Nervous system

About: Nervous system is a research topic. Over the lifetime, 16729 publications have been published within this topic receiving 847181 citations.

Ryk-mediated Wnt repulsion regulates posterior-directed growth of corticospinal tract

Abstract: Guidance cues along the longitudinal axis of the CNS are poorly understood. Wnt proteins attract ascending somatosensory axons to project from the spinal cord to the brain. Here we show that Wnt proteins repel corticospinal tract (CST) axons in the opposite direction. Several Wnt genes were found to be expressed in the mouse spinal cord gray matter, cupping the dorsal funiculus, in an anterior-to-posterior decreasing gradient along the cervical and thoracic cord. Wnts repelled CST axons in collagen gel assays through a conserved high-affinity receptor, Ryk, which is expressed in CST axons. Neonatal spinal cord secretes diffusible repellent(s) in an anterior-posterior graded fashion, with anterior cord being stronger, and the repulsive activity was blocked by antibodies to Ryk (anti-Ryk). Intrathecal injection of anti-Ryk blocked the posterior growth of CST axons. Therefore, Wnt proteins may have a general role in anterior-posterior guidance of multiple classes of axons.

Planarian homologs of netrin and netrin receptor are required for proper regeneration of the central nervous system and the maintenance of nervous system architecture

Abstract: Conserved axon guidance mechanisms are essential for proper wiring of the nervous system during embryogenesis; however, the functions of these cues in adults and during regeneration remain poorly understood. Because freshwater planarians can regenerate a functional central nervous system (CNS) from almost any portion of their body, they are useful models in which to study the roles of guidance cues during neural regeneration. Here, we characterize two netrin homologs and one netrin receptor family member from Schmidtea mediterranea . RNAi analyses indicate that Smed-netR ( netrin receptor ) and Smed-netrin2 are required for proper CNS regeneration and that Smed-netR may mediate the response to Smed-netrin2 . Remarkably, Smed-netR and Smed-netrin2 are also required in intact planarians to maintain the proper patterning of the CNS. These results suggest a crucial role for guidance cues, not only in CNS regeneration but also in maintenance of neural architecture.

Expression of FGF receptor gene in rat development

Abstract: We examined the expression of FGF-receptor (FGF-R) mRNA during rat development with in situ hybridization histochemistry. Embryonic tissues (E9, E12, E14, E17) and postnatal neural tissues (P1, P7, P14, adult) were examined. We detected significant levels of FGF-R mRNA in various tissues at different developmental stages. As postulated by previous studies using other methods, FGF-R gene expression was observed primarily in mesoderm- and neuroectoderm-derived tissues. In the nervous system, the pattern of gene expression was developmentally regulated; in embryos, FGF-R mRNA was mainly detected in the ependymal layer of the central nervous system (CNS). Postnatally, FGF-R transcripts were observed in specific neuronal populations, such as hippocampal neurons. FGF-R mRNA was also found in sensory systems such as trigeminal and dorsal root ganglia in late stage embryos; however, FGF-R mRNA decreased in the postnatal period. FGF-R mRNA expression was modulated in the developing retina: FGF-R messages were observed in the pigment epithelium and neuroblast layer at embryonic stages; in the postnatal period, they were found in the ganglion cell and inner granular layer. In non-neuronal embryonic tissues, a wide variety of organs expressed FGF-R message. Particularly, the prevertebral column, bone, kidney and skin showed high levels of expression. These observations reinforce the idea that FGF exerts effects on the development of various tissues.

New Neuronal Growth Factors

Abstract: The complexity and remarkable specificity found in the nervous system chal­ lenge the investigator to identify molecular mechanisms guiding neuronal development. Cell-cell interactions mediated by diffusible substances have frequently been suggested to play an important role. Studies on naturally occurring cell death in the nervous system provided early evidence for such interactions by demonstrating that neuronal survival beyond a critical period in development requires interaction between the neurons and the postsynaptic target tissue (for a review see Oppenheim 1981). The discovery of Nerve Growth Factor (NGF) raised the possibility that neuronal development, includ­ ing target-dependent neuronal survival, might be mediated by diffusible mole­ cules. NGF can be isolated as a 140,000 dalton protein complex (7S NGF) of heterologous subunits or as a 26,500 dalton component (beta-NGF) containing two identical polypeptide chains. Experiments in vivo indicate that NGF can reverse naturally occurring as well as experimentally induced cell death in sympathetic and sensory neurons; moreover, anti-NGF antibodies in vivo can block the development of the sympathetic nervous system (for reviews see Thoenen & Barde 1980, Hamburger et al 1981, Levi-Monta1cini 1982). That NGF might also influence the choice of targets contacted by neurons is suggested by studies in cell culture showing that NGF can change the direction of neuritic growth (Gundersen & Barrett 1979) and can help shape the neuritic tree maintained by the neuron (Campenot 1982). Naturally occurring cell death has been documented for almost every popula­ tion of vertebrate neurons studied (Oppenheim 1981), and every neuron is faced with the problem of finding appropriate target cells. Only sensory and sympathetic neurons, however, have been convincingly shown to depend on

Complete ablation of the neurotrophin receptor p75NTR causes defects both in the nervous and the vascular system.

Abstract: We identified a protein isoform of the common neurotrophin receptor p75NTR that arises from alternative splicing of exon III in the p75NTR locus. Because this protein is left intact in the previously described p75NTR mutant mouse line1, we generated a new p75NTR mutant allele. Mice homozygous for this mutation lack both protein isoforms, display severe nervous system defects and reveal a previously unknown role of p75NTR in the formation of blood vessels.