paragraph “Neurotransmitter secretion”), its extrasynaptic secretion from PNS axons has not been demonstrated. Couple of existing experimental information suggest that neuronal activity controls myelination also within the mature PNS. Subfunctional soleus nerve fibers in hindlimb-unloaded rats exhibit decreased myelin thickness (Canu et al., 2009). Administration of ATP modulates myelin lipid constitution in frog SN preparations (Kutuzov NP et al., 2013). Regardless of whether and how neuronal function is affected by these changes needs additional investigation.TROPHIC AND METABOLIC Help OF NEURONSIn neuropathy modelsDown Up Down Previously published dataa-o UpTranscriptional regulation pDuring developmentCx29,32, andCx37 ,40, andCxCxNeuronal activity is dependent upon the upkeep of axonal integrity and energetic status. Each nmSCs and mSCs deliver neurotropic and metabolic support to adjacent neurons (Griffin and Thompson, 2008; Nave, 2010). This assistance is below the handle of axonal activity. In response to ES and ATP, cultured SCs secrete nerve development factor (NGF) and brain-derived neurotropic element (BDNF), respectively, promoting axonal development (Figure 1H) (Verderio et al., 2006; Huang et al., 2010). In addition, chemical depolarization triggers vesicular transport of molecules from SCs to axons (Figure 1I) at the least in invertebrates (Eyman et al., 2007). Reported molecular cargo of SC-to-axon transported vesicles incorporates ribosome-bound mRNA, cytoskeletal components and heat-shock proteins (Court et al., 2008; Cocucci et al., 2009; Lopez-Verrilli and Court, 2012). Their exact contributions to axonal function under physiological situations are nonetheless unknown. Despite the fact that data relating to glia-to-axon metabolic assistance in the PNS is scarce, inferences could possibly be made from CNS information. Neuronal activity triggers exosome transfer of metabolic enzymes from oligodendrocytes to neurons (Fruhbeis et al., 2013), also as release of lactate from astrocytes and uptake by neurons (Barros, 2013). Equivalent power transfer processes may well happen in the PNS. ES in SN increases O2 uptake and glucose consumption, and SCs appear to be the principle metabolic SN niche (Heller and Hesse, 1961). Additionally, in vivo genetic disruption of mitochondria power production in otherwise functional mouse SCs severely impairs the structure and function of peripheralSubtypesTable 1 | ContinuedGAP-junctionsl-nFamiliesCxk-mCx29,32, and 43 in mSCs; Cx32, and in iSCs, Cx 29 in iSCsFrontiers in Cellular Neurosciencej Loretiwww.frontiersin.orgNovember 2013 | Volume 7 | Short article 228 |Samara et al.PNS glia-neuron communicationfibers (Viader et al., 2011; Funfschilling et al., 2012), suggesting that there may well be SC-to-neuron power transfer also inside the PNS. However, its characterization, and prospective regulation by neuro.