Early Neurogenesis (early + neurogenesi)

Distribution by Scientific Domains

Selected Abstracts

Genetic analysis of early neurogenesis: Dedicated to the scientific contributions of Jose A. Campos-Ortega (1940,2004),

Volker Hartenstein
Abstract Jose Campos-Ortega stands out as one of the pioneers of developmental-genetic studies of early neurogenesis. He also liked to reflect about the history of science: how one discovery leads to the next, and what role individuals play in the progress of science. He had indeed started to work on a book describing the history of developmental genetics during the last year of his life. His goal in this book was to "explain how developmental genetics originated, how it transformed developmental biology and, while doing so, how it contributed to achieve the biological synthesis." In the following, I would like to reflect on the origin and growth of the field Campos-Ortega contributed so much. In doing so, it is of particular interest to consider his scientific roots, and the manner in which he entered the stage of developmental genetics. I believe that Campos-Ortega's unusual scientific background influenced in an important manner the way in which he shaped the study of early neurogenesis. Developmental Dynamics 235:2003,2008, 2006. 2006 Wiley-Liss, Inc. [source]

The essential haematopoietic transcription factor Scl is also critical for neuronal development

Cara K. Bradley
Abstract The basic helix-loop-helix (bHLH) transcription factor Scl displays tissue-restricted expression and is critical for the establishment of the haematopoietic system; loss of Scl results in embryonic death due to absolute anaemia. Scl is also expressed in neurons of the mouse diencephalon, mesencephalon and metencephalon; however, its requirement in those sites remains to be determined. Here we report conditional deletion of Scl in neuronal precursor cells using the Cre/LoxP system. Neuronal-Scl deleted mice died prematurely, were growth retarded and exhibited an altered motor phenotype characterized by hyperactivity and circling. Moreover, ablation of Scl in the nervous system affected brain morphology with abnormal neuronal development in brain regions known to express Scl under normal circumstances; there was an almost complete absence of Scl-null neurons in the hindbrain and partial loss of Scl-null neurons in the thalamus and midbrain from early neurogenesis onwards. Our results demonstrate a crucial role for Scl in the development of Scl-expressing neurons, including ,-aminobutyric acid (GABA)ergic interneurons. Our study represents one of the first demonstrations of functional overlap of a single bHLH protein that regulates neural and haematopoietic cell development. This finding underlines Scl's critical function in cell fate determination of mesodermal as well as neuroectodermal tissues. [source]

Dynamic expression of de novo DNA methyltransferases Dnmt3a and Dnmt3b in the central nervous system

Jian Feng
Abstract To explore the role of DNA methylation in the brain, we examined the expression pattern of de novo DNA methyltransferases Dnmt3a and Dnmt3b in the mouse central nervous system (CNS). By comparing the levels of Dnmt3a and Dnmt3b mRNAs and proteins in the CNS, we showed that Dnmt3b is detected within a narrow window during early neurogenesis, whereas Dnmt3a is present in both embryonic and postnatal CNS tissues. To determine the precise pattern of Dnmt3a and Dnmt3b gene expression, we carried out X-gal histochemistry in transgenic mice in which the lacZ marker gene is knocked into the endogenous Dnmt3a or Dnmt3b gene locus (Okano et al. [1999] Cell 99:247,257). In Dnmt3b - lacZ transgenic mice, X-gal-positive cells are dispersed across the ventricular zone of the CNS between embryonic days (E) 10.5 and 13.5 but become virtually undetectable in the CNS after E15.5. In Dnmt3a - lacZ mice, X-gal signal is initially observed primarily in neural precursor cells within the ventricular and subventricular zones between E10.5 and E17.5. However, from the newborn stage to adulthood, Dnmt3a X-gal signal was detected predominantly in postmitotic CNS neurons across all the regions examined, including olfactory bulb, cortex, hippocampus, striatum, and cerebellum. Furthermore, Dnmt3a signals in CNS neurons increase during the first 3 weeks of postnatal development and then decline to a relatively low level in adulthood, suggesting that Dnmt3a may be of critical importance for CNS maturation. Immunocytochemistry experiments confirmed that Dnmt3a protein is strongly expressed in neural precursor cells, postmitotic CNS neurons, and oligodendrocytes. In contrast, glial fibrillary acidic protein-positive astrocytes exhibit relatively weak or no Dnmt3a immunoreactivity in vitro and in vivo. Our data suggest that whereas Dnmt3b may be important for the early phase of neurogenesis, Dnmt3a likely plays a dual role in regulating neurogenesis prenatally and CNS maturation and function postnatally. 2005 Wiley-Liss, Inc. [source]

Emanuel Miller Lecture: Early onset depressions , meanings, mechanisms and processes

Ian M. Goodyer
Background:, Depressive syndromes in children and adolescents constitute a serious group of mental disorders with considerable risk for recurrence. A more precise understanding of aetiology is necessary to improve treatment and management. Methods:, Three neuroactive agents are purported to be involved in the aetiology of these disorders: serotonin, brain-derived neurotrophic factor and cortisol. A literature review was conducted to determine their contributions to the emergence of unipolar depressions in the adolescent years. Results:, Serotonin, brain-derived neurotrophic factor and cortisol may operate in concert within two distinct functional frameworks: atypical early epigenesis arising in the first few years of life and resulting in the formation of a vulnerable neuronal network involving in particular the amygdala and ventral prefrontal cortex. Individuals with this vulnerability are likely to show impaired mood regulation when faced with environmental demands during adolescence and over the subsequent decades; and acquired neuroendangerment, a pathological brain process leading to reduced synaptic plasticity, in particular in the hippocampus and perhaps the nucleus accumbens and ventral tegmentum. This may result in motivational, cognitive and behavioural deficits at any point in the lifespan most apparent at times of environmental demand. Conclusions:, The characteristics, course and outcome of a depressive episode may depend on the extent of the involvement of both atypical early neurogenesis and acquired neuroendangerment. [source]