Human NRTN (Neurturin) ELISA Kit

The aim of this study was to establish a rapid atrial pacing-induced canine model of atrial fibrillation in studying the effects of low-level vagus nerve stimulation (LLVNS) on atrial fibrillation and the underlying mechanisms for those effects. Adult beagle dogs were randomly assigned to 3 groups: a sham operation group (sham group), a fast left atrial appendage 12-hour pacing group (pacing group), and a 12-hour pacing + LLVNS group (LLVNS group). All dogs underwent tests for their left and right atrial effective refractory period at various time points, after which they were killed, and samples of atrial and anterior right ganglionated plexi tissue were removed and microscopically examined. As pacing times increased, the mean effective refractory period in the pacing group became significantly shortened. The pacing group and the LLVNS group did show significant differences (P < 0.001). Three groups showed significant differences in their atrial myocardial periodic acid-Schiff-positive area staining densities. Anterior right ganglionated plexi expressions of nerve growth factor and neurturin (NRTN) in the sham group and the LLVNS group were lower than those in the pacing group (nerve growth factor in 3 groups were (36.35 +/- 6.18) x 1000, (86.35 +/- 5.63) x 1000, and (40.50 +/- 7.24) x 1000 mu m(2)/mm(2), P < 0.001; NRTN in 3 groups were (39.28 +/- 7.80) x 1000, (80.24 +/- 6.56) x 1000, (40.45 +/- 6.97) x 1000 mu m(2)/mm(2), P < 0.001). Therefore, LLVNS not only reverses the effect of fast pacing-induced atrial electrical remodeling in dogs but also exerts structural effects and stimulates remodeling of autonomic nerves.

Embryonic stem (ES) cells are genetically manipulable pluripotential cells that can be differentiated in vitro into neurons, oligodendrocytes, and astrocytes. Given their potential utility as a source of replacement cells for the injured nervous system and the likelihood that transplantation interventions might include co-application of growth factors, we examined the effects of neurotrophin and GDNF family ligands on the survival and excitotoxic vulnerability of ES cell-derived neurons (ES neurons) grown in vitro. ES cells were differentiated down a neural lineage in vitro using the 4-/4+ protocol (Bain et al., Dev Biol 168:342-57, 1995). RT-PCR demonstrated expression of receptors for neurotrophins and GDNF family ligands in ES neural lineage cells. Neuronal expression of GFRalpha1, GFRalpha2, and ret was confirmed by immunocytochemistry. Exposure to 30-100 ng/ml GDNF or neurturin (NRTN) resulted in activation of ret. Addition of NT-3 and GDNF did not increase cell division but did increase the number of neurons in the cultures 7 days after plating. Pretreatment with NT-3 enhanced the vulnerability of ES neurons to NMDA-induced death (100 muM NMDA for 10 min) and enhanced the NMDA-induced increase in neuronal [Ca(2+)](i), but did not alter expression of NMDA receptor subunits NR2A or NR2B. In contrast, pretreatment with GDNF reduced the vulnerability of ES neurons to NMDA-induced death while modestly enhancing the NMDA-induced increase in neuronal [Ca(2+)](i). These findings demonstrate that the response of ES-derived neurons to neurotrophins and GDNF family ligands is largely similar to that of other cultured central neurons. (C) 2004 Elsevier Inc. All rights reserved.