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Neuron Migration (neuron + migration)
Selected AbstractsMultiple mechanisms mediate motor neuron migration in the zebrafish hindbrainDEVELOPMENTAL NEUROBIOLOGY, Issue 2 2010Stephanie M. Bingham Abstract The transmembrane protein Van gogh-like 2 (Vangl2) is a component of the noncanonical Wnt/Planar Cell Polarity (PCP) signaling pathway, and is required for tangential migration of facial branchiomotor neurons (FBMNs) from rhombomere 4 (r4) to r5-r7 in the vertebrate hindbrain. Since vangl2 is expressed throughout the zebrafish hindbrain, it might also regulate motor neuron migration in other rhombomeres. We tested this hypothesis by examining whether migration of motor neurons out of r2 following ectopic hoxb1b expression was affected in vangl2, (trilobite) mutants. Hoxb1b specifies r4 identity, and when ectopically expressed transforms r2 to an "r4-like" compartment. Using time-lapse imaging, we show that GFP-expressing motor neurons in the r2/r3 region of a hoxb1b -overexpressing wild-type embryo migrate along the anterior-posterior (AP) axis. Furthermore, these cells express prickle1b (pk1b), a Wnt/PCP gene that is specifically expressed in FBMNs and is essential for their migration. Importantly, GFP-expressing motor neurons in the r2/r3 region of hoxb1b -overexpressing trilobite mutants and pk1b morphants often migrate, even though FBMNs in r4 of the same embryos fail to migrate longitudinally (tangentially) into r6 and r7. These observations suggest that tangentially migrating motor neurons in the anterior hindbrain (r1-r3) can use mechanisms that are independent of vangl2 and pk1b functions. Interestingly, analysis of tri; val double mutants also suggests a role for vangl2 -independent factors in neuronal migration, since the valentino mutation partially suppresses the trilobite mutant migration defect. Together, the hoxb1b and val experiments suggest that multiple mechanisms regulate motor neuron migration along the AP axis of the zebrafish hindbrain. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2010 [source] Netrin 1-mediated chemoattraction regulates the migratory pathway of LHRH neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2004Gerald A. Schwarting Abstract Luteinizing hormone-releasing hormone (LHRH) neurons migrate from the vomeronasal organ (VNO) to the forebrain in all mammals studied. In mice, the direction of LHRH neuron migration is dependent upon axons that originate in the VNO, but bypass the olfactory bulb and project caudally into the basal forebrain. Thus, factors that guide this unique subset of vomeronasal axons that comprise the caudal vomeronasal nerve (cVNN) are candidates for regulating the migration of LHRH neurons. We previously showed that deleted in colorectal cancer (DCC) is expressed by neurons that migrate out of the VNO during development [Schwarting et al. (2001) J. Neurosci., 21, 911,919]. We examined LHRH neuron migration in Dcc,/, mice and found that trajectories of the cVNN and positions of LHRH neurons are abnormal. Here we extend these studies to show that cVNN trajectories and LHRH cell migration in netrin 1 (Ntn1) mutant mice are also abnormal. Substantially reduced numbers of LHRH neurons are found in the basal forebrain and many LHRH neurons migrate into the cerebral cortex of Ntn1 knockout mice. In contrast, migration of LHRH cells is normal in Unc5h3rcm mutant mice. These results are consistent with the idea that the chemoattraction of DCC+ vomeronasal axons by a gradient of netrin 1 protein in the ventral forebrain guides the cVNN, which, in turn, determines the direction of LHRH neuron migration in the forebrain. Loss of function through a genetic deletion in either Dcc or Ntn1 results in the migration of many LHRH neurons to inappropriate destinations. [source] Rho kinase activates ezrin-radixin-moesin (ERM) proteins and mediates their function in cortical neuron growth, morphology and motility in vitroJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2007Matilda A. Haas Abstract The ezrin-radixin-moesin (ERM) family of proteins contribute to cytoskeletal processes underlying many vital cellular functions. Their previously elucidated roles in non-neuronal cells are an indication of their potential importance in CNS neurons. The specific mechanisms of their activation are unknown, but are likely to depend on factors such as the cell type and biological context. For ERM proteins to become active they must be phosphorylated at a specific C-terminal threonine residue. In non-neuronal cells, several kinases, including the Rho GTPase family member Rho kinase, have been identified as capable of phosphorylating the C-terminal threonine. In these experiments we have investigated specifically the potential role of Rho kinase mediated ERM activation in cortical neurons, utilizing a new pharmacologic inhibitor of Rho kinase and quantitative analysis of aspects of neuronal functions potentially mediated by ERM proteins. Rho kinase inhibition significantly suppressed aspects of neuronal development including neurite initiation and outgrowth, as well as growth cone morphology, with a concomitant loss of phosphorylated ERM immunolabeling in areas associated with neuronal growth. The ability of the Rho kinase inhibitor to decrease the amount of pERM protein was shown by immunoblotting. Post-injury responses were negatively affected by Rho kinase inhibition, namely by a significant decrease in the number of regenerative neurites. We investigated a novel role for ERM proteins in neuron migration using a post-injury motility assay, where Rho kinase inhibition resulted in significant and drastic reduction in neuron motility and phosphorylated ERM immunolabeling. Thus, Rho kinase is an important activator of ERMs in mediating specific neuronal functions. © 2006 Wiley-Liss, Inc. [source] An automatic integrated approach for stained neuron detection in studying neuron migrationMICROSCOPY RESEARCH AND TECHNIQUE, Issue 2 2010Yue Huang Abstract Neurons that come to populate the six-layered cerebral cortex are born deep within the developing brain in the surface of the embryonic cerebral ventricles. It is very important to detect these neurons for studying histogenesis of the brain and abnormal migration that had been linked to cognitive deficits, mental retardation, and motor disorders. The visualization of labeled cells in brain sections was performed by immunocytochemical examination and its image data were documented to microscopic pictures. Based on the fact, automatic accurate neurons labeling is prerequisite instead of time-consuming manual labeling. In this article, a fully automated image processing approach is proposed to detect all the stained neurons in microscopic images. First of all, dark stained neurons are achieved by thresholding in blue channel of image. And then a modified fuzzy c-means clustering method, called alternative fuzzy c-means is applied to achieve higher classification accuracy in extracting constraint factor. Finally, watershed based on gradient vector flow is employed to the constraint factor image to segment all the neurons, including clustered neurons. The results demonstrate that the proposed method can be a useful tool in neuron image analysis. Microsc. Res. Tech. 2010. © 2009 Wiley-Liss, Inc. [source] | ||||||||||