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Thread: Fish offer clues to spinal cord renewal

  1. #1

    Fish offer clues to spinal cord renewal

    Fish offer clues to spinal cord renewal
    April 6, 2011




    (PhysOrg.com) -- Spinal cord injuries are devastating, but fish may be the key to finding a cure.Research shows adult fish that sustain a spinal cord injury have the miraculous ability to not only regenerate the spinal cord, but to recover function as well — meaning they are able to perform tasks they were able to do prior to the injury.





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    For the past four years, biology department chair Günther Zupanc and his research associate, Ruxandra Sîrbulescu, have been studying this stunning recovery in fish.

    Their research was recently published in the journal Brain Research Reviews.

    Zupanc’s team is examining how fish are able to regenerate the spinal cord in hopes of ultimately finding a way to replicate this process in humans. "To cure spinal cord injury would be amazing and incredible for people who are suffering," Zupanc said.

    read....

    http://www.physorg.com/news/2011-04-...d-renewal.html

  2. #2
    Senior Member FasterNow's Avatar
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    "Humans have some regeneration potential. The trick will be to unravel the hidden potential of humans, and fish may show us how to do that."

    I didn't know fish had so much spinal cord regenerative ability. Thanks manouli.
    Injured 7-22-06, T-11 T-12 complete. [Holds up cardboard sign] "Will work for returns."
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  3. #3
    Dr. Günther K. H. Zupanc studies a fish called zebrafish. He is a good scientist and has contributed significantly to the field but this tiny fish was reported to be able to regenerate more than two decades ago and many laboratories have been studying spinal cord injury in this fish.

    At the W. M. Keck Center at Rutgers, the laboratory of Melitta Schachner has been studying spinal cord regeneration in zebrafish for several years. Yu, et al. [1] recently reported that application of the extracellular matrix glycoprotein tenascin-C promotes swiming recovery in the adult zebrafish. In a second paper, Yu, et al. [2] showed that the microRNA miR-133b is essential for functional recovery after spinal cord injury in adult zebrafish. Guo, et al. [3] recently reported that the transcription factor Sox11b is involved in the regeneration of the adult zebrafish.

    The Schachner laboratory has long been engaged in zebrafish studies. In 1997, Becker, et al. [4] had earlier described axonal regrowth after spinal cord tansection in the adult zebrafish, associated with the expression of specific cell recognition molecules [5]. In 2003, Schweitzer, et. al. [6] reported the expression of protein zero is increased in lesioned axon pathways in spinal cord of adult zebrafish. In 2004, Becker, et al. [7] reported that L1.1 is involved in spinal cord regeneration in adult zebrafish. In 2005, Becker, et al. [8] characterized the differences in regenerative responses of neuronal cell populations after spinal cord transection in zebrafish.

    After 2005, after she moved to Rutgers, Schachner continued to collaborate with Becker. For example, Reimer, et al. [9] from the Becker laboratory has shown motor neuronal regeneration in adult zebrafish. Schweitzer, et al. [10] showed that contactin1a expression is associated with oligodendrocyte differentiation and axonal regeneration in spinal cord of adult zebrafish.

    A search for papers by Zupanc yielded four publications from 2005-2009 [11-15]. Unfortunately, the paper that is referred to by this press release has not yet been published and I will comment further when it becomes available.

    References

    1. Yu YM, Cristofanilli M, Valiveti A, Ma L, Yoo M, Morellini F and Schachner M The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish. Neuroscience W. M. Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, 604 Allison Road, NJ 08854, USA. Adult zebrafish, by virtue of exhibiting spontaneous recovery after spinal lesion, have evolved into a paradigmatic vertebrate model system to identify novel genes vital for successful regeneration after spinal cord injury. Due to a remarkable level of conservation between zebrafish and human genomes, such genes, once identified, could point to possibilities for addressing the multiple issues on how to deal with functional recovery after spinal cord injury in humans. In the current study, the extracellular matrix glycoprotein tenascin-C was studied in the zebrafish spinal cord injury model to assess the often disparate functions of this multidomain molecule under in vivo conditions. This in vivo study was deemed necessary since in vitro studies had shown discrepant functional effects on neurite outgrowth: tenascin-C inhibits neurite outgrowth when presented as a molecular barrier adjacent to a conducive substrate, but enhances neurite outgrowth when presented as a uniform substrate. Thus, our current study addresses the question as to which of these features prevails in vivo: whether tenascin-C reduces or enhances axonal regrowth after injury in a well accepted vertebrate model of spinal cord injury. We show upregulation of tenascin-C expression in regenerating neurons of the nucleus of median longitudinal fascicle (NMLF) in the brainstem and spinal motoneurons. Inhibition of tenascin-C expression by antisense oligonucleotide (morpholino) resulted in impaired locomotor recovery, reduced regrowth of axons from brainstem neurons and reduced synapse formation by the regrowing brainstem axons on spinal motoneurons, all vital indicators of regeneration. Our results thus point to an advantageous role of tenascin-C in promoting spinal cord regeneration, by promoting axonal regrowth and synapse formation in the spinal cord caudal to the lesion site after injury.

    2. Yu YM, Gibbs KM, Davila J, Campbell N, Sung S, Todorova TI, Otsuka S, Sabaawy HE, Hart RP and Schachner M MicroRNA miR-133b is essential for functional recovery after spinal cord injury in adult zebrafish. Eur J Neurosci W. M. Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, NJ, USA The Cancer Institute of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ, USA. MicroRNAs (miRNAs) play important roles during development and also in adult organisms by regulating the expression of multiple target genes. Here, we studied the function of miR-133b during zebrafish spinal cord regeneration and show upregulation of miR-133b expression in regenerating neurons of the brainstem after transection of the spinal cord. miR-133b has been shown to promote tissue regeneration in other tissue, but its ability to do so in the nervous system has yet to be tested. Inhibition of miR-133b expression by antisense morpholino (MO) application resulted in impaired locomotor recovery and reduced regeneration of axons from neurons in the nucleus of the medial longitudinal fascicle, superior reticular formation and intermediate reticular formation. miR-133b targets the small GTPase RhoA, which is an inhibitor of axonal growth, as well as other neurite outgrowth-related molecules. Our results indicate that miR-133b is an important determinant in spinal cord regeneration of adult zebrafish through reduction in RhoA protein levels by direct interaction with its mRNA. While RhoA has been studied as a therapeutic target in spinal cord injury, this is the first demonstration of endogenous regulation of RhoA by a microRNA that is required for spinal cord regeneration in zebrafish. The ability of miR-133b to suppress molecules that inhibit axon regrowth may underlie the capacity for adult zebrafish to recover locomotor function after spinal cord injury.

    3. Guo Y, Ma L, Cristofanilli M, Hart RP, Hao A and Schachner M (2010). Transcription factor Sox11b is involved in spinal cord regeneration in adult zebrafish. Neuroscience 172: 329-41. W.M. Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers, the State University of New Jersey, Piscataway, NJ 08854, USA. Adult zebrafish have the ability to recover from spinal cord injury and exhibit re-growth of descending axons from the brainstem to the spinal cord. We performed gene expression analysis using microarray to find damage-induced genes after spinal cord injury, and found that Sox11b mRNA is up-regulated at 11 days after injury. However, the functional relevance of Sox11b for regeneration is not known. Here, we report that the up-regulation of Sox11b mRNA after spinal cord injury is mainly localized in ependymal cells lining the central canal and in newly differentiating neuronal precursors or immature neurons. Using an in vivo morpholino-based gene knockout approach, we demonstrate that Sox11b is essential for locomotor recovery after spinal cord injury. In the injured spinal cord, expression of the neural stem cell associated gene Nestin, and the proneural gene Ascl1a (Mash1a), which are involved in the self-renewal and cell fate specification of endogenous neural stem cells, respectively, is regulated by Sox11b. Our data indicate that Sox11b promotes neuronal determination of endogenous stem cells and regenerative neurogenesis following spinal cord injury in the adult zebrafish. Enhancing Sox11b expression to promote proliferation and neurogenic determination of endogenous neural stem cells after injury may be a promising strategy in restorative therapy after spinal cord injury in mammals.

    4. Becker T, Wullimann MF, Becker CG, Bernhardt RR and Schachner M (1997). Axonal regrowth after spinal cord transection in adult zebrafish. J Comp Neurol 377: 577-95. Department of Neurobiology, Swiss Federal Institute of Technology, Honggerberg, Zurich, Switzerland. rmlab@ucl.edu. Using axonal tracers, we characterized the neurons projecting from the brain to the spinal cord as well as the terminal fields of ascending spinal projections in the brain of adult zebrafish with unlesioned or transected spinal cords. Twenty distinct brain nuclei were found to project to the spinal cord. These nuclei were similar to those found in the closely related goldfish, except that additionally the parvocellular preoptic nucleus, the medial octavolateralis nucleus, and the nucleus tangentialis, but not the facial lobe, projected to the spinal cord in zebrafish. Terminal fields of axons, visualized by anterograde tracing, were seen in the telencephalon, the diencephalon, the torus semicircularis, the optic tectum, the eminentia granularis, and throughout the ventral brainstem in unlesioned animals. Following spinal cord transection at a level approximately 3.5 mm caudal to the brainstem/spinal cord transition zone, neurons in most brain nuclei grew axons beyond the transection site into the distal spinal cord to the level of retrograde tracer application within 6 weeks. However, the individually identifiable Mauthner cells were never seen to do so up to 15 weeks after spinal cord transection. Nearly all neurons survived axotomy, and the vast majority of axons that had grown beyond the transection site belonged to previously axotomized neurons as shown by double tracing. Terminal fields were not re-established in the torus semicircularis and the eminentia granularis following spinal cord transection.

    5. Becker T, Bernhardt RR, Reinhard E, Wullimann MF, Tongiorgi E and Schachner M (1998). Readiness of zebrafish brain neurons to regenerate a spinal axon correlates with differential expression of specific cell recognition molecules. J Neurosci 18: 5789-803. Department of Neurobiology, Swiss Federal Institute of Technology, Honggerberg, CH-8093 Zurich, Switzerland. We analyzed changes in the expression of mRNAs for the axonal growth-promoting cell recognition molecules L1.1, L1.2, and neural cell adhesion molecule (NCAM) after a rostral (proximal) or caudal (distal) spinal cord transection in adult zebrafish. One class of cerebrospinal projection nuclei (represented by the nucleus of the medial longitudinal fascicle, the intermediate reticular formation, and the magnocellular octaval nucleus) showed a robust regenerative response after both types of lesions as determined by retrograde tracing and/or in situ hybridization for GAP-43. A second class (represented by the nucleus ruber, the nucleus of the lateral lemniscus, and the tangential nucleus) showed a regenerative response only after proximal lesion. After distal lesion, upregulation of L1.1 and L1.2 mRNAs, but not NCAM mRNA expression, was observed in the first class of nuclei. The second class of nuclei did not show any changes in their mRNA expression after distal lesion. After proximal lesion, both classes of brain nuclei upregulated L1.1 mRNA expression (L1.2 and NCAM were not tested after proximal lesion). In the glial environment distal to the spinal lesion, labeling for L1.2 mRNA but not L1.1 or NCAM mRNAs was increased. These results, combined with findings in the lesioned retinotectal system of zebrafish (Bernharnhardt et al., 1996), indicate that the neuron-intrinsic regulation of cell recognition molecules after axotomy depends on the cell type as well as on the proximity of the lesion to the neuronal soma. Glial reactions differ for different regions of the CNS.

    6. Becker T, Bernhardt RR, Reinhard E, Wullimann MF, Tongiorgi E and Schachner M (1998). Readiness of zebrafish brain neurons to regenerate a spinal axon correlates with differential expression of specific cell recognition molecules. J Neurosci 18: 5789-803. Department of Neurobiology, Swiss Federal Institute of Technology, Honggerberg, CH-8093 Zurich, Switzerland. We analyzed changes in the expression of mRNAs for the axonal growth-promoting cell recognition molecules L1.1, L1.2, and neural cell adhesion molecule (NCAM) after a rostral (proximal) or caudal (distal) spinal cord transection in adult zebrafish. One class of cerebrospinal projection nuclei (represented by the nucleus of the medial longitudinal fascicle, the intermediate reticular formation, and the magnocellular octaval nucleus) showed a robust regenerative response after both types of lesions as determined by retrograde tracing and/or in situ hybridization for GAP-43. A second class (represented by the nucleus ruber, the nucleus of the lateral lemniscus, and the tangential nucleus) showed a regenerative response only after proximal lesion. After distal lesion, upregulation of L1.1 and L1.2 mRNAs, but not NCAM mRNA expression, was observed in the first class of nuclei. The second class of nuclei did not show any changes in their mRNA expression after distal lesion. After proximal lesion, both classes of brain nuclei upregulated L1.1 mRNA expression (L1.2 and NCAM were not tested after proximal lesion). In the glial environment distal to the spinal lesion, labeling for L1.2 mRNA but not L1.1 or NCAM mRNAs was increased. These results, combined with findings in the lesioned retinotectal system of zebrafish (Bernharnhardt et al., 1996), indicate that the neuron-intrinsic regulation of cell recognition molecules after axotomy depends on the cell type as well as on the proximity of the lesion to the neuronal soma. Glial reactions differ for different regions of the CNS.

    7. Becker CG, Lieberoth BC, Morellini F, Feldner J, Becker T and Schachner M (2004). L1.1 is involved in spinal cord regeneration in adult zebrafish. J Neurosci 24: 7837-42. Zentrum fur Molekulare Neurobiologie, Universitat Hamburg, D-20246 Hamburg, Germany. tcbecker@zmnh.uni-hamburg.de. Adult zebrafish, in contrast to mammals, regrow axons descending from the brainstem after spinal cord transection. L1.1, a homolog of the mammalian recognition molecule L1, is upregulated by brainstem neurons during axon regrowth. However, its functional relevance for regeneration is unclear. Here, we show with a novel morpholino-based approach that reducing L1.1 protein expression leads to impaired locomotor recovery as well as reduced regrowth and synapse formation of axons of supraspinal origin after spinal cord transection. This indicates that L1.1 contributes to successful regrowth of axons from the brainstem and locomotor recovery after spinal cord transection in adult zebrafish.

    8. 1. Becker T, Lieberoth BC, Becker CG and Schachner M (2005). Differences in the regenerative response of neuronal cell populations and indications for plasticity in intraspinal neurons after spinal cord transection in adult zebrafish. Mol Cell Neurosci 30: 265-78. Zentrum fur Molekulare Neurobiologie, Universitat Hamburg, Martinistr. 52, D-20246 Hamburg, Germany. In zebrafish, the capacity to regenerate long axons varies among different populations of axotomized neurons after spinal cord transection. In specific brain nuclei, 84-92% of axotomized neurons upregulate expression of the growth-related genes GAP-43 and L1.1 and 32-51% of these neurons regrow their descending axons. In contrast, 16-31% of spinal neurons with axons ascending to the brainstem upregulate these genes and only 2-4% regrow their axons. Dorsal root ganglion (DRG) neurons were not observed to regrow their ascending axons or to increase expression of GAP-43 mRNA. Expression of L1.1 mRNA is high in unlesioned and axotomized DRG neurons. In the lesioned spinal cord, expression of growth-related molecules is increased in a substantial population of non-axotomized neurons, suggesting morphological plasticity in the spinal-intrinsic circuitry. We propose that locomotor recovery in spinal-transected adult zebrafish is influenced less by recovery of ascending pathways, but more by regrowth of descending tracts and rearrangement of intraspinal circuitry.

    9. Reimer MM, Sorensen I, Kuscha V, Frank RE, Liu C, Becker CG and Becker T (2008). Motor neuron regeneration in adult zebrafish. J Neurosci 28: 8510-6. Centre for Neuroscience Research, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Summerhall, Edinburgh EH9 1QH, United Kingdom. The mammalian spinal cord does not regenerate motor neurons that are lost as a result of injury or disease. Here we demonstrate that adult zebrafish, which show functional spinal cord regeneration, are capable of motor neuron regeneration. After a spinal lesion, the ventricular zone shows a widespread increase in proliferation, including slowly proliferating olig2-positive (olig2+) ependymo-radial glial progenitor cells. Lineage tracing in olig2:green fluorescent protein transgenic fish indicates that these cells switch from a gliogenic phenotype to motor neuron production. Numbers of undifferentiated small HB9+ and islet-1+ motor neurons, which are double labeled with the proliferation marker 5-bromo-2-deoxyuridine (BrdU), are transiently strongly increased in the lesioned spinal cord. Large differentiated motor neurons, which are lost after a lesion, reappear at 6-8 weeks after lesion, and we detected ChAT+/BrdU+ motor neurons that were covered by contacts immunopositive for the synaptic marker SV2. These observations suggest that, after a lesion, plasticity of olig2+ progenitor cells may allow them to generate motor neurons, some of which exhibit markers for terminal differentiation and integration into the existing adult spinal circuitry.

    10. Schweitzer J, Gimnopoulos D, Lieberoth BC, Pogoda HM, Feldner J, Ebert A, Schachner M, Becker T and Becker CG (2007). Contactin1a expression is associated with oligodendrocyte differentiation and axonal regeneration in the central nervous system of zebrafish. Mol Cell Neurosci 35: 194-207. Institut fur die Biosynthese Neuraler Strukturen, Zentrum fur Molekulare Neurobiologie, University of Hamburg, D-20246 Hamburg, Germany. Contactin1a (Cntn1a) is a zebrafish homolog of contactin1 (F3/F11/contactin) in mammals, an immunoglobulin superfamily recognition molecule of neurons and oligodendrocytes. We describe conspicuous Cntn1a mRNA expression in oligodendrocytes in the developing optic pathway of zebrafish. In adults, this expression is only retained in glial cells in the intraretinal optic fiber layer, which contains 'loose' myelin. After optic nerve lesion, oligodendrocytes re-express Cntn1a mRNA independently of the presence of regenerating axons and retinal ganglion cells upregulate Cntn1a expression to levels that are significantly higher than those during development. After spinal cord lesion, expression of Cntn1a mRNA is similarly increased in axotomized brainstem neurons and white matter glial cells in the spinal cord. In addition, reduced mRNA expression in the trigeminal/anterior lateral line ganglion in erbb3-deficient mutant larvae implies Cntn1a in Schwann cell differentiation. These complex regulation patterns suggest roles for Cntn1a in myelinating cells and neurons particularly in successful CNS regeneration.

    11. Zupanc GK, Wellbrock UM, Sirbulescu RF and Rajendran RS (2009). Generation, long-term persistence, and neuronal differentiation of cells with nuclear aberrations in the adult zebrafish brain. Neuroscience 159: 1338-48. School of Engineering and Science, Jacobs University Bremen, Bremen, Germany. g.zupanc@jacobs-university.de. Zebrafish, like other teleosts, continuously produce new cells in numerous regions of the adult brain. Immunolabeling employing antisera against phosphorylated histone-H3 and 5-bromo-2'-deoxyuridine revealed that approximately 6%-7% of such cells exhibited nuclear aberrations. These aberrations, presumably the result of mitotic segregation defects, included single and multiple laggards (both during metaphase and anaphase) and anaphase bridges. Cells with such aberrations persisted long-term and comprised, when examined 7.5 months after their generation, approximately 2.5% of the total population of adult-born cells. The drop in relative frequency of aberrations in the course of further development appears to be caused by elimination of cells with nuclear aberrations, presumably by apoptotic cell death. The cells with nuclear aberrations that persisted long-term were capable of neuronal differentiation, as demonstrated by combining anti-5-bromo-2'-deoxyuridine immunohistochemistry with immunostaining against the neuronal marker protein Hu or the enzyme tyrosine hydroxylase, a marker of catecholaminergic neurons. We hypothesize that the alterations in chromosome number and/or chromosome structure caused by nuclear aberrations do not necessarily result in loss of vital functions or in tumorigenesis. Instead, cells with such aberrations are able to undergo what appears to be normal development.

    12. Zupanc GK (2008). Adult neurogenesis and neuronal regeneration in the brain of teleost fish. J Physiol Paris 102: 357-73. School of Engineering and Science, Jacobs University Bremen, Bremen, Germany. g.zupanc@jacobs-university.de. Whereas adult neurogenesis appears to be a universal phenomenon in the vertebrate brain, enormous differences exist in neurogenic potential between "lower" and "higher" vertebrates. Studies in the gymnotiform fish Apteronotus leptorhynchus and in zebrafish have indicated that the relative number of new cells, as well as the number of neurogenic sites, are at least one, if not two, orders of magnitude larger in teleosts than in mammals. In teleosts, these neurogenic sites include brain regions homologous to the mammalian hippocampus and olfactory bulb, both of which have consistently exhibited neurogenesis in all species examined thus far. The source of the new cells in the teleostean brain are intrinsic stem cells that give rise to both glial cells and neurons. In several brain regions, the young cells migrate, guided by radial glial fibers, to specific target areas where they integrate into existing neural networks. Approximately half of the new cells survive for the rest of the fish's life, whereas the other half are eliminated through apoptotic cell death. A potential mechanism regulating development of the new cells is provided by somatic genomic alterations. The generation of new cells, together with elimination of damaged cells through apoptosis, also enables teleost fish rapid and efficient neuronal regeneration after brain injuries. Proteome analysis has identified a number of proteins potentially involved in the individual regenerative processes. Comparative analysis has suggested that differences between teleosts and mammals in the growth of muscles and sensory organs are key to explain the differences in adult neurogenesis that evolved during phylogenetic development of the two taxa.

    13. Hinsch K and Zupanc GK (2007). Generation and long-term persistence of new neurons in the adult zebrafish brain: a quantitative analysis. Neuroscience 146: 679-96. School of Engineering and Science, Jacobs University Bremen,(1) P.O. Box 750 561, D-28725 Bremen, Germany. Zebrafish, like other teleosts, are distinguished by their enormous potential to produce new neurons in many parts of the adult brain. By labeling S-phase cells with the thymidine analog 5-bromo-2'-deoxyuridine (BrdU), quantitative analysis demonstrated that, on average, 6000 new cells were generated in the entire adult brain within any 30 min period. This corresponds to roughly 0.06% of the total number of brain cells. Part of these cells underwent a second round of cell division a few days after their generation so that 10 days post-BrdU administration, when the cells have exited the mitotic cycle, approximately 10,000 BrdU-labeled cells were present in the entire brain. At post-BrdU survival times of 446-656 days, on average 4600 BrdU-labeled cells were found, suggesting that approximately 46% of the cells present at 10 days persisted in the adult zebrafish brain. Combination of BrdU-labeling of mitotic cells with immunostaining against Hu showed that roughly 47% of the BrdU-labeled cells that persisted in the brain expressed this neuronal marker protein. Taken together, the results of this investigation demonstrate that at least half of the cells generated in the adult zebrafish brain develop into neurons and are likely to persist for the rest of the fish's life.

    14. Zupanc GK, Hinsch K and Gage FH (2005). Proliferation, migration, neuronal differentiation, and long-term survival of new cells in the adult zebrafish brain. J Comp Neurol 488: 290-319. School of Engineering and Science, International University Bremen, D-28725 Bremen, Germany. g.zupanc@iu-bremen.de. In contrast to mammals, fish exhibit an enormous potential to produce new cells in the adult brain. By labeling mitotically dividing cells with 5-bromo-2'-deoxyuridine (BrdU), we have characterized the development of these cells in the zebrafish (Danio rerio). Proliferation zones were located in specific regions of the olfactory bulb, dorsal telencephalon (including a region presumably homologous to the mammalian hippocampus), preoptic area, dorsal zone of the periventricular hypothalamus, optic tectum, torus longitudinalis, vagal lobe, parenchyma near the rhombencephalic ventricle, and in a region of the medulla oblongata lateral to the vagal motor nucleus, as well as in all three subdivisions of the cerebellum, the valvula cerebelli, the corpus cerebelli, and the lobus caudalis cerebelli. In the valvula cerebelli and the corpus cerebelli, the young cells migrated from their site of origin in the molecular layers to the corresponding granule cell layers. By contrast, in the lobus caudalis cerebelli and optic tectum, no indication of a migration of the newly generated cells over wider distances could be obtained. BrdU-labeled cells remained present in the brain over at least 292 days post-BrdU administration, indicating a long-term survival of a significant portion of the newly generated cells. The combination of BrdU immunohistochemistry with immunolabeling against the neural marker protein Hu, or with retrograde tracing, suggested a neuronal differentiation in a large portion of the young cells.

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