PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “GANGLIA, SPINAL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources

Nerve growth factors in chick tissues.

Bioassays of factors promoting nerve growth in embryonic ganglia are described. Chick embryo extract evokes fiber outgrowth in both sympathetic and ciliary ganglia explanted into a collagen gel. The response is not suppressed by antibodies directed against mouse nerve growth factor (NGF). Chick embryo extract also supported survival of neurons in both intact and dissociated ganglia. In addition to these non-NGF activities, preliminary evidence is presented for the release of a NGF-like factor from cultured iris of the adult chick.

Animals↗

Regulation of growth cone morphology by nerve growth factor: a comparative study by scanning electron microscopy.

The object of this study was to document and analyze local regulation by nerve growth factor (NGF) of neuronal growth cone properties and to explore the possible diversity of this effect in various NGF-responsive preparations. In particular, scanning electron microscopy was used to characterize the morphology of neuronal growth cones in cultures of dissociated chick embryo dorsal root ganglia (DRG) under conditions of continuous NGF exposure, withdrawal of NGF for 5-6 hr, and restoration of NGF for various times. Comparison was made with similarly manipulated cultures of dissociated newborn rat sympathetic ganglia and neurite-bearing PC12 pheochromocytoma cells. The growth cones of most of the continuously NGF-treated DRG neurons (cultured on poly-L-lysine or collagen-coated glass coverslips) had relatively compact central flattened areas and numerous prominent filopodia. Withdrawal of NGF resulted in a marked spreading of the central growth cone area so that the average maximum width of this structure increased by about threefold as compared to nondeprived cultures. The mean number and lengths of filopodia were unaffected. Restoration of NGF brought about, over a time course of tens of minutes, a return of the original type of growth cone morphology. Rather different responses were observed for the sympathetic neuron and PC12 cultures. Here, surface ruffles, only rarely seen in the chick cultures, were a major feature of the growth cones, whereas filopodia, though present, were less prominent. Removal of NGF led to loss of ruffles and to rounding up of the growth cones; NGF readdition elicited a rapid (less than 30 sec) reinitiation of ruffling and a more gradual (over tens of minutes) respreading of growth cones. These findings illustrate not only that NGF can regulate growth cone properties, but also that there is a diversity as to how this is manifested. Possible mechanisms and biological roles for this regulation are discussed.

Animals↗

Myelin protein expression in dissociated superior cervical ganglia and dorsal root ganglia cultures.

Schwann cells of the adult rat superior cervical ganglia (SCG) synthesize negligible levels of the major myelin glycoprotein, P0, in vivo. This suggests that the sympathetic axons of the SCG are deficient in one of more components involved in the regulation of myelin protein expression. Here we have compared the ability of neurites from neonatal rat SCG and embryonic rat dorsal root ganglia (DRG) to induce Schwann cell expression of myelin proteins after growth in culture using a serum-free medium. Steady-state P0 mRNA levels in the SCG and DRG culture paradigms were determined with a sensitive polymerase chain reaction (PCR) assay that amplified cDNA produced by reverse transcription of mRNA. This semiquantitative assay showed a linear response to increasing amounts of P0 and actin mRNA and required substantially less cellular RNA than typical hybridization techniques. Using the PCR assay, we found that SCG cultures contained significantly lower amounts of P0 mRNA than did DRG cultures. To further confirm that SCG cultures have negligible expression of myelin proteins, immunoblot analyses were done to examine the steady-state levels of both P0 and myelin basic protein. While nonmyelinating DRG cultures had readily detectable amounts of these myelin-specific proteins, neither could be demonstrated in the SCG cultures. The data indicate that SCG neurites lack one or more signals needed to induce myelin protein expression. Employing SCG and DRG cultures in comparative biochemical studies should prove useful in identifying the axonal molecule(s) involved in the regulation of myelin protein expression.

Actins↗

Neuronotrophic effects of skeletal muscle fractions on neurite development.

Soluble fractions of chick embryonic skeletal muscle stimulated radial outgrowth of long neurites from peripheral ganglia. Dorsal root ganglia were more responsive to the growth stimulus of muscle fractions than sympathetic ganglia. Muscle fractions from chicks immobilized with d-tubocurarine chloride (dtc) were significantly more effective in stimulating growth than normal muscle fractions. Neuritic outgrowth stimulated by muscle fractions was not blocked by antisera to the Nerve Growth Factor (NGF) indicating that these neuronotrophic effects were not due to NGF.

Animals↗

Faster nerve regeneration after sciatic nerve injury in mice over-expressing basic fibroblast growth factor.

Basic fibroblast growth factor (FGF-2) is expressed in the peripheral nervous system and is up-regulated after nerve lesion. It has been demonstrated that administration of FGF-2 protects neurons from injury-induced cell death and promotes axonal regrowth. Using transgenic mice over-expressing FGF-2 (TgFGF-2), we addressed the importance of endogenously generated FGF-2 on sensory neuron loss and sciatic nerve regeneration. After sciatic nerve transection, wild-type and transgenic mice showed the same degree of cell death in L5 spinal ganglia. Also, the number of chromatolytic, eccentric, and pyknotic sensory neurons was not changed under elevated levels of FGF-2. Morphometric evaluation of intact nerves from TgFGF-2 mice revealed no difference in number and size of myelinated fibers compared to wild-type mice. One week after crush injury, the number of regenerated axons was doubled and the myelin thickness was significantly smaller in transgenic mice. After 2 and 4 weeks, morphometric analysis and functional tests revealed no differences in recovery of sensory and motor nerve fibers. To study the role of FGF-2 over-expression on Schwann cell proliferation during the early regeneration process, we used BrdU-labeling to mark dividing cells. In transgenic mice, the number of proliferating cells was significantly increased distal to the crush site compared to wild-types. We propose that endogenously synthesized FGF-2 influences early peripheral nerve regeneration by regulating Schwann cell proliferation, axonal regrowth, and remyelination.

Animals↗

The history of the discovery of the nerve growth factor.

The Nerve Growth Factor (NGF) is the progenitor of a family of growth factors which is still expanding. The history of its discovery is very colorful; it is a rare combination of scientific reasoning, intuition, fortuities, and good luck. In addition, I believe that the collaboration of three scientists with very different backgrounds contributed to the success: I had grown up in a laboratory of experimental embryology, Dr. Levi-Montalcini came from neurology, and Dr. Stanley Cohen was from biochemistry. The decision where to begin the history of a discovery is always arbitrary. I shall give my reasons why I begin this story with my wing bud extirpations on chick embryos and the analysis of the effects of the operation on the development of spinal nerve centers, published in 1934. Of course, I am aware of the fact that the analysis of neurogenesis had been pioneered by Dr. R. G. Harrison and his students at Yale University since the beginning of this century. It should be mentioned that their experiments had been done on amphibian embryos. My own interest in problems of neurogenesis dates back to my Ph.D. thesis in the Zoology Department of Professor H. Spemann at the University of Freiburg in (the Federal Republic of) Germany; it dealt with the influence of the nervous system on the development of limbs in frog embryos. After I had obtained some inconclusive results I did the crucial experiment of producing nerveless legs. I removed the lumbar part of the spinal cord and the spinal ganglia before the outgrowth of nerve fibers. The nerveless legs developed normally in every respect, but the muscles atrophied eventually.

Animals↗

Neurotrophic influence of denervated sciatic nerve on adult dorsal root ganglion neurons.

Isolated adult frog dorsal root ganglion neurons survive in vitro in a defined medium for more than 4 weeks and extend processes. When co-cultured with a 1-mm piece of peripheral nerve the average total process length per neuron was 10 times longer than that of control neurons by 8 days, and the processes had a significantly different morphology from that of control neurons. This influence on process length increased with increasing time of nerve denervation prior to co-culturing. These results suggest the release of a neurotrophic factor/s from the cells of the peripheral nerve. The neurotrophic influence was completely blocked by antibodies against mouse nerve growth factor (NGF). Although NGF increased the average process length by twofold over control neurons, its influence nerve reached that of the nerve-released factor, and the NGF-induced processes had a distinctly different morphology. The frog nerve-released factor promoted process outgrowth from E11 chick sympathetic ganglia, although the process number, length, and their fasciculation differed greatly from those induced by NGF. These results suggest that the nerve-released factor/s are immunologically and functionally related to NGF but have not established whether a single factor or an aggregate of several secreted molecules are responsible. This article presents a new preparation in which the varied influences of different neurotrophic factors can be studied in great detail on large populations of isolated adult vertebrate neurons and sets the stage for the characterization and isolation of the frog peripheral nerve neurotrophic factor, as well as examining the influence of this factor on neuronal morphology and its ability to direct process outgrowth.

Animals↗

Expression of trk and neurotrophin mRNA in dorsal root and sympathetic ganglia of the quail during development.

The nerve growth factor (NGF) family of neurotrophins exerts effects by binding to products of the trk family of proto-oncogenes. We examined the expression of both trk and neurotrophin mRNA during the entire range of development of quail dorsal root ganglia (DRG) and sympathetic ganglia (SG) using in situ hybridization and reverse transcriptase-polymerase chain reaction (RT-PCR). TrkC mRNA was present in neurons or their precursors from the time of formation of DRG (stage 18, embryonic day 2.5 [E2.5]) and throughout development. The number of labeled cells changed, however, from a majority to a minority at later developmental stages. Expression of trkA mRNA was not detected in DRG until stage 30 (E6) by in situ hybridization, although results with RT-PCR were positive at stage 23 (E3.5). Labeling was always detected on a majority of neurons or their precursors. SG exhibited low levels of trkC mRNA during the later stages of development, whereas trkA mRNA was present from stage 34 onward in most neurons. We have also shown that NGF, neurotrophin-3 (NT-3), and brain-derived neurotrophic factor (BDNF) mRNA were present at all stages examined (stages 23 through 45 for DRG, stages 35-36 and 45 for SG). In DRG, NGF mRNA expression was limited to support cells, whereas NT-3 and BDNF mRNA were detected in both neurons and support cells. These results suggest that neurotrophins could serve a local function in developing ganglia, which can be correlated with the presence of their respective receptors.

Animals↗

Association of tracheoesophageal anomalies with visceral and parietal malformations in a human embryo (Carnegie stage 21).

A human embryo (Carnegie stage 21) with tracheoesophageal malformations (esophageal atresia and tracheoesophageal fistula) and anomalies at the caudal end of the embryo (anorectal atresia, rectovesical fistula, vertebral and notochordal defects, and agenesis of the metanephros) was studied. Other anomalies observed were: absence of right umbilical artery, fusion of spinal ganglia, and absence of cloacal outlet of mesonephric ducts. The possible pathogenesis of these associated malformations is discussed.

Abnormalities, Multiple↗

Laminets: laminin- and netrin-related genes expressed in distinct neuronal subsets.

Laminins and netrins are families of related secreted proteins known to play critical roles in guiding the growth of peripheral and central axons, respectively. Here we report the identification of two novel cell surface glycoproteins that we name laminets because they resemble both laminins and netrins. Laminet-1 and -2 are selectively expressed in neurons, each in a distinct subset that includes populations in forebrain, midbrain, hindbrain, spinal cord, and spinal ganglia. In several forebrain regions, including main relays of the central olfactory pathway, laminet-1 and -2 are expressed in nonoverlapping neuronal subsets. Both laminets are subject to alternative splicing which, in the case of laminet-1, generates at least 10 distinct isoforms, each of which contains a unique combination of potential binding sites for ligands or counterreceptors. Their complex patterns of distribution and isoform diversity, along with their homology to known axon guidance molecules, suggest that laminets contribute to the patterning of neuronal connections.

Alternative Splicing↗

Age pigments in different populations of peripheral neurons in vivo and in vitro.

The distribution and ultrastructure of lipopigments in the rat sympathetic, vagus and spinal ganglion neurons were studied in vivo and in vitro using fluorescence and electron microscopy. Newborn, 3-6 mo and 24-30 mo-old male Wistar rats were used. In vivo, the age pigments in the sympathetic neurons showed a tendency to form unipolar or bipolar caps, whereas in the vagus and spinal ganglion neurons pigment granules were packed in the peripheral area of the perikarya during aging. Ultrastructurally, lipid-like vacuoles and a rather homogeneous matrix were the components shared by pigment bodies of all types of peripheral neurons. However, pigment granules in sympathetic neurons frequently had a third, osmiophilic component, which likely represents neuromelanin. In vitro, the cytoplasmic area occupied by autofluorescent pigments was increased in most of the neurons. Some neurons, however, showed the same amount of lipopigments as in vivo. In electron microscopy, age pigment granules typical of each type of neuron were found, and their number and intracellular distribution seemed to be comparable with those in vivo. In most of the neurons cultured from all ages and of all types of ganglion, there appeared to be accumulations of another, very homogeneous and large type of pigment body. In some cases, they were structurally connected with classical pigment bodies or they had a finger print-like substructure. Large homogeneous pigment bodies were also seen in surrounding satellite cells. All these changes were most frequently seen in cultures of spinal ganglia from old animals. It is concluded that although classical age pigments maintain their characteristics in cultured peripheral neurons, there is, in addition, a rapid accumulation of ceroid-like pigments, which may be caused by the inability of the cultured neurons to cope with increased peroxidative damage.

Aging↗

Capsaicin-induced local effector responses, autonomic reflexes and sensory neuropeptide depletion in the pig.

Systemic capsaicin pretreatment (total cumulative dose 50 mg/kg administered s.c. over 2h) was performed in pigs under pentobarbitone anaesthesia and the effects on sensory and sympatho-adrenal mechanisms were examined acutely and 2 days after treatment. During pretreatment with capsaicin, pronounced sensory and sympatho-adrenal activation were noticed. This resulted in a several-fold increase in the systemic arterial plasma levels of calcitonin gene-related peptide (CGRP), neurokinin A (NKA), noradrenaline (NA), adrenaline (Adr) and neuropeptide Y (NPY), and a slight increase (39%) in plasma cortisol. Simultaneously, there was marked tachycardia, an increase in blood pressure, total skin erythema and some bronchoconstriction, all lasting for about 30 min. Upon repeated injections tachyphylaxis was observed. 2 days after capsaicin pretreatment, basal plasma levels of the neuropeptides, catecholamines and cortisol as well as basal cardiovascular and pulmonary parameters were similar in control and capsaicin-treated pigs. The tissue content of CGRP and NKA was reduced by 50-65% in the airways and by 80-90% in the skin 2 days after capsaicin pretreatment. In contrast, the CGRP content was unchanged or increased (by 195%) in the nodose and spinal ganglia, respectively. The corresponding tissue levels of vasoactive intestinal polypeptide (VIP) and NPY were basically unchanged in capsaicin-treated pigs. A bolus injection of capsaicin (1 mg/kg i.v.) in control animals resulted in a marked increase in plasma catecholamines and NPY, concomitant with elevation in blood pressure and heart rate. These effects were preceded by an initial bradycardia and decrease in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Innervation of the large arteries and heart of the toad (Bufo marinus) by adrenergic and peptide-containing neurons.

The innervation of the major arteries and heart of the toad (Bufo marinus) was examined by use of glyoxylic acid-induced catecholamine fluorescence and peptide immunohistochemistry. All arteries possessed a moderate to dense plexus of adrenergic axons, which also showed neuropeptide Y-like immunoreactivity (NPY-LI). Some adrenergic axons in the intracardiac vagal trunks showed NPY-LI, but the varicose adrenergic axons innervating the cardiac muscle of the atria and ventricle, and the coronary blood vessels did not display NPY-LI. About half of the nerve cell bodies in the anterior sympathetic chain ganglia with dopamine-beta-hydroxylase-LI (DBH-LI) also contained NPY-LI. The nerve cell bodies with DBH-LI alone were generally larger (median diameter 30 micron) than those with both DBH-LI and NPY-LI (median diameter 20 micron). Some cell bodies showing DBH-LI alone were surrounded by boutons with NPY-LI but not DBH-LI. Axons that displayed simultaneously both substance P-LI (SP-LI) and calcitonin gene-related peptide-LI (CGRP-LI) also formed a plexus around all arteries studied, being particularly dense around the mesenteric and pulmonary arteries. These axons are most likely sensory since SP-LI was reduced by capsaicin treatment, and nerve cell bodies with both SP-LI and CGRP-LI were found in dorsal root ganglia and the vagal ganglion. A dense plexus of axons showing somatostatin-LI was located around the pulmonary artery and its main intrapulmonary branches. A few nerves with vasoactive intestinal polypeptide-LI were found around the dorsal aorta and pulmonary artery. No perivascular nerves with enkephalin-LI were observed. Reversed-phase, high-pressure liquid chromatography of acid extracts of the large arteries showed that the major peaks of NPY-LI and SP-LI co-eluted with porcine NPY (1-36) and synthetic SP (1-11), respectively. Thus, the location and structure of these peptides in perivascular nerves has been highly conserved during vertebrate evolution.

Adrenergic Fibers↗

Immunoreactivity for phosphorylated 200-kDa neurofilament subunit is heterogeneously expressed in human sympathetic and primary sensory neurons.

This study was undertaken to investigate whether human sensory and sympathetic neurons contain phosphorylated neurofilament proteins, and whether they may be classified on the basis of this property, as in other mammalian species. The distribution of the phosphorylated 200-kDa neurofilament protein subunit (p200-NFP) was investigated in lumbar sympathetic and dorsal root ganglia by means of the RT97 monoclonal antibody (against p200-NFP). The intensity of immunostaining, and the size of neuronal body profiles were measured in order to define different neuron subclasses. In dorsal root ganglia, most of the neuronal profiles (96%) were p200-NFP immunoreactive, and the intensity of immunostaining was not related to neuronal perikarya size. In the lumbar paravertebral sympathetic ganglia, virtually all neurons displayed p200-NFP immunoreactivity, and the intensity of immunolabelling was also independent of the size of the neuronal somata. These results demonstrate heterogeneity in the expression of p200-NFP immunoreactivity in human sympathetic and sensory neurons. In contrast to other mammalian species, RT97 immunolabelling cannot be used as a discriminative marker for the two main types of human primary sensory neurons. On the other hand, our findings provide evidence for the occurrence of phosphorylated neurofilaments within peripheral neuron cell bodies.

Adult↗

Distribution and origin of the peripheral innervation of rat cervical esophagus.

Several neurotransmitters, neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), galanin, enkephalin, calcitonin-gene related peptide (GGRP), substance P, as well as nitric oxide synthase (NOS), and the noradrenergic marker tyrosine-hydroxylase (TH) were localized by immunocytochemistry in the cervical esophagus of rat. Nerve fibers containing the neuropeptides, NOS, and TH were distributed in the myenteric plexus, around muscle bundles and small blood vessels. Injection of the retrograde tracer True Blue (TB) into the cervical esophagus resulted in the appearance of labeled nerve cell bodies in the superior cervical, the stellate, the nodose, the sphenopalatine, the dorsal root ganglia at levels C2-C7, and in local ganglia close to the thyroid. Most of the TB-labeled nerve cell bodies in the superior cervical ganglia contained NPY. In the stellate ganglion, a few labeled nerve cell bodies contained VIP whereas an additional few cell bodies stored VIP. In local ganglia, the majority of labeled cell bodies contained VIP. In the nodose ganglion and cervical dorsal root ganglia, the majority of the labeled nerve cell bodies stored CGRP. The results indicate that the cervical esophagus has a dense innervation with multiple neurotransmitters emanating from several ganglia. As judged by the pattern of nerve fiber distribution, they may regulate esophageal peristalsis and blood flow, some of them possibly in a cooperative manner.

Amino Acid Oxidoreductases↗

Galactosialidosis: neuropathological findings in a case of the late-infantile type.

The neuropathological findings in a 13-year-old Japanese male showing decrease of sialidase and beta-galactosidase activities are reported. The patient was the product of normal pregnancy to consanguineous parents. He started to sit at 8 months, stand at 20 months and walk at age of 2; mental retardation, visual disturbance, cerebellar ataxia, myoclonus and epilepsy developed by the age of 10, and he died at 13. Neuropathological investigation revealed neuronal loss and storage. Severe loss of neurons was observed in the thalamus, globus pallidus, lateral geniculate body, gracile nucleus, Purkinje and retinal ganglion cells. Marked ballooning was seen in the Betz cells and neurons in the basal forebrain, the motor neurons in the cranial nerve nuclei and spinal cord, and in the trigeminal and spinal ganglia. The storage material varied in staining from region to region and from neuron to neuron. Electron microscopic investigation revealed a variety of intracytoplasmic and intranuclear inclusions: membranous cytoplasmic bodies, parallel, wavy-lamellar or tortuous tubular structures, lipofuscin-like irregular-shaped pleomorphic bodies, and cytoplasmic vacuoles with fine granules and lamellar materials. The severity of the neuronal loss did not seem to correlate with the amount of the storage materials, but with the presence of tortuous tubular inclusion.

Brain↗

Opposite effects of diabetes and galactosaemia on adenosine triphosphatase activity in rat nervous tissue.

This study measured the ouabain-sensitive adenosine triphosphatase activity in sciatic nerve, lumbar dorsal root ganglia and superior cervical ganglia from control rats, rats with 8 weeks streptozotocin-induced diabetes and rats fed a diet containing 20% galactose for 8 weeks. Whilst the sciatic nerves of the diabetic rats showed a 42% reduction in ouabain-sensitive adenosine triphosphatase activity, the galactose-fed rats showed an increase of 124% (p less than 0.01 and p less than 0.005, respectively, compared to controls). There was also a reduction (by 30% compared to controls; p less than 0.05) in the ouabain-sensitive adenosine triphosphatase activity of the dorsal root ganglia from the diabetic rats, but their superior cervical ganglia did not show a significant fall. The ganglia of the galactosaemic rats showed no change in ouabain-sensitive adenosine triphosphatase activity compared to controls. These changes coexisted with increases in appropriate polyol pathway metabolites in all tissues of both diabetic and galactosaemic rats. There were also depletions of myo-inositol in the sciatic nerves and dorsal root ganglia of diabetic and galactosaemic rats, but their superior cervical ganglia contained levels of myo-inositol which were similar to those of controls. The nerves of the galactosaemic rats showed increased water content; the nerves of the diabetic rats did not. The data argue against a simple relationship between myo-inositol depletion and impaired Na/K adenosine triphosphatase activity in association with exaggerated polyol pathway flux in peripheral nervous tissue.

Adenosine Triphosphatases↗