JOURNAL OF NEUROIMAGING, Issue 4 2007
Pin Lin Kei MBChB
ABSTRACT Decompression sickness (DCS) typically causes changes in the white matter of the spinal cord on MR imaging. We present a case of DCS in a scuba diver with dorsal white matter lesions typical of venous infarction. In addition, some central gray matter involvement was noted. Characteristic features of venous spinal cord infarction can be recognized on MR imaging in DCS but may be more extensive in severe cases. [source]

Comparison of Localization of the Neurokinin 1 Receptor and Nitric Oxide Synthase with Calbindin D Labelling in the Rat Spinal Cord

ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 3 2000
M. Nazli
Summary A comparison of the localization of the neurokinin 1 (NK1) receptor and nitric oxide synthase with calbindin D labelling in the lumbar spinal cord was carried out in the rat using immunocytochemistry. Considerable regional variations were observed. Application of the antibody to calbindin D resulted in dense staining in laminae I and II and light staining in the other laminae. Occasional scattered cells were seen in the deep laminae and in the lamina X, the ventral horn and the lateral spinal nucleus. The results indicate that neurones expressing calbindin D, NK1 receptor and NOS are three separate populations in the dorsal horn of the lumbar spinal cord. [source]

Cavernous Malformations of the Brain and Spinal Cord

ANZ JOURNAL OF SURGERY, Issue 12 2009
FRACS, John D. Laidlaw MB BS
No abstract is available for this article. [source]

Chronic Pain after Spinal Cord Injury: Results of a Long-Term Study

PAIN MEDICINE, Issue 7 2010
Ehsan Modirian MD
Abstract Objective., Chronic pain after spinal cord injury (SCI) is a common and considerable complication and may continue for a long time. Design., During a 2-year survey, 13.9 ± 3.0 years after injury, a total of 1,295 war-related spinal cord injury survivors were thoroughly examined by physical and rehabilitation specialists and all relevant data, consisting of type and site of pain as well as exacerbating or palliative factors, were recorded. Patients., The mean age of the survivors was 35.9 ± 7.2; 98.5% were male and 1.5% were female. The level of injury was cervical in 9.3%, thoracic in 67%, and lumbosacral in 23.7%, with 8.1% tetraplegic and 89.1% paraplegic. About 89.8% had complete spinal cord injuries and 10.2% had incomplete spinal cord injuries, based on sensory and motor testing. Results., Spinal cord related pain was reported in 64.9% of the subjects; 8.8% reported a history of pain but had no complaint at the time of examination, and 26.3% had never suffered from any pain. Patients suffering from lumbar spinal cord injury reported the highest percent of pain perception, with pain detected in 83.5% of these patients. Common sites of reported pain were the distal lower extremities (46.5%), proximal lower extremities (40.9%), pelvic girdle (24.5%), and upper limbs (5.7%). Conclusion., Spinal cord injury-related pain interferes with daily activities of patients and significantly influences their quality of life. [source]

Abnormal substance P release from the spinal cord following injury to primary sensory neurons

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2000
Marzia Malcangio
Abstract The neuropeptide substance P (SP) modulates nociceptive transmission within the spinal cord. Normally, SP is uniquely contained in a subpopulation of small-calibre axons (A,- and C-fibres) within primary afferent nerve. However, it has been shown that after nerve transection, besides being downregulated in small axons, SP is expressed de novo in large myelinated A,-fibres. In this study we investigated whether, following peripheral nerve injury, SP was released de novo from the spinal cord after selective activation of A,-fibres. Spinal cords with dorsal roots attached were isolated in vitro from rats 2 weeks following distal sciatic axotomy or proximal spinal nerve lesion (SNL). The ipsilateral dorsal roots were electrically stimulated for two consecutive periods at low- or high-threshold fibre strength, spinal cord superfusates were collected and SP content was determined by radioimmunoassay. SNL, but not axotomized or control rat cords, released significant amounts of SP after selective activation of A,-fibres. Not only do these data support the idea that A, myelinated fibres contribute to neuropathic pain by releasing SP, they also illustrate the importance of the proximity of the lesion to the cell body. [source]

Diffusion tensor magnetic resonance imaging in spinal cord injury

CONCEPTS IN MAGNETIC RESONANCE, Issue 3 2008
Benjamin M. Ellingson
Abstract Noninvasive assessment of spinal cord integrity following injury is critical for precise diagnosis, prognosis, and surgical intervention strategies. Diffusion weighted imaging and diffusion tensor imaging are more sensitive to the underlying spinal cord microstructure than traditional imaging techniques. As a result, diffusion imaging is emerging as the clinical technique for imaging the spinal cord after trauma, surgery or during progressive degenerative diseases. This review describes the basic physics of diffusion imaging using magnetic resonance, techniques used to visualize diffusion measurements, and expected changes in diffusion measurements following spinal cord injury. © 2008 Wiley Periodicals, Inc.Concepts Magn Reson Part A 32A: 219,237, 2008. [source]

Functional magnetic resonance imaging of the human brain and spinal cord by means of signal enhancement by extravascular protons

CONCEPTS IN MAGNETIC RESONANCE, Issue 1 2003
P.W. Stroman
Abstract A review of functional magnetic resonance imaging (fMRI) signal changes in spin,echo image data is presented. Spin,echo fMRI data from the human brain and spinal cord show a consistent departure from that expected with blood oxygen level dependent (BOLD) contrast. Studies to investigate this finding demonstrate fMRI signal changes of 2.5% in the spinal cord and 0.7% in the brain at 1.5 T, which is extrapolated to an echo time of zero. Consistent evidence of a non-BOLD contrast mechanism arising from a proton-density change at sites of neuronal activation is demonstrated. A mathematical model and physiological explanation for signal enhancement by extravascular protons is also presented. © 2003 Wiley Periodicals, Inc. Concepts Magn Reson 16A: 28,34, 2003 [source]

The role of inhibitory neurotransmission in locomotor circuits of the developing mammalian spinal cord

ACTA PHYSIOLOGICA, Issue 2 2009
H. Nishimaru
Abstract Neuronal circuits generating the basic coordinated limb movements during walking of terrestrial mammals are localized in the spinal cord. In these neuronal circuits, called central pattern generators (CPGs), inhibitory synaptic transmission plays a crucial part. Inhibitory synaptic transmission mediated by glycine and GABA is thought to be essential in coordinated activation of muscles during locomotion, in particular, controlling temporal and spatial activation patterns of muscles of each joint of each limb on the left and right side of the body. Inhibition is involved in other aspects of locomotion such as control of speed and stability of the rhythm. However, the precise roles of neurotransmitters and their receptors mediating inhibitory synaptic transmission in mammalian spinal CPGs remain unclear. Moreover, many of the inhibitory interneurones essential for output pattern of the CPG are yet to be identified. In this review, recent advances on these issues, mainly from studies in the developing rodent spinal cord utilizing electrophysiology, molecular and genetic approaches are discussed. [source]

Could chronic pain and spread of pain sensation be induced and maintained by glial activation?

ACTA PHYSIOLOGICA, Issue 1-2 2006
E. Hansson
Abstract An injury often starts with acute physiological pain, which becomes inflammatory or neuropathic, and may sometimes become chronic. It has been proposed recently that activated glial cells, astrocytes and microglia within the central nervous system could maintain the pain sensation even after the original injury or inflammation has healed, and convert it into chronic by altering neuronal excitability. Glial cell activation has also been proposed to be involved in the phenomenon of spread of pain sensation ipsilaterally or to the contralateral side (i.e. mirror image pain). Substance P and calcitonin gene-related peptide, released due to an inflammatory process, interact with the endothelial cells of the blood,spinal cord and blood,brain barriers. The barriers open partially and substances may influence adjacent glial cells. Such substances are also released from neurones carrying the ,pain message' all the way from the injury to the cerebral cortex. Pro-inflammatory cytokines may be released from the microglial cells, and astroglial Ca2+ -transients or oscillations may spread within the astroglial networks. One theory is that Ca2+ -oscillations could facilitate the formation of new synapses. These new synapses could establish neuronal contacts for maintaining and spreading the pain sensation. If this theory holds true, it is possible that Ca2+ waves, production of cytokines and growth factors could be modified by selective anti-inflammatory drugs to achieve a balance in the activities of the different intercellular and intracellular processes. This paper reviews current knowledge about glial mechanisms underlying the phenomena of chronic pain and spread of the pain sensation. [source]

Differential expression and localization of neuronal intermediate filament proteins within newly developing neurites in dissociated cultures of Xenopus laevis embryonic spinal cord

CYTOSKELETON, Issue 1 2001
Jayanthi Undamatla
Abstract The molecular subunit composition of neurofilaments (NFs) progressively changes during axon development. In developing Xenopus laevis spinal cord, peripherin emerges at the earliest stages of neurite outgrowth. NF-M and XNIF (an ,-internexin-like protein) appear later, as axons continue to elongate, and NF-L is expressed after axons contact muscle. Because NFs are the most abundant component of the vertebrate axonal cytoskeleton, we must understand why these changes occur before we can fully comprehend how the cytoskeleton regulates axon growth and morphology. Knowing where these proteins are localized within developing neurites and how their expression changes with cell contact is essential for this understanding. Thus, we examined by immunofluorescence the expression and localization of these NF subunits within dissociated cultures of newly differentiating spinal cord neurons. In young neurites, peripherin was most abundant in distal neuritic segments, especially near branch points and extending into the central domain of the growth cone. In contrast, XNIF and NF-M were usually either absent from very young neurites or exhibited a proximal to distal gradient of decreasing intensity. In older neurites, XNIF and NF-M expression increased, whereas that of peripherin declined. All three of these proteins became more evenly distributed along the neurites, with some branches staining more intensely than others. At 24 h, NF-L appeared, and in 48-h cultures, its expression, along with that of NF-M, was greater in neurites contacting muscle cells, arguing that the upregulation of these two subunits is dependent on contact with target cells. Moreover, this contact had no effect on XNIF or peripherin expression. Our findings are consistent with a model in which peripherin plays an important structural role in growth cones, XNIF and NF-M help consolidate the intermediate filament cytoskeleton beginning in the proximal neurite, and increased levels of NF-L and NF-M help further solidify the cytoskeleton of axons that successfully reach their targets. Cell Motil. Cytoskeleton 49:16,32, 2001. © 2001 Wiley-Liss, Inc. [source]

Neuroanatomy and neurophysiology of itch

DERMATOLOGIC THERAPY, Issue 4 2005
Joanna Wallengren
ABSTRACT:, The specific pathway of "pure," histaminergic itch is traced from the mechano-insensitive nerve fibers in the skin to their central cortical projections. Neuropathic itch created at different levels of this anatomical pathway is reviewed. In this review the present author discusses damage to pruritoceptors in the skin, entrapment syndromes, damage to spinal ganglia, nerve root impingement, injury of the spinal cord, and cerebral damage in the distribution of the middle cerebral artery, capsula interna, or thalamus. Itch in inflamed skin resulting from interactions between nerve transmitters and other mediators of inflammation is described. [source]

Repulsive guidance of axons of spinal sensory neurons in Xenopus laevis embryos: Roles of Contactin and notochord-derived chondroitin sulfate proteoglycans

DEVELOPMENT GROWTH & DIFFERENTIATION, Issue 7 2005
Naoko Fujita
An immunoglobulin superfamily neuronal adhesion molecule, Contactin, has been implicated in axon guidance of spinal sensory neurons in Xenopus embryos. To identify the guidance signaling molecules that Contactin recognizes in tailbud embryos, an in situ binding assay was performed using recombinant Contactin-alkaline phosphatase fusion protein (Contactin-AP) as a probe. In the assay of whole-mount or sectioned embryos, Contactin-AP specifically bound to the notochord and its proximal regions. This binding was completely blocked by either digestion of embryo sections with chondroitinase ABC or pretreatment of Contactin-AP with chondroitin sulfate A. When the spinal cord and the notochord explants were co-cultured in collagen gel, growing Contactin-positive spinal axons were repelled by notochord-derived repulsive activity. This repulsive activity was abolished by the addition of either a monoclonal anti-Contactin antibody, chondroitin sulfate A or chondroitinase ABC to the culture medium. An antibody that recognizes chondroitin sulfate A and C labeled immunohistochemically the notochord in embryo sections and the collagen gel matrix around the cultured notochord explant. Addition of chondroitinase ABC into the culture eliminated the immunoreactivity in the gel matrix. These results suggest that the notochord-derived chondroitin sulfate proteoglycan acts as a repulsive signaling molecule that is recognized by Contactin on spinal sensory axons. [source]

Anomalous development of brain structure and function in spina bifida myelomeningocele

DEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 1 2010
Jenifer Juranek
Abstract Spina bifida myelomeningocele (SBM) is a specific type of neural tube defect whereby the open neural tube at the level of the spinal cord alters brain development during early stages of gestation. Some structural anomalies are virtually unique to individuals with SBM, including a complex pattern of cerebellar dysplasia known as the Chiari II malformation. Other structural anomalies are not necessarily unique to SBM, including altered development of the corpus callosum and posterior fossa. Within SBM, tremendous heterogeneity is reflected in the degree to which brain structures are atypical in qualitative appearance and quantitative measures of morphometry. Hallmark structural features of SBM include overall reductions in posterior fossa and cerebellum size and volume. Studies of the corpus callosum have shown complex patterns of agenesis or hypoplasia along its rostral-caudal axis, with rostrum and splenium regions particularly susceptible to agenesis. Studies of cortical regions have demonstrated complex patterns of thickening, thinning, and gyrification. Diffusion tensor imaging studies have reported compromised integrity of some specific white matter pathways. Given equally complex ocular motor, motor, and cognitive phenotypes consisting of relative strengths and weaknesses that seem to align with altered structural development, studies of SBM provide new insights to our current understanding of brain structure,function associations. © 2010 Wiley-Liss, Inc. Dev Disabil Res Rev 2010;16:23,30. [source]

Activity-based restorative therapies: Concepts and applications in spinal cord injury-related neurorehabilitation

DEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 2 2009
Cristina L. Sadowsky
Abstract Physical rehabilitation following spinal cord injury-related paralysis has traditionally focused on teaching compensatory techniques, thus enabling the individual to achieve day-to-day function despite significant neurological deficits. But the concept of an irreparable central nervous system (CNS) is slowly being replaced with evidence related to CNS plasticity, repair, and regeneration, all related to persistently maintaining appropriate levels of neurological activity both below and above the area where the damage occurred. It is now possible to envision functional repair of the nervous system by implementing rehabilitative interventions. Making the transition from "bench to bedside" requires careful analysis of existing basic science evidence, strategic focus of clinical research, and pragmatic implementation of new therapeutic tools. Activity, defined as both function specific motor task and exercise appears to be a necessity for optimization of functional, metabolic, and neurological status in chronic paralysis. Crafting a comprehensive rehabilitative intervention focused on functional improvement through neurological gains seems logical. The terms activity-based restorative therapies, activity-based therapies, and activity-based rehabilitation have been coined in the last 10 years to describe a new fundamental approach to deficits induced by neurological paralysis. The goal of this approach is to achieve activation of the neurological levels located both above and below the injury level using rehabilitation therapies. This article reviews basic and clinical science evidence pertaining to implementation of physical activity and exercise as a therapeutic tool in the management of chronic spinal cord-related neurological paralysis. © 2009 Wiley-Liss, Inc. Dev Disabil Res Rev 2009;15:112,116. [source]

Planar cell polarity effector gene Fuzzy regulates cilia formation and Hedgehog signal transduction in mouse

DEVELOPMENTAL DYNAMICS, Issue 12 2009
Westley Heydeck
Abstract Precise planar cell polarity (PCP) is critical for the development of multiple organ systems in animals. A group of core-PCP proteins are recognized to play crucial roles in convergent extension and other PCP-related processes in mammals. However, the functions of another group of PCP-regulating proteins, the PCP-effector proteins, are yet to be fully studied. In this study, the generation and characterization of a mouse mutant for the PCP effector gene Fuzzy (Fuz) is reported. Fuz homozygous mutants are embryonically lethal, with multiple defects including neural tube defects, abnormal dorsal/ventral patterning of the spinal cord, and defective anterior/posterior patterning of the limb buds. Fuz mutants also exhibit abnormal Hedgehog (Hh) signaling and inefficient proteolytic processing of Gli3. Finally, a significant decrease in cilia was found in Fuz homozygous mutants. In conclusion, Fuz plays an important role in cilia formation, Hh signal transduction, and embryonic development in mammals. Developmental Dynamics 238:3035,3042, 2009. © 2009 Wiley-Liss, Inc. [source]

Cloning and characterization of voltage-gated calcium channel alpha1 subunits in Xenopus laevis during development

DEVELOPMENTAL DYNAMICS, Issue 11 2009
Brittany B. Lewis
Abstract Voltage-gated calcium channels play a critical role in regulating the Ca2+ activity that mediates many aspects of neural development, including neural induction, neurotransmitter phenotype specification, and neurite outgrowth. Using Xenopus laevis embryos, we describe the spatial and temporal expression patterns during development of the 10 pore-forming alpha1 subunits that define the channels' kinetic properties. In situ hybridization indicates that CaV1.2, CaV2.1, CaV2.2, and CaV3.2 are expressed during neurula stages throughout the neural tube. These, along with CaV1.3 and CaV2.3, beginning at early tail bud stages, and CaV3.1 at late tail bud stages, are detected in complex patterns within the brain and spinal cord through swimming tadpole stages. Additional expression of various alpha1 subunits was observed in the cranial ganglia, retina, olfactory epithelium, pineal gland, and heart. The unique expression patterns for the different alpha1 subunits suggests they are under precise spatial and temporal regulation and are serving specific functions during embryonic development. Developmental Dynamics 238:2891,2902, 2009. © 2009 Wiley-Liss, Inc. [source]

The embryonic expression patterns and the knockdown phenotypes of zebrafish ADP-ribosylation factor-like 6 interacting protein gene

DEVELOPMENTAL DYNAMICS, Issue 1 2009
Hsing-Yen Huang
Abstract ADP-ribosylation factor-like 6 (Arl6) mutation is linked to human disease and Arl6 interacts with Arl6 interacting protein (Arl6ip). However, the expression pattern and function of Arl6ip during embryogenesis are unknown. To confirm whether abnormal Arl6ip function might result in embryonic defects in zebrafish, we examined the expression patterns of arl6ip during embryogenesis, and they were maternally expressed and exhibited in the brain, optic primordia, hypochord, spinal cord, myotome, heart, fin-bud, kidney, trunk, and retina. Knockdown of Arl6ip revealed the following phenotypic defects: microphthalmia, disorganized pigment pattern, flat head, defective tectum, deficient pectoral fins, abnormal pneumatic duct, pericardial edema, and deformed trunk. Particularly, histological dissection of the retinae of arl6ip -morphants revealed that neuronal differentiation is severely delayed, resulting in no formation of retinal layers. We further confirmed that opsins of arl6ip -morphants were not transcribed. Based on this evidence, Arl6ip may play important roles in zebrafish ocular, heart, and fin-bud development. Developmental Dynamics 238:232,240, 2009. © 2008 Wiley-Liss, Inc. [source]

An olig2 reporter gene marks oligodendrocyte precursors in the postembryonic spinal cord of zebrafish

DEVELOPMENTAL DYNAMICS, Issue 12 2007
Hae-Chul Park
Abstract Continuous production of new neurons and glia in adult mammals occurs within specialized proliferation zones of the forebrain. Neural cell proliferation and neurogenesis is more widespread in adult amphibians, reptiles, and fish but the identity of neural stem cell populations in these organisms has not been fully described. We investigated expression of a reporter gene driven by olig2 regulatory DNA at postembryonic stages in zebrafish. We show that olig2 expression marks a discrete population of spinal cord radial glia in larvae and adults that divide continuously. olig2+ radial glia have hallmarks of stem cells and their divisions appear to be asymmetric, producing new oligodendrocytes but not neurons or astrocytes. Developmental Dynamics 236:3402,3407, 2007. © 2007 Wiley-Liss, Inc. [source]

Rab23 GTPase is expressed asymmetrically in Hensen's node and plays a role in the dorsoventral patterning of the chick neural tube

DEVELOPMENTAL DYNAMICS, Issue 11 2007
Naixin Li
Abstract The mouse Rab23 protein, a Ras-like GTPase, inhibits signaling through the Sonic hedgehog pathway and thus exerts a role in the dorsoventral patterning of the spinal cord. Rab23 mouse mutant embryos lack dorsal spinal cord cell types. We cloned the chicken Rab23 gene and studied its expression in the developing nervous system. Chick Rab23 mRNA is initially expressed in the entire neural tube but retracts to the dorsal alar plate. Unlike in mouse, we find Rab23 in chick already expressed asymmetrically during gastrulation. Ectopic expression of Rab23 in ventral midbrain induced dorsal genes (Pax3, Pax7) ectopically and reduced ventral genes (Nkx2.2 and Nkx6) without influencing cell proliferation or neurogenesis. Thus, in the developing brain of chick embryos Rab23 acts in the same manner as described for the caudal spinal cord in mouse. These data indicate that Rab23 plays an important role in patterning the dorso-ventral axis by dorsalizing the neural tube. Developmental Dynamics 236:2993,3006, 2007. © 2007 Wiley-Liss, Inc. [source]

Regionalized expression of ADAM13 during chicken embryonic development

DEVELOPMENTAL DYNAMICS, Issue 3 2007
Juntang Lin
Abstract ADAMs are a family of membrane proteins possessing a disintegrin domain and a metalloprotease domain, which have functions in cell,cell adhesion, cell,matrix adhesion, and protein shedding, respectively. ADAMs are involved in morphogenesis and tissue formation during embryonic development. In the present study, chicken ADAM13 was cloned and identified, and its expression was investigated by semiquantitative reverse transcriptase-polymerase chain reaction and in situ hybridization during chicken embryonic development. Our results show that ADAM13 expression is temporally and spatially regulated in chicken embryos. At early developmental stages, ADAM13 is expressed in the head mesenchyme, which later develops into the craniofacial skeleton, in the branchial arches, and in the meninges surrounding the brain. Furthermore, ADAM13 mRNA was also detected in several tissues and organs, such as the somites and their derived muscles, the meninges surrounding the spinal cord, the dorsal aorta, the developing kidney, and several digestive organs. Developmental Dynamics 236:862,870, 2007. © 2007 Wiley-Liss, Inc. [source]

Developmental analysis of activin-like kinase receptor-4 (ALK4) expression in Xenopus laevis

DEVELOPMENTAL DYNAMICS, Issue 2 2005
Yumei Chen
Abstract The type I transforming growth factor-beta (TGF,) receptor, activin-like kinase-4 (ALK4), is an important regulator of vertebrate development, with roles in mesoderm induction, primitive streak formation, gastrulation, dorsoanterior patterning, and left,right axis determination. To complement previous ALK4 functional studies, we have analyzed ALK4 expression in embryos of the frog, Xenopus laevis. Results obtained with reverse transcriptase-polymerase chain reaction indicate that ALK4 is present in both the animal and vegetal poles of blastula stage embryos and that expression levels are relatively constant amongst embryos examined at blastula, gastrula, neurula, and early tail bud stages. However, the tissue distribution of ALK4 mRNA, as assessed by whole-mount in situ hybridization, was found to change over this range of developmental stages. In the blastula stage embryo, ALK4 is detected in cells of the animal pole and the marginal zone. During gastrulation, ALK4 is detected in the outer ectoderm, involuting mesoderm, blastocoele roof, dorsal lip, and to a lesser extent, in the endoderm. At the onset of neurulation, ALK4 expression is prominent in the dorsoanterior region of the developing head, the paraxial mesoderm, and midline structures, including the prechordal plate and neural folds. Expression in older neurula stage embryos resolves to the developing brain, somites, notochord, and neural crest; thereafter, additional sites of ALK4 expression in tail bud stage embryos include the spinal cord, otic placode, developing eye, lateral plate mesoderm, branchial arches, and the bilateral heart fields. Together, these results not only reflect the multiple developmental roles that have been proposed for this TGF, receptor but also define spatiotemporal windows in which ALK4 may function to modulate fundamental embryological events. Developmental Dynamics 232:393,398, 2005. © 2004 Wiley-Liss, Inc. [source]

Retinoic acid, a regeneration-inducing molecule

DEVELOPMENTAL DYNAMICS, Issue 2 2003
Malcolm Maden
Abstract Retinoic acid (RA) is the biologically active metabolite of vitamin A. It is a low molecular weight, lipophilic molecule that acts on the nucleus to induce gene transcription. In amphibians and mammals, it induces the regeneration of several tissues and organs and these examples are reviewed here. RA induces the "super-regeneration" of organs that can already regenerate such as the urodele amphibian limb by respecifying positional information in the limb. In organs that cannot normally regenerate such as the adult mammalian lung, RA induces the complete regeneration of alveoli that have been destroyed by various noxious treatments. In the mammalian central nervous system (CNS), which is another tissue that cannot regenerate, RA does not induce neurite outgrowth as it does in the embryonic CNS, because one of the retinoic acid receptors, RAR,2, is not up-regulated. When RAR,2 is transfected into the adult spinal cord in vitro, then neurite outgrowth is stimulated. In all these cases, RA is required for the development of the organ, in the first place suggesting that the same gene pathways are likely to be used for both development and regeneration. This suggestion, therefore, might serve as a strategy for identifying potential tissue or organ targets that have the capacity to be stimulated to regenerate. Developmental Dynamics 226:237,244, 2003.© 2003 Wiley-Liss, Inc. [source]

Electroporation as a tool to study in vivo spinal cord regeneration

DEVELOPMENTAL DYNAMICS, Issue 2 2003
K. Echeverri
Abstract Tailed amphibians such as axolotls and newts have the unique ability to fully regenerate a functional spinal cord throughout life. Where the cells come from and how they form the new structure is still poorly understood. Here, we describe the development of a technique that allows the visualization of cells in the living animal during spinal cord regeneration. A microelectrode needle is inserted into the lumen of the spinal cord and short rapid pulses are applied to transfer the plasmids encoding the green or red fluorescent proteins into ependymal cells close to the plane of amputation. The use of small, transparent axolotls permits imaging with epifluorescence and differential interference contrast microscopy to track the transfected cells as they contribute to the spinal cord. This technique promises to be useful in understanding how neural progenitors are recruited to the regenerating spinal cord and opens up the possibility of testing gene function during this process. Developmental Dynamics 226:418,425, 2003. © 2003 Wiley-Liss, Inc. [source]

Expression of the ETS transcription factor ER81 in the developing chick and mouse hindbrain

DEVELOPMENTAL DYNAMICS, Issue 3 2002
Yan Zhu
Abstract ER81 is an ETS domain-containing transcription factor, which is expressed in various developing tissues and organs of the embryo and in pools of developing spinal motor neurons and proprioceptive sensory neurons. Analysis of mice lacking ER81 function showed that this gene played an important role in the establishment of sensory-motor circuitry in the spinal cord. Here, we investigate the expression pattern of er81 in the hindbrain of both chick and mouse embryos. We find that er81 is expressed in a subpopulation of inferior olive neurons, which send their projections to the caudal cerebellum. © 2002 Wiley-Liss, Inc. [source]

Cloning and expression of three zebrafish roundabout homologs suggest roles in axon guidance and cell migration

DEVELOPMENTAL DYNAMICS, Issue 2 2001
Jeong-Soo Lee
Abstract We report the cloning and expression patterns of three novel zebrafish Roundabout homologs. The Roundabout (robo) gene encodes a transmembrane receptor that is essential for axon guidance in Drosophila and Robo family members have been implicated in cell migration. Analysis of extracellular domains and conserved cytoplasmic motifs shows that zebrafish Robo1 and Robo2 are orthologs of mammalian Robo1 and Robo2, respectively, while zebrafish Robo3 is likely to be an ortholog of mouse Rig-1. The three zebrafish robos are expressed in distinct but overlapping patterns during embryogenesis. They are highly expressed in the developing nervous system, including the olfactory system, visual system, hindbrain, cranial ganglia, spinal cord, and posterior lateral line primordium. They are also expressed in several nonneuronal tissues, including somites and fin buds. The timing and patterns of expression suggest roles for zebrafish robos in axon guidance and cell migration. Wiley-Liss, Inc. © 2001 Wiley-Liss, Inc. [source]

Cervical spinal cord injury following cephalic presentation and delivery by Caesarean section

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 4 2001
C Morgan MD MRCP MRCPCH
We describe a term infant with an acute spinal cord injury following emergency Caesarean section. Foetal movements were normal on the day that the mother was admitted for postterm induction of labour. Caesarean section was performed because of foetal distress and failure to progress during labour. The initial clinical picture suggested acute birth asphyxia. The presence of a high cervical spine injury became more obvious as the clinical picture evolved over the next 7 days. A discontinuity of the cervical spinal cord at C4,5 was confirmed on MRI. Spontaneous respiration failed to develop and intensive care was withdrawn on day 15. No evidence of trauma, or a vascular, neurological, or congenital anomaly of the cervical spinal cord was found at post mortem. The absence of a similar case following cephalic presentation and Caesarean section made bereavement couselling of the parents especially difficult. [source]

Gliomatosis cerebri in a 10,year-old girl masquerading as diffuse encephalomyelitis and spinal cord tumour

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 2 2001
Sandeep Jayawant
Gliomatosis cerebri is the unifying term used when diffuse glial infiltration occurs throughout the cerebral hemispheres. The very few cases reported in children have presented with intractable epilepsy, corticospinal tract deficits, unilateral tremor, headaches, and developmental delay. Antemortem diagnosis is difficult because of the vagueness of the physical, radiological and pathological findings. Adult cases may simulate an acute diffuse encephalomyelitis and show postmortem evidence of a marked swelling of the spinal cord. Apparently benign intracranial hypertension with papilloedema has also been recorded. We report a 10,year-old girl who presented with a history and physical signs suggestive of benign intracranial hypertension. A diffuse encephalomyelopathy occurred, which was complicated by spinal cord swelling, followed by deterioration and death. Gliomatosis cerebri affecting the brain and spinal cord was found at postmortem examination. [source]

Vascular endothelial growth factor prevents G93A-SOD1-induced motor neuron degeneration

DEVELOPMENTAL NEUROBIOLOGY, Issue 13 2009
J. Simon Lunn
Abstract Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disorder characterized by selective loss of motor neurons (MNs). Twenty percent of familial ALS cases are associated with mutations in Cu2+/Zn2+ superoxide dismutase (SOD1). To specifically understand the cellular mechanisms underlying mutant SOD1 toxicity, we have established an in vitro model of ALS using rat primary MN cultures transfected with an adenoviral vector encoding a mutant SOD1, G93A-SOD1. Transfected cells undergo axonal degeneration and alterations in biochemical responses characteristic of cell death such as activation of caspase-3. Vascular endothelial growth factor (VEGF) is an angiogenic and neuroprotective growth factor that can increase axonal outgrowth, block neuronal apoptosis, and promote neurogenesis. Decreased VEGF gene expression in mice results in a phenotype similar to that seen in patients with ALS, thus linking loss of VEGF to the pathogenesis of MN degeneration. Decreased neurotrophic signals prior to and during disease progression may increase MN susceptibility to mutant SOD1-induced toxicity. In this study, we demonstrate a decrease in VEGF and VEGFR2 levels in the spinal cord of G93A-SOD1 ALS mice. Furthermore, in isolated MN cultures, VEGF alleviates the effects of G93A-SOD1 toxicity and neuroprotection involves phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling. Overall, these studies validate the usefulness of VEGF as a potential therapeutic factor for the treatment of ALS and give valuable insight into the responsible signaling pathways and mechanisms involved. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2009 [source]

Glutamate drives the touch response through a rostral loop in the spinal cord of zebrafish embryos

DEVELOPMENTAL NEUROBIOLOGY, Issue 12 2009
Thomas Pietri
Abstract Characterizing connectivity in the spinal cord of zebrafish embryos is not only prerequisite to understanding the development of locomotion, but is also necessary for maximizing the potential of genetic studies of circuit formation in this model system. During their first day of development, zebrafish embryos show two simple motor behaviors. First, they coil their trunks spontaneously, and a few hours later they start responding to touch with contralateral coils. These behaviors are contemporaneous until spontaneous coils become infrequent by 30 h. Glutamatergic neurons are distributed throughout the embryonic spinal cord, but their contribution to these early motor behaviors in immature zebrafish is still unclear. We demonstrate that the kinetics of spontaneous coiling and touch-evoked responses show distinct developmental time courses and that the touch response is dependent on AMPA-type glutamate receptor activation. Transection experiments suggest that the circuits required for touch-evoked responses are confined to the spinal cord and that only the most rostral part of the spinal cord is sufficient for triggering the full response. This rostral sensory connection is presumably established via CoPA interneurons, as they project to the rostral spinal cord. Electrophysiological analysis demonstrates that these neurons receive short latency AMPA-type glutamatergic inputs in response to ipsilateral tactile stimuli. We conclude that touch responses in early embryonic zebrafish arise only after glutamatergic synapses connect sensory neurons and interneurons to the contralateral motor network via a rostral loop. This helps define an elementary circuit that is modified by the addition of sensory inputs, resulting in behavioral transformation. © 2009 Wiley Periodicals, Inc. Develop Neurobiol 2009 [source]

Developmental characteristics of AMPA receptors in chick lumbar motoneurons

DEVELOPMENTAL NEUROBIOLOGY, Issue 11 2007
Xianglian Ni
Abstract Ca2+ fluxes through ionotropic glutamate receptors regulate a variety of developmental processes, including neurite outgrowth and naturally occurring cell death. In the CNS, NMDA receptors were originally thought to be the sole source of Ca2+ influx through glutamate receptors; however, AMPA receptors also allow a significant influx of Ca2+ ions. The Ca2+ permeability of AMPA receptors is regulated by the insertion of one or more edited GluR2 subunits. In this study, we tested the possibility that changes in GluR2 expression regulate the Ca2+ permeability of AMPA receptors during a critical period of neuronal development in chick lumbar motoneurons. GluR2 expression is absent between embryonic day (E) 5 and E7, but increases significantly by E8 in the chick ventral spinal cord. Increased GluR2 protein expression is correlated with parallel changes in GluR2 mRNA in the motoneuron pool. Electrophysiological recordings of kainate-evoked currents indicate a significant reduction in the Ca2+ -permeability of AMPA receptors between E6 and E11. Kainate-evoked currents were sensitive to the AMPA receptor blocker GYKI 52466. Application of AMPA or kainate generates a significant increase in the intracellular Ca2+ concentration in E6 spinal motoneurons, but generates a small response in older neurons. Changes in the Ca2+ -permeability of AMPA receptors are not mediated by age-dependent changes in the editing pattern of GluR2 subunits. These findings raise the possibility that Ca2+ influx through Ca2+ -permeable AMPA receptors plays an important role during early embryonic development in chick spinal motoneurons. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007 [source]