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Radial Migration (radial + migration)

Distribution by Scientific Domains
Life Sciences85%

Selected Abstracts

Radial migration of developing microglial cells in quail retina: A confocal microscopy study

GLIA, Issue 3 2004
Ana Sánchez-López
Abstract Microglial cells spread within the nervous system by tangential and radial migration. The cellular mechanism of tangential migration of microglia has been described in the quail retina but the mechanism of their radial migration has not been studied. In this work, we clarify some aspects of this mechanism by analyzing morphological features of microglial cells at different steps of their radial migration in the quail retina. Microglial cells migrate in the vitreal half of the retina by successive jumps from the vitreal border to progressively more scleral levels located at the vitreal border, intermediate regions, and scleral border of the inner plexiform layer (IPL). The cellular mechanism used for each jump consists of the emission of a leading thin radial process that ramifies at a more scleral level before retraction of the rear of the cell. Hence, radial migration and ramification of microglial cells are simultaneous events. Once at the scleral border of the IPL, microglial cells migrate through the inner nuclear layer to the outer plexiform layer by another mechanism: they retract cell processes, become round, and squeeze through neuronal bodies. Microglial cells use radial processes of s-laminin-expressing Müller cells as substratum for radial migration. Levels where microglial cells stop and ramify at each jump are always interfaces between retinal strata with strong tenascin immunostaining and strata showing weak or no tenascin immunoreactivity. When microglial cell radial migration ends, tenascin immunostaining is no longer present in the retina. These findings suggest that tenascin plays a role in the stopping and ramification of radially migrating microglial cells. © 2004 Wiley-Liss, Inc. [source]

Emerging topics in Reelin function

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2010
Eckart Förster
Abstract Reelin signalling in the early developing cortex regulates radial migration of cortical neurons. Later in development, Reelin promotes maturation of dendrites and dendritic spines. Finally, in the mature brain, it is involved in modulating synaptic function. In recent years, efforts to identify downstream signalling events induced by binding of Reelin to lipoprotein receptors led to the characterization of novel components of the Reelin signalling cascade. In the present review, we first address distinct functions of the Reelin receptors Apoer2 and Vldlr in cortical layer formation, followed by a discussion on the recently identified downstream effector molecule n-cofilin, involved in regulating actin cytoskeletal dynamics required for coordinated neuronal migration. Next, we discuss possible functions of the recently identified Reelin,Notch signalling crosstalk, and new aspects of the role of Reelin in the formation of the dentate radial glial scaffold. Finally, progress in characterizing the function of Reelin in modulating synaptic function in the adult brain is summarized. The present review has been inspired by a session entitled ,Functions of Reelin in the developing and adult hippocampus', held at the Spring Hippocampal Research Conference in Verona/Italy, June 2009. [source]

Transient maternal hypothyroxinemia at onset of corticogenesis alters tangential migration of medial ganglionic eminence-derived neurons

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2005
Estela Cuevas
Abstract Correct positioning of cortical neurons during development depends on the radial migration of the projection neurons and on the coordinated tangential and radial migrations of the subcortically generated interneurons. As previously shown, a transient and moderate maternal deficiency in thyroxin during early corticogenesis alters the radial migration of projection neurons. To determine if a similar effect might also affect tangential migration of medial ganglionic eminence (MGE)-derived neurons at the origin of cortical interneurons, explants of MGE from green fluorescent protein (GFP)-transgenic embryos were implanted into flat cortical mounts from wild-type embryos. The distances covered and the preferential migration (medially) of GFP-MGE neurons from embryos of hypothyroxinemic dams are not affected in their tangential migration into wild-type control cortices. In contrast, when GFP-MGE neurons from embryos of control or hypothyroxinemic dams migrate within cortices from embryos of hypothyroxinemic dams, the GFP-MGE-derived neurons lose their preferential direction of migration, although they still migrate for long distances throughout the cortex. Our results show that maternal hypothyroxinemia alters the tangential migration of GFP-MGE-derived neurons in the neocortex of the progeny and suggest that this alteration is not derived from the migratory neurons themselves but through undefined short- and long-range cues responsible for the guidance of their migration. [source]

Radial migration of developing microglial cells in quail retina: A confocal microscopy study

GLIA, Issue 3 2004
Ana Sánchez-López
Abstract Microglial cells spread within the nervous system by tangential and radial migration. The cellular mechanism of tangential migration of microglia has been described in the quail retina but the mechanism of their radial migration has not been studied. In this work, we clarify some aspects of this mechanism by analyzing morphological features of microglial cells at different steps of their radial migration in the quail retina. Microglial cells migrate in the vitreal half of the retina by successive jumps from the vitreal border to progressively more scleral levels located at the vitreal border, intermediate regions, and scleral border of the inner plexiform layer (IPL). The cellular mechanism used for each jump consists of the emission of a leading thin radial process that ramifies at a more scleral level before retraction of the rear of the cell. Hence, radial migration and ramification of microglial cells are simultaneous events. Once at the scleral border of the IPL, microglial cells migrate through the inner nuclear layer to the outer plexiform layer by another mechanism: they retract cell processes, become round, and squeeze through neuronal bodies. Microglial cells use radial processes of s-laminin-expressing Müller cells as substratum for radial migration. Levels where microglial cells stop and ramify at each jump are always interfaces between retinal strata with strong tenascin immunostaining and strata showing weak or no tenascin immunoreactivity. When microglial cell radial migration ends, tenascin immunostaining is no longer present in the retina. These findings suggest that tenascin plays a role in the stopping and ramification of radially migrating microglial cells. © 2004 Wiley-Liss, Inc. [source]

Revisiting two local constraints of the Galactic chemical evolution

MONTHLY NOTICES OF THE ROYAL ASTRONOMICAL SOCIETY, Issue 4 2006
M. Haywood
ABSTRACT I review the uncertainties in two observational local constraints of the Galactic disc chemical evolution: the metallicity distribution of long-lived dwarfs and the age,metallicity relation. Analysing most recent data, it is shown first that the observed metallicity distribution at solar galactocentric radius, designed with standard methods, is more fit to a closed-box model than to the infall metallicity distribution. We argue that this is due to the specific contribution of the thick-disc population, which has been overlooked both in the derivation of the observed metallicity distribution and in the standard chemical evolution models. Although this agreement disqualifies the metallicity distribution as the best supportive (indirect) evidence for infall, we argue that the evolution must be more complex than described by either the closed-box or the standard infall models. It is then shown that recent determinations of the age,metallicity distribution (AMD) from large Strömgren photometric surveys are dominated by noise resulting from systematic biases in metallicities and effective temperatures. These biases are evaluated and a new AMD is obtained, where particularities of the previous determinations are phased out. The new age,metallicity relation shows a mean increase limited to about a factor of 2 in Z over the disc age. It is shown that below 3 Gyr, the dispersion in metallicity is about 0.1 dex, which, given the observational uncertainties in the derived metallicities, is compatible with the small cosmic dispersion measured on the interstellar medium and meteoritic pre-solar dust grains. A population that is progressively older and more metal rich arises at a metallicity greater than that of the Hyades, to reach [Fe/H],+0.5 dex at ages greater than 5 Gyr. We suggest that this is best explained by radial migration. A symmetrical widening of the metallicity interval towards lower values is seen at about the same age, which is attributed to a similar cause. Finally, the new derived ages are sufficiently consistent that an age,metallicity relation within the thick disc is confirmed. These new features altogether draw a picture of the chemical evolution in the solar neighbourhood where dynamical effects and complexity in the AMD dominate, rather than a generalized high dispersion at all ages. [source]

Distinct roles of neuropilin 1 signaling for radial and tangential extension of callosal axons

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2009
Yumiko Hatanaka
Abstract Cortical excitatory neurons migrate from their origin in the ventricular zone (VZ) toward the pial surface. During migration, these neurons exhibit a stellate shape in the intermediate zone (IZ), transform into bipolar cells, and then initiate radial migration, extending a trailing process, which may lead to an axon. Here we examined the role of neuropilin 1 (NRP1) in these developmental events. Both NRP1 mRNA and protein were highly expressed in the IZ, where stellate-shaped cells were located. DiI labeling experiments showed that neuronal migration occurred normally in Nrp1 mutant mice up to embryonic day (E) 14.5, the latest day to which the mutant survives, with only subtle axonal defasciculation. However, interference with Nrp1 signaling at a later stage caused pathfinding errors: when a dominant negative form of Nrp1 was electroporated into the cortical VZ cells at E12.5 or E15.5 and examined perinatally, guidance errors were found in tangential axonal extension toward the midline. In contrast, no significant effect was noted on the migration of cortical excitatory neurons. These findings indicate that NRP1 plays an important role in the guidance of callosal axons originating from cortical excitatory neurons but does not support a role in their migration. Moreover, insofar as radial axonal extension within the cortical plate was unaffected, the present findings imply that molecular mechanisms for the axonal extension of excitatory neurons within the cortical plate are distinct from those in the white matter. J. Comp. Neurol. 514:215,225, 2009. © 2009 Wiley-Liss, Inc. [source]

Transient maternal hypothyroxinemia at onset of corticogenesis alters tangential migration of medial ganglionic eminence-derived neurons

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2005
Estela Cuevas
Abstract Correct positioning of cortical neurons during development depends on the radial migration of the projection neurons and on the coordinated tangential and radial migrations of the subcortically generated interneurons. As previously shown, a transient and moderate maternal deficiency in thyroxin during early corticogenesis alters the radial migration of projection neurons. To determine if a similar effect might also affect tangential migration of medial ganglionic eminence (MGE)-derived neurons at the origin of cortical interneurons, explants of MGE from green fluorescent protein (GFP)-transgenic embryos were implanted into flat cortical mounts from wild-type embryos. The distances covered and the preferential migration (medially) of GFP-MGE neurons from embryos of hypothyroxinemic dams are not affected in their tangential migration into wild-type control cortices. In contrast, when GFP-MGE neurons from embryos of control or hypothyroxinemic dams migrate within cortices from embryos of hypothyroxinemic dams, the GFP-MGE-derived neurons lose their preferential direction of migration, although they still migrate for long distances throughout the cortex. Our results show that maternal hypothyroxinemia alters the tangential migration of GFP-MGE-derived neurons in the neocortex of the progeny and suggest that this alteration is not derived from the migratory neurons themselves but through undefined short- and long-range cues responsible for the guidance of their migration. [source]