The Role of Growth Factors in the Control of Neurogenesis

Rohrer, Hermann

doi:10.1111/j.1460-9568.1990.tb00013.x

Cited by 73 publications

(16 citation statements)

References 185 publications

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“…It will allow a quantitative characterization of the cells of each of these populations as they move through the successive phases of the proliferative cycle and exit from the cycle. Considered in this light, the present analysis and others to come in this series relate to broader current themes in developmental neurobiology, which include the determinants and behaviors of separate neuronal lineages (Cepko, 1988;McConnell and Kaznowski, 199 l), the operation of clonal mechanics in cortical histogenesis (Rakic, 1988;Austin and Cepko, 1990;Crandall and Herrup, 1990;Cepko, 1990, 1992), and the molecular mechanisms, including both the effect of growth factors (Cattaneo and McKay, 1990;Rivera and Greenberg, 1990;Rohrer, 1990) and intrinsic genetic operators (Murray and Kirschner, 1989, 199 l), that regulate the cell cycle itself.…”

Section: Cytogenesismentioning

confidence: 97%

Cell cycle parameters and patterns of nuclear movement in the neocortical proliferative zone of the fetal mouse

1993

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Cytogenesis is the critical determinant of the total number of neurons that contribute to the formation of the cerebral cortex and the rate at which the cells are produced. Two distinct cell populations constitute the proliferative population, a pseudostratified ventricular epithelium (PVE) lying within the ventricular zone (VZ) at the margin of the ventricle, and a secondary proliferative population that is intermixed with the PVE within the VZ but also is distributed through the overlying subventricular and intermediate zones of the cerebral wall. The present analysis, based upon cumulative S-phase labeling of the proliferative cells with 5-bromo-2′-deoxyuridine, is principally concerned with the PVE of the gestational-day-14 (E14) murine cerebral wall. It has immediate but also more far reaching general objectives. The most immediate objective, essential to the design and interpretation of later experiments, is to provide estimates of critical parameters of cytogenesis for the PVE. The growth fraction is virtually 100%. The lengths of the overall cell cycle, S-, G2+M-m, and G1-phases are 15.1 hr, 3.8 hr, 2 hr, and 9.3 hr, respectively. The PVE is homogeneous with respect to cell cycle length. For methodological considerations, these estimates are more accurate than estimates of the same parameters obtained in earlier analyses based upon S-phase labeling with tritiated thymidine. It is particularly with respect to a shorter length of S-phase determined here that the present values are different from those obtained with thymidine. At a more innovative level, the temporal and spatial resolution of nuclear movement made possible by the methods developed here will allow, in a way not previously attempted, a fine-grained tracking of nuclear movement as cells execute the successive stages of the cell cycle or exit the cycle subsequent to mitosis. Such observations are pertinent to our understanding of the regulatory mechanisms of neocortical histogenesis and the cell biological mechanisms that govern the proliferative cycle of the ventricular epithelium itself. It is known that the velocity of nuclear movement in the PVE is maximum in G2 (fourfold increase from S- phase) and minimum in M and early G1.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Cytogenesismentioning

confidence: 97%

Cell cycle parameters and patterns of nuclear movement in the neocortical proliferative zone of the fetal mouse

1993

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“…NGF is secreted by nerve targets and stimulates sympathetic neurite outgrowth in vitro (Coughlin et al, 1977;Carnpenot, 1982;Davies et al, 1987;Levi-Montalcini et al, 1990;Matsuoka et al, 1991). A number of other factors have also been demonstrated to support survival and induce neurite outgrowth (Gospodarowicz 1989;Rohrer 1990;TessierLavigne and Placzek, 1991).…”

Section: Introductionmentioning

confidence: 94%

Lymphoid tissues induce NGF‐dependent and NGF‐independent neurite outgrowth from rat superior cervical ganglia explants in culture

Kannan

Stead

Goldsmith

et al. 1994

J of Neuroscience Research

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Induction of neurite outgrowth from superior cervical ganglia (SCG) by rat lymphoid tissues was studied using a tissue culture model. Neonatal rat SCG were cultured with 6-12-week-old rat thymus, spleen, or mesenteric lymph node (MLN) explants in a Matrigel layer, in defined culture medium without exogenous nerve growth factor (NGF). SCG were also co-cultured with neonatal rat heart (as positive control) or spinal cord (SC; as negative control). To determine whether inflammation affects the ability of lymphoid tissues to induce neurite outgrowth, we also examined MLN at various times after infecting rats with Nip-postrongylus brasiliensis (Nb-MLN). In one series of experiments, a single lymphoid tissue explant was surrounded by four SCG at a distance of 1 mm. The extent of neurite outgrowth was determined by counting the number of neurites 0.5 mm away from each ganglion at several time points. Adult thymus and, to a lesser extent, spleen had strong stimulatory effects on neurite outgrowth from SCG after 12 hr or more in culture. For thymus tissue, this was similar to the positive control heart explants. MLN from normal rats had minimal effect on neurite outgrowth; however, Nb-MLN showed a time-dependent enhancement of the neurite outgrowth, maximal at 3 weeks after infection. The relative efficacy of neurite outgrowth induction (heart > or = thymus > or = Nb-MLN > or spleen > or = MLN > or = SC) was confirmed in a second series of experiments where one SCG was surrounded by three different tissue explants. We then examined the role of 2.5S NGF, a well-known trophic factor for sympathetic nerves, in the lymphoid tissue-induced neurite outgrowth. Anti-NGF treatment of co-cultures of SCG and heart almost completely blocked the neurite outgrowth. Anti-NGF also significantly inhibited thymus- and spleen-induced neurite outgrowth, but not as effectively as heart-induced neuritogenesis (93, 80, and 77% inhibition at 24 hr; 86, 70, and 68% inhibition at 48 hr for heart, thymus, and spleen, respectively). On the other hand, anti-NGF inhibited only 8% of neurite outgrowth induced by 3-week post-infection Nb-MLN at 24 hr, and 41% at 48 hr. These data show that several adult rat lymphoid tissues exert neurotrophic/tropic effects. The predominant growth factor in thymus and spleen is NGF, while Nb-MLN produces factor(s) which is (are) immunologically distinguishable from NGF.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…The chicken embryo in ovo has been widely used as a model to study the effect of various growth factors [16,17], and drugs including ethanol [11,12,18,19], caffeine [20], nicotine [12,21], and narcotics [21,22] on various organ systems. Additionally, the chick model has been utilized to study neurogenesis [23], angiogenesis [24], oncogenic transformation [14,15] and bacterial pathogenesis and toxicity [25 -27]. Because glucose is an essential component of embryonic development and metabolism, the expression of glucose transporters during embryogenesis may be relevant to studies examining the effect of drugs, growth factors, or chemicals on embryonic metabolism and/or structure.…”

mentioning

confidence: 99%

Differential expression of glucose transporters during chick embryogenesis

Carver¹,

Shibley²,

Pennington

et al. 2001

CMLS, Cell. Mol. Life Sci.

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The patterns of Glut1 and Glut3 glucose transporter protein and mRNA expression were assessed during embryogenesis of chicken brain and skeletal muscle, Glut4 protein levels were also evaluated in skeletal muscle and heart, and Glut1 was examined in the developing heart and liver. Glut1 protein expression was detectable throughout brain ontogeny but was highest during early development. Glut1 mRNA levels in the brain remained very high throughout development. Glut3 protein was highest very early and very late and mRNA was highest during the last half of development. In embryonic skeletal muscle, the levels of Glut1 and Glut3 proteins and mRNA were highest very early, and declined severely by mid-development. Glut1 protein and mRNA in the heart also peaked early and then decreased steadily. Although Glut1 mRNA levels were consistently high in the embryonic liver, Glut1 protein expression was not detected. These results suggest that (1) Glut1 is developmentally regulated in chick brain, skeletal muscle, and heart, (2) Glut1 mRNA is present in liver but does not appear to be translated, (3) Glut3 in brain increases developmentally but is virtually absent in muscle, and (4) Glut4 protein and mRNA appear to be absent from chick heart and skeletal muscle.

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The Role of Growth Factors in the Control of Neurogenesis

Cited by 73 publications

References 185 publications

Cell cycle parameters and patterns of nuclear movement in the neocortical proliferative zone of the fetal mouse

Cell cycle parameters and patterns of nuclear movement in the neocortical proliferative zone of the fetal mouse

Lymphoid tissues induce NGF‐dependent and NGF‐independent neurite outgrowth from rat superior cervical ganglia explants in culture

Differential expression of glucose transporters during chick embryogenesis

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