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PubMed2025

Formation of sensory maps: New tools reveal novel insights into neural development.

The development of functional neural circuits depends on the navigation of neurites (axons and dendrites) through spatially complex and molecularly diverse environments to their appropriate targets. How these processes maneuver through dense surroundings to reach their targets is a long-standing question in neuroscience. Studies of sensory systems have been especially enlightening for identifying cues that underlie connectivity due to their organization as stereotyped neural maps. Recent advances in imaging, connectomics, and genomics have profoundly deepened our understanding of these processes and uncovered new mechanisms regulating circuit development. In this review, we discuss studies of Drosophila sensory systems that provide new insights into axon and dendritic targeting, partner identification and selection, and subcellular refinement. We highlight related or divergent findings in other systems and provide an outlook for future studies.

Animals↗

PubMed2005

Neural development by transplanted human embryonal carcinoma stem cells expressing green fluorescent protein.

For many years, researchers have investigated the fate and potential of neuroectodermal cells during the development of the central nervous system. Although several key factors that regulate neural differentiation have been identified, much remains unknown about the molecular mechanisms that control the fate and specification of neural subtypes, especially in humans. Human embryonal carcinoma (EC) stem cells are valuable research tools for the study of neural development; however, existing in vitro experiments are limited to inducing the differentiation of EC cells into only a handful of cell types. In this study, we developed and characterized a novel EC cell line (termed TERA2.cl.SP12-GFP) that carries the reporter molecule, green fluorescent protein (GFP). We demonstrate that TERA2.cl.SP12-GFP stem cells and their differentiated neural derivatives constitutively express GFP in cells grown both in vitro and in vivo. Cellular differentiation does not appear to be affected by insertion of the transgene. We propose that TERA2.cl.SP12-GFP cells provide a valuable research tool to track the fate of cells subsequent to transplantation into alternative environments and that this approach may be particularly useful to investigate the differentiation of human neural tissues in response to local environmental signals.

Animals↗

PubMed2003

Anomalies in the developing neural and visceral head skeleton of the Australian lungfish, Neoceratodus forsteri.

Several anomalies occur in the developing neural and visceral head skeleton of young specimens of Neoceratodus forsteri that have been reared under laboratory conditions. These include anomalies of the basicranium and its derivatives, aberrations of the anterior mandible and hyoid apparatus, and abnormalities in the articulation of the jaws and the elements that produce them. Apart from the occasional absence of the basihyal, and failure of the quadrate processes to form, the anomalies are not deficiencies. Most involve malformations of parts of the neurocranium and visceral skeleton, inappropriate articulations or fusions between elements, disunity in structures that are normally fused and the appearance of supernumerary elements. The incidence of chondral anomalies, generally higher than aberrations that occur in the dermal skeleton in juvenile lungfish, ranges from 1-10% in laboratory reared individuals that have not been subjected to experimental interference. The anomalies differ from those found in many amphibian populations, in the field and in the laboratory, because they involve the cranium, and not the limbs, and the lungfish have not been exposed to the factors that cause anomalies in the amphibians. It is unlikely that the existence of those anomalies, if it is reflected in the wild population, places a selective pressure on the lungfish, because, in a normal season, less than 1% of the total number of eggs produced survive to be recruited into the adult population.

Animals↗

PubMed1997

Expression of B-type endothelin receptor gene during neural development.

Mutations of the B-type endothelin receptor (ETRB) gene have been found to cause defects in the development of enteric neurons, which resulted in aganglionic megacolon in rodents and humans. To determine the distribution of ETRB mRNA during neural development, mainly in the CNS, in situ hybridization was applied at various developmental stages of rat. ETRB gene was abundantly expressed prenatally in the ventricular and subventricular zones, as well as postnatally in the ependymal and subependymal cells. ETRB mRNA was also strongly detected prenatally in the dorsal root ganglia, as well as postnatally in the cerebellar Bergmann glial cells and epithelial cells of choroid plexus. Our data suggest that ETRB acts as a regulator in the differentiation, proliferation, or migration of neural cells during development.

Animals↗

PubMedDate not supplied

Networks of gene regulation, neural development and the evolution of general capabilities, such as human empathy.

A network of gene regulation organized in a hierarchical and combinatorial manner is crucially involved in the development of the neural network, and has to be considered one of the main substrates of genetic change in its evolution. Though qualitative features may emerge by way of the accumulation of rather unspecific quantitative changes, it is reasonable to assume that at least in some cases specific combinations of regulatory parts of the genome initiated new directions of evolution, leading to novel capabilities of the brain. These notions are applied, in this paper, to the evolution of the capability of cognition-based human empathy. It is suggested that it has evolved as a secondary effect of the evolution of strategic thought. Development of strategies depends on abstract representations of one's own possible future states in one's own brain to allow assessment of their emotional desirability, but also on the representation and emotional evaluation of possible states of others, allowing anticipation of their behaviour. This is best achieved if representations of others are connected to one's own emotional centres in a manner similar to self-representations. For this reason, the evolution of the human brain is assumed to have established representations with such linkages. No group selection is involved, because the quality of strategic thought affects the fitness of the individual. A secondary effect of this linkage is that both the actual states and the future perspectives of others elicit vicarious emotions, which may contribute to the motivations of altruistic behaviour.

Biological Evolution↗

PubMed1981

Analysis of mesenchyme in the developing hind limb of Rana pipiens larvae with implications for neural development.

Mesenchyme in the hind limbs of Rana pipiens tadpoles may serve as an important influence on the development of specific neural structures involved in limb innervation. Thus a histological quantification of mesenchyme was undertaken to identify landmark stages with respect to mesenchyme presence and neural events. Mesenchyme remained as a high percentage of the limb tissue until stage V (Taylor-Kollros stages, '46), after which it declined dramatically until its virtual absence after stage XI. The volume of mesenchyme, however, was greatest at stages VIII-IX. Periods of high and low mesenchyme content were correlated in time with potential limb involvement in regulating limb innervation and motor neuron loss from the lateral motor columns. This provides additional evidence for developmental relationships between events of the limb and neural tissues.

Animals↗

PubMed1997

Hematolymphopoietic and inflammatory cytokines in neural development.

It is now clear that cytokines traditionally viewed as immune modulators participate in inflammatory responses within the adult nervous system. However, in the developing nervous system hematolymphopoietic cytokines also play a role unrelated to neural-immune interactions. Instead, many of these factors subserve primary regulatory functions related both to the morphogenesis and to the cellular maturation of the central and peripheral nervous systems. This article focuses specifically on cytokine actions in neural development.

Animals↗

PubMed2004

BMP controls nitric oxide-mediated regulation of cell numbers in the developing neural tube.

Balanced cell proliferation and cell death determines neural precursor cell numbers in early stages of neural tube (NT) development. We have previously shown that nitric oxide (NO) regulates cell numbers locally in the NT of eight to 12 somite embryos. Here, we demonstrate that bone morphogenetic protein-4 (BMP-4), which is expressed in the ectoderm and dorsal NT at these developmental stages, induces programmed cell death (PCD) and promotes entry into the S-phase, via nitric oxide synthase (NOS) activity. These effects can be reversed by BMP-4 antagonists, such as follistatin and noggin, or by specific NOS inhibitors, resulting in low NO levels that facilitate mitosis and reduce PCD. Ectopic BMP-4 induction of PCD is restricted to the dorsal NT, whereas promotion of the S-phase is evenly observed across the dorsal-ventral (D-V) axis. Prolonged exposure to either BMP-4 or NOS inhibitors, which results in high or low NO levels, respectively, causes NT defects. The results presented here throw new light on the BMP signaling pathway. The local presence of BMP-4 helps to regulate cell numbers in the developing NT by a NO-mediated pathway, which is essential for normal NT formation.

Animals↗

PubMed1997

Evolutionarily conserved mechanisms regulating neural development: lessons from the development of Drosophila peripheral nervous systems.

Functions of genes regulating the development of Drosophila peripheral nervous systems are summarized herein. These genes can be classified into 6 groups: <1> prepattern genes, <2> proneural genes, <3> neurogenic genes, <4> neuronal precursor genes, <5> neuronal precursor type selector genes, and <6> cell-division and lineage genes. The mechanisms described herein provide excellent paradigms in the regulation of the development of other tissues in Drosophila, as well as in other organisms, including vertebrates. The roles of two different inhibitory mechanisms, i.e. Notch-signaling and Argos, in the development of Drosophila neural precursor cells are also discussed.

Animals↗

PubMed1990

Developing neural crest cells in culture: correlation of cytochrome oxidase activity with SSEA-1 and dopamine-beta-hydroxylase immunoreactivity.

This study examines possible changes in energy demands by developing neural crest cells in vitro using cytochrome oxidase (C.O.) histochemistry and immunohistochemical labeling of adrenergic (autonomic) cells and primary sensory neurons. Cytochrome oxidase is a key enzyme for oxidative metabolism and energy production, and it is used as a sensitive metabolic marker for neurons in the brain and dorsal root ganglia. In primary neural crest cell cultures, C.O. staining intensities differ among 4 distinct cellular populations (sensory neurons, adrenergic cells, pigment cells, and non-neuronal neural crest cells). At all stages, pigment cells exhibit extremely low C.O. staining. Neurons (both primary sensory and adrenergic cells) have higher C.O. activity than other cell types such as non-neuronal neural crest cells. This indicates that neurons have higher energy demands and presumably higher levels of functional activity than other cell types at least under the present culture conditions. All neurons in neural crest cell cultures elevate their energy demands during development, implying that energy metabolism and functional activity increase with neuronal maturation. At all stages, early determined sensory neurons exhibit more intense C.O. staining than late-developing sensory neurons. The difference in C.O. activity between the two populations of sensory neurons may be caused by different levels of functional activity due to their different time course of development. Tetrodotoxin (TTX) at 0.5-1 microM concentrations causes a decrease in the level of C.O. activity in the early determined sensory neurons, which may be correlated with a decrease in the functional activity of these neurons. Triple staining combining C.O. histochemistry with indirect immunofluorescence of antibodies against the stage specific embryonic antigen-1 (SSEA-1, which labels quail sensory neurons) and dopamine-beta-hydroxylase (DBH, which labels adrenergic cells) distinguish the level of C.O. activity between sensory neurons and autonomic cells. DBH+ cells exhibit relatively low C.O. staining. However, the C.O. activity among SSEA-1+ neurons varies from high to low levels. In general, SSEA-1+ sensory neurons are much more C.O. reactive than DBH+ autonomic cells. This suggests that developing sensory neurons in culture may have higher spontaneous and/or synaptic activity than autonomic neurons.

Animals↗

PubMed1987

Effect of repeated treatment with a gamma-aminobutyric acid receptor agonist on postnatal neural development in rats.

The effect of treatment with the gamma-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1- and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons.

Animals↗

PubMed1999

NeuroD regulates multiple functions in the developing neural retina in rodent.

The expression and function of the basic helix-loop-helix (bHLH) transcription factor NeuroD were studied in the developing neural retina in rodent. neuroD was expressed in areas of undetermined retinal cells as well as developing photoreceptors and amacrine interneurons. Expression was maintained in a subset of mature photoreceptors in the adult retina. Using both loss-of-function and gain-of-function approaches, NeuroD was found to play multiple roles in retinal development. (1) NeuroD was found to be a critical regulator of the neuron versus glial cell fate decision. Retinal explants derived from NeuroD-null mice demonstrated a three- to fourfold increase in Müller glia. Forced expression of neuroD in progenitors in rat using retroviruses hastened cell cycle withdrawal and blocked gliogenesis in vivo. (2) NeuroD appeared to regulate interneuron development, favouring amacrine over bipolar differentiation. Forced NeuroD expression resulted in an increase in amacrine interneurons and a decrease in bipolar interneurons. In the complementary experiment, retinae derived from NeuroD-null mice demonstrated a twofold increase in bipolar interneurons and a delay in amacrine differentiation. (3) NeuroD appeared to be essential for the survival of a subset of rod photoreceptors. In conclusion, these results implicate NeuroD in a variety of developmental functions including cell fate determination, differentiation and neuron survival.

Animals↗

PubMed1989

A triple-labeling method: HRP anterograde tract tracing combined with double immunofluorescent cell staining in developing neural tissue of the rat.

In this paper we describe a triple-labeling technique on a single section of developing nervous tissue. This labelling consists of a histochemical visualization of anterogradely transported horseradish peroxidase (HRP), within outgrowing rat corticospinal tract fibers and a double immunofluorescence labelling against glial fibrillary acidic protein (GFAP) and vimentin, being specific markers for astrocytes and their precursors, respectively. For the visualization of the anterogradely transported HRP, tetramethylbenzidine (TMB) is used as a chromogen with ammonium heptamolybdate (AHM) as a stabilizer followed by an additional diaminobenzidine-cobalt incubation to prevent washing out the HRP-TMB-AHM reaction product during the subsequent immunohistochemistry. Thereafter, double immunofluorescence labelling is carried out on the same section by adding simultaneously polyclonal anti-GFAP and monoclonal anti-vimentin which are then visualized with antisera conjugated with tetramethylrhodamine-isothiocynate (TRITC) and fluorescein-isothiocyanate (FITC) respectively as markers. Since the above mentioned visualization of the anterogradely transported HRP does not affect the immunofluorescence labelling, the methods enables within a single cryosection of developing neural tissue, the localization and identification of both outgrowing axons and their adjacent differentiating glial cells. In addition the method can easily be adapted for triple labelling of HRP tract tracing in conjunction with double immunofluorescence histochemistry of neurotransmitters.

Animals↗

PubMed2005

Regulation of neural development by glial cell line-derived neurotrophic factor family ligands.

Glial cell line-derived neurotrophic factor (GDNF) and its three relatives constitute a novel family of neurotrophic factors, the GDNF family ligands. These factors signal through a multicomponent receptor complex comprising a glycosylphosphatidylinositol-anchored cell surface molecule (GDNF family receptor (GFR) alpha) and RET tyrosine kinase, triggering the activation of multiple signaling pathways in responsive cells. Recent gene-targeting studies have demonstrated that GDNF family ligands are essential for the development of a diverse set of neuronal populations and we have now started to understand how these ligands uniquely regulate the formation and sculpting of the nervous system. Recent studies have also revealed interactions by multiple extracellular signals during neural development. The deciphering of GDNF family ligand signaling in neural cells promises to provide vital new insights into the development and pathology of the nervous system.

Animals↗

PubMed1998

Structural modification of fibroblast growth factor-binding heparan sulfate at a determinative stage of neural development.

Heparan sulfate (HS) glycosaminoglycans are essential modulators of fibroblast growth factor (FGF) activity and appear to act by coupling particular forms of FGF to appropriate FGF receptors. During neural development, one particular HS proteoglycan is able to rapidly switch its potentiating activity from FGF-2, as neural precursor cell proliferation occurs, to FGF-1, as neuronal differentiation occurs. Using various analytical techniques, including chemical and enzymatic cleavage, low pressure chromatography, and strong anion-exchange high performance liquid chromatography, we have analyzed the different HSs expressed during these crucial developmental stages. There are distinct alterations in patterns of 6-O-sulfation, total chain length, and the number of sulfated domains of the HS from the more mature embryonic brain. These changes correlate with a switch in the ability of the HS to potentiate the actions of FGF-1 in triggering cell differentiation. It thus appears that each HS pool is designed to function in the modulation of an intricate interaction with a specific growth factor and its cognate receptor, and suggests tightly regulated expression of specific, bioactive disaccharide sequences. The data can be used to construct a simple model of controlled variations in HS chain structure which have functional consequences at a crucial stage of neuronal maturation.

Animals↗

PubMed2005

Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways.

Bmi-1 is required for the post-natal maintenance of stem cells in multiple tissues including the central nervous system (CNS) and peripheral nervous system (PNS). Deletion of Ink4a or Arf from Bmi-1(-/-) mice partially rescued stem cell self-renewal and stem cell frequency in the CNS and PNS, as well as forebrain proliferation and gut neurogenesis. Arf deficiency, but not Ink4a deficiency, partially rescued cerebellum development, demonstrating regional differences in the sensitivity of progenitors to p16Ink4a and p19Arf. Deletion of both Ink4a and Arf did not affect the growth or survival of Bmi-1(-/-) mice or completely rescue neural development. Bmi-1 thus prevents the premature senescence of neural stem cells by repressing Ink4a and Arf, but additional pathways must also function downstream of Bmi-1.

Animals↗

PubMed1987

Changes in neural cell adhesion molecule (NCAM) structure during vertebrate neural development.

Changes in carbohydrate and polypeptide form of the neural cell adhesion molecule (NCAM) have been documented during the development of central nervous system tissue in both chicken and frog. The carbohydrate variations reflect a high and low content of polysialic acid, and for the two vertebrates examined the expression of these forms is similar. At very early stages of neural development NCAM with a low content of polysialic acid is present, during histogenesis of the central nervous system NCAM with a high content of polysialic acid dominates, and there is a gradual return to NCAM with a low content of polysialic acid as the animals approach maturity. In contrast, the order of expression of the major NCAM polypeptide forms is different in the chicken and frog. These findings suggest that changes in sialic acid are a fundamental aspect of the function of NCAM in development, whereas NCAM polypeptide differences may affect events associated with a particular vertebrate. Studies have demonstrated that a decreased sialic acid content enhances the adhesion properties of NCAM. On this basis, we propose that NCAM with a low content of polysialic acid functions both to maintain integrity of neuroepithelium during morphogenesis of the early embryo and to stabilize differentiated structures in the adult, while the decreased adhesive function of NCAM with a high content of polysialic acid provides more plasticity in cell interactions during cell migration, axon outgrowth, and formation of neural circuits.

Animals↗

PubMed2004

Neural development and the ontogeny of central nervous system tumors.

Recent evidence argues that the oncogenesis and growth of CNS tumors occurs through dysregulated molecular and cellular mechanisms of neural development. New insights have emerged that have had a significant impact on both research and treatment of these cancers.

Journal Article↗