[Normal histology of the peripheral nervous system; the synaptic junctions; anatomic and experimental studies].
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Humans↗
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Glial-Schwann cell specialisations at the central-peripheral nervous system transition of a cyclostome: an ultrastructural study.
This study describes for the first time the central (CNS)-peripheral (PNS) nervous system transitional zone (TZ) of a member of the vertebrate class Agnatha, namely, the sea lamprey. It is concerned in particular with the glial tissue contribution to the TZ and the Schwann cell-CNS interface. Plastic-embedded specimens of spinal cord and nerve roots were examined using light and electron microscopy. At the TZ of each root a glial barrier, continuous with and similar in form to the surrounding glia limitans, stretches across the nerve bundle. In possessing such a barrier the lamprey TZ follows the general vertebrate pattern and differs from the Cephalochordata and invertebrates where a corresponding barrier is absent. The glial barrier is of similar thickness to the glia limitans generally, unlike in the mammal where it is thicker at the TZ than elsewhere. All lamprey axons are unmyelinated peripherally and most of them traverse the glial TZ barrier singly in individual tunnels. In this they resemble mammalian axons of similar calibre (which are, however, myelinated), but differ from unmyelinated mammalian axons, which generally traverse it in bundles. The lamprey TZ has specialisations not found in mammals. These include prominent, multiple interconnected strata of microfilament bundles which are continuous deeply with glial filament bundles and which lie under the surface plasmalemma of the glia limitans, to which they are connected by hemidesmosomes. Features of the mature lamprey TZ resemble those of developing mammalian TZs. For example, slender Schwann cell processes extend below the cord surface and become closely apposed to glial processes. In addition, together with the axon, the TZ glial processes and the basal lamina, they bound an extensive periaxonal network of spaces at the TZ, into which fine Schwann cell processes project. Accordingly, the networks could represent a primitive form of node gap.
Animals↗
Motor axon pathfinding in the peripheral nervous system.
Functional motor performance is dependent upon the correct assemblage of neural circuitry, a process initiated during embryonic development. How is the complicated neural circuitry that underlies functional behavior formed? During early stages of development, motor neurons extend their axons in a precise manner to their target destinations where they form fine synaptic connections. This process is not random but rather, highly stereotyped and specific. Results of recent studies indicate that positive and negative molecules influence particular steps in the navigation of motor axons to their targets. These molecules include, but are not limited to, members of the Semaphorin family and their receptors, Neuropilins and Plexins, Slits and their Robo receptors, members of the Eph family, extracellular matrix molecules, Hepatocyte Growth Factor/Scatter Factor, peanut agglutinin-binding glycoproteins, and neural cell adhesion molecule. The developing avian peripheral nervous system has served as an excellent model system for many years for studies of the basic cellular interactions that underlie motor axon pathfinding. The principal advantage for the experimental use of the avian embryo is the ease of access to early developmental events. Fine microsurgical manipulations, difficult at best in mouse embryonic development, are readily accomplished in avian embryos and have provided a powerful approach to unraveling the cellular interactions that govern motor axon pathfinding. These approaches, combined in recent years with molecular biology, have begun to produce critical insights into the mechanisms that sculpt cellular architecture during neural development.
Animals↗
Studies with antisera against peripheral nervous system myelin and myelin basic proteins. I. Effects of antiserum upon living cultures of nervous tissue.
We studied the effects of antiserum against rat peripheral nervous system (PNS) myelin, rat or chicken central nervous system myelin basic protein (BP), or rabbit P2 protein from PNS myelin on myelinated cultures containing only rat dorsal root ganglion neurons and Schwann cells. While anti-PNS myelin serum consistently produced segmental PNS demyelination, anti-BP serum and anti-P2 serum did not. The culture results suggest that the myelin PNS proteins P1 (identical to basic protein from central nervous system myelin) and P2 are not exposed on the extracellular surfaces of myelin-related Schwann cells in tissue culture.
Animals↗
The effect of 5-bromodeoxyuridine on remyelination in the peripheral nervous system of the mouse.
The thymidine analogue, 5-bromodeoxyuridine (BrdU), has been used in an attempt to manipulate experimentally the proliferative response of the Schwann cell population that follows induction of segmental demyelination in the peripheral nervous system. It was found that in the presence of BrdU, a significant number of Schwann cells displayed a susceptibility to the agent, in that they could be 'held' in the pro-myelinated state. It is suggested that there is some regulatory transition requiring the priming of the Schwann cell genome for myelination that occurs before the remyelinating phase of repair can be started, but after the establishment of the Schwann cell/axon relationship.
Animals↗
Differential distribution of (Na,K)-ATPase alpha isoform mRNAs in the peripheral nervous system.
mRNA transcripts for 3 isoforms of the alpha subunit of (Na,K)-ATPase have been previously identified in the nervous system (designated alpha 1, alpha 2, and alpha 3). In order to study the localization and expression of the different alpha isoforms in the peripheral nervous system, we prepared probes from the unique 3' untranslated region of alpha 1 cDNA, and from the translated region of alpha 3 cDNA. These probes were used in dot blot and in situ hybridization assays of rat spinal cord, dorsal root ganglia (DRG), and sciatic nerve. Within the ventral horn of lumbar spinal cord, alpha 1 mRNA was found in a discrete set of laterally placed motor neurons, while alpha 3 was found in all the identified neurons of the spinal cord, including those motor neurons containing alpha 1. In the lumbar DRG, alpha 3 was uniformly distributed in DRG neurons, while alpha 1 was abundant in some neurons but little or none was found in other neurons. Satellite cells contained neither isoform. Schwann cells in sciatic nerve were labeled with the alpha 1 probe in a perinuclear distribution, but contained no detectable alpha 3. Dot blot analysis showed alpha 1 and alpha 3 in spinal cord and DRG, but only alpha 1 in peripheral nerve.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Pressure wave injuries to the nervous system caused by high-energy missile extremity impact: Part I. Local and distant effects on the peripheral nervous system--a light and electron microscopic study on pigs.
Pigs were used for studies of effects on the peripheral nervous tissue of pressure waves induced by impact and passage through the left thigh of high-energy missiles. The short-lasting pressure waves were demonstrated to move close to the speed of sound and to have a spectrum of high frequencies and large amplitudes. The sciatic nerve in the contralateral leg showed no hemorrhage or major deformation. Both immediately after the missile impact and after 48 hr the myelin sheaths in the contralateral sciatic nerve showed deformation. Myelin was bulging into the axon, dislocating the axoplasm. The nodes of Ranvier could be exposed to an increased extent. Electron microscopic examination revealed decreased number of microtubules immediately after the trauma, persisting even after 48 hr in the largest axon. Schwann cells showed, especially after 48 hr, signs of damage and swelling. Similar changes, although less extensive, were noticed in the phrenic nerves as well as in unmyelinated axons in both sciatic and phrenic nerves. It is concluded that a high-energy missile hit in the thigh of a pig, caused structurally demonstrable dislocations of myelin sheaths, and disarrangement of cytoskeleton and endoplasmic reticulum in axons as well as other signs of damage. The changes may interfere with the normal functions of peripheral and autonomic nerves.
Abdomen↗
Neurons of the peripheral nervous system express thymidine phosphorylase.
Platelet-derived endothelial cell growth factor (PD-ECGF) is an angiogenic factor which recently has been shown to be identical to thymidine phosphorylase. We describe here, high levels of expression of PD-ECGF/thymidine phosphorylase in neurons of the peripheral nervous system (PNS) but very little in the central nervous system (CNS). Monoclonal and polyclonal antibodies were used for the staining of sections of dorsal root ganglia, sympathetic cervical ganglia and the enteric plexus as well as the brain and spinal cord. In addition, in situ hybridisation confirmed the results of immunohistochemistry. The possible role of thymidine phosphorylase in the PNS is discussed.
Animals↗
Peripheral nervous system involvement in a patient with large T-cell lymphoma arising from a pre-existing mycosis fungoides.
A 29-year-old man was examined for disseminated erythematous scaling patches and plaques and reddish, partially ulcerated nodules. Histological examination showed a dense, diffuse, epidermotropic infiltrate located in the entire dermis to the subcutaneous tissue, composed mainly of large pleomorphic T lymphocytes. Immunohistochemistry revealed positivity of neoplastic cells for T-cell-associated markers, negativity for CD30 antigen and for B-cell markers. Polymerase chain reaction analysis detected a clonal amplification of T-cell receptor gamma. Based on clinicopathological and molecular findings, the diagnosis of large T-cell lymphoma (LCL) arising from a pre-existing mycosis fungoides was made. Seven months after primary diagnosis, meningeal and peripheral nervous system involvement developed with no other evidence of systemic disease. Despite chemotherapy and radiation therapy, the patient died 3 months after the diagnosis of nervous system involvement. In patients with cutaneous LCL, mild neurological symptoms may precede the complete diagnostic picture by some weeks. A rapid and fatal progression characterizes the clinical course of the disease.
Adult↗
Differential expression of sodium channel mRNAs in rat peripheral nervous system and innervated tissues.
RNA blot hybridization analyses using probes specific for sodium channels I, II and III revealed high levels of sodium channel I mRNA and low levels of sodium channel II and III mRNAs in peripheral nervous system (PNS) tissues. The developmental expression patterns of these mRNAs were generally similar to those described for the central nervous system. The small amounts of sodium channel I and III mRNAs present in tongue muscle were greatly reduced after partial denervation. Expression of the three sodium channels thus appears to be restricted to the nervous system. Putative novel additional mRNAs, specifically expressed in the PNS, were detected with a probe that recognizes nucleotide sequences common to sodium channels I, II and III.
Animals↗
Hoxb-8 gain-of-function transgenic mice exhibit alterations in the peripheral nervous system.
To understand the developmental role of Hoxb-8, this relatively 5' Hoxb gene was ectopically expressed in embryonic regions where only more 3' Hox genes are normally expressed. Hoxb-8 coding sequences driven by a retinoic acid receptor beta2 promoter fragment were introduced in the mouse germ line by pronuclear injection. The promoter was chosen with the aim to extend rostrally the expression domain of the gene in neurectoderm and mesoderm at the time of development when Hox gene expression domains are being established. Embryos developing from DNA-injected zygotes, and from transgenic mouse lines were analyzed. Pattern alterations were observed in transgenic embryos, some of which involved the peripheral nervous system. Spinal ganglia in the mouse are first detectable around embryonic day 9.5. By day 11.5, the first of these ganglia (C1, Froriep's ganglion) has degenerated in the mouse and other amniotes. In contrast, this first ganglion did persist in the Hoxb-8 gain-of-function transgenic mice. We have started to take advantage of the phenotype of transgenic versus wild-type embryos to understand the mechanisms underlying the ontogeny and degeneration of Froriep's ganglion in wild-type mice, and the role of Hoxb-8 in C1 maintenance in transgenic embryos. The present work describes a morphological, histological and immunocytological analysis of both the degenerating and the permanent C1, and a preliminary characterization of the axonal extensions from the transgenic C1. We discuss the methodology of generating gain-of-function transgenic mice to study the genetics of pattern formation along the antero-posterior axis, and the usefulness of analyzing these particular Hoxb-8 transgenic embryos to understand some aspects of the ontogenesis and development of the upper cervical dorsal root ganglia.
Animals↗
GAP-43 is expressed by nonmyelin-forming Schwann cells of the peripheral nervous system.
Recently it has been demonstrated that the growth-associated protein GAP-43 is not confined to neurons but is also expressed by certain central nervous system glial cells in tissue culture and in vivo. This study has extended these observations to the major class of glial cells in the peripheral nervous system, Schwann cells. Using immunohistochemical techniques, we show that GAP-43 immunoreactivity is present in Schwann cell precursors and in mature non-myelin-forming Schwann cells both in vitro and in vivo. This immunoreactivity is shown by Western blotting to be a membrane-associated protein that comigrates with purified central nervous system GAP-43. Furthermore, metabolic labeling experiments demonstrate definitively that Schwann cells in culture can synthesize GAP-43. Mature myelin-forming Schwann cells do not express GAP-43 but when Schwann cells are removed from axonal contact in vivo by nerve transection GAP-43 expression is upregulated in nearly all Schwann cells of the distal stump by 4 wk after denervation. In contrast, in cultured Schwann cells GAP-43 is not rapidly upregulated in cells that have been making myelin in vivo. Thus the regulation of GAP-43 appears to be complex and different from that of other proteins associated with nonmyelin-forming Schwann cells such as N-CAM, glial fibrillary acidic protein, A5E3, and nerve growth factor receptor, which are rapidly upregulated in myelin-forming cells after loss of axonal contact. These observations suggest that GAP-43 may play a more general role in the nervous system than previously supposed.
Animals↗
[The brothers of Jumiege--the peripheral nervous system in early French mythology].
This article reviews the process of discovery of the nervous system from Pythagoras (570-500 BC) to Galen (130-201 AD). After Galen, no anatomical studies were performed before the renaissance. According to a legend, probably produced for political reasons, two brothers, sons of the French king Clovis II, revolted against their father and were sentenced to loose their physical powers by having the nerves of their arms and legs cut. They were then set adrift on the river Seine, stranding at the Jumiège monastery. The earliest written version of this legend stems from the fourteenth century; it was probably a part of the local French mythology. This indicates that the existence of the peripheral nervous system, and therefore also in part the knowledge contained in the early anatomical works, quite early may have been more or less known outside academic circles.
France↗
Expression of the large myelin-associated glycoprotein isoform during the development in the mouse peripheral nervous system.
The developmental maximum expression of the large myelin-associated glycoprotein isoform (L-MAG) protein prior to that of the small myelin-associated glycoprotein isoform (S-MAG) in both the central and peripheral nervous systems (CNS, PNS) in mice was shown by immunoblotting techniques using specific antibodies to the L-MAG protein and the S-MAG protein. Both the L-MAG protein and the S-MAG protein were expressed earlier in the PNS than in the CNS, which reflects earlier myelination in the PNS. The peak of the L-MAG protein concentration was 8 days in the sciatic nerve and 15 days in the brainstem. The concentration of the S-MAG protein in the sciatic nerve reached a peak at 15 days, whereas in the brainstem it increased rapidly between 15 and 20 days and gradually thereafter. Thus, the preceding maximum expression of the L-MAG during active myelination in the PNS demonstrated here as well as in the CNS strongly suggests an important role for L-MAG in myelin formation.
Aging↗
Studies of adhesion molecules mediating interactions between cells of peripheral nervous system indicate a major role for L1 in mediating sensory neuron growth on Schwann cells in culture.
The involvement of the adhesion molecules L1, N-CAM, and J1 in adhesion and neurite outgrowth in the peripheral nervous system was investigated. We prepared Schwann cells and fibroblasts (from sciatic nerves) and neurons (from dorsal root ganglia) from 1-d mice. These cells were allowed to interact with each other in a short-term adhesion assay. We also measured outgrowth of dorsal root ganglion neurons on Schwann cell and fibroblast monolayers. Schwann cells (which express L1, N-CAM, and J1) adhered most strongly to dorsal root ganglion neurons by an L1-dependent mechanism and less by N-CAM and J1. Schwann cell-Schwann cell adhesion was mediated by L1 and N-CAM, but not J1. Adhesion of fibroblasts (which express N-CAM, but not L1 or J1) to neurons or Schwann cells was mediated by L1 and N-CAM and not J1. However, inhibition by L1 and N-CAM antibodies was found to be less pronounced with fibroblasts than with Schwann cells. N-CAM was also strongly involved in fibroblast-fibroblast adhesion. Neurite outgrowth was most extensive on Schwann cells and less on fibroblasts. A difference in extent of neurite elongation was seen between small- (10-20 microns) and large- (20-35 microns) diameter neurons, with the larger neurons tending to exhibit longer neurites. Fab fragments of polyclonal L1, N-CAM, and J1 antibodies exerted slightly different inhibitory effects on neurite outgrowth, depending on whether the neurites were derived from small or large neurons. L1 antibodies interfered most strikingly with neurite outgrowth on Schwann cells (inhibition of 88% for small and 76% for large neurons), while no inhibition was detectable on fibroblasts. Similarly, although to a smaller extent than L1, N-CAM appeared to be involved in neurite outgrowth on Schwann cells and not on fibroblasts. Antibodies to J1 only showed a very small effect on neurite outgrowth of large neurons on Schwann cells. These observations show for the first time that identified adhesion molecules are potent mediators of glia-dependent neurite formation and attribute to L1 a predominant role in neurite outgrowth on Schwann cells which may be instrumental in regeneration.
Animals↗
Inducible nitric oxide synthase (iNOS) in immune-mediated demyelination and Wallerian degeneration of the rat peripheral nervous system.
The inducible isoform of nitric oxide synthase (iNOS), produces nitric oxide (NO) from l-arginine in response to inflammatory stimuli. NO sub-serves different functions from cytotoxicity to neuroprotection and triggers either necrosis or apoptosis. This study shows by Northern blot analysis that during experimental allergic neuritis (EAN), at the beginning of clinical signs, there is a transient extensive iNOS mRNA induction in nerve roots, in which morphology is mainly characterized by severe demyelination, but not in sciatic nerve, where scattered axonal degeneration is evident. Immunocytochemistry performed on teased nerve fibers and ultrastructural analysis showed that iNOS was localized in both inflammatory and Schwann cells, and the study of cell membrane permeability detected with fluorescent dyes showed a diffuse necrotic phenotype in the whole peripheral nervous system (PNS). With EAN clinical progression toward spontaneous recovery, endoneurial iNOS was rapidly down-regulated and in nerve roots almost all cells shifted their membrane permeability to an apoptotic phenotype, while necrosis persisted in sciatic nerve, until complete clinical recovery, when both root and nerve returned to normal. During wallerian degeneration following sciatic nerve transection, iNOS was undetectable in PNS, while endoneurial cell membrane had a diffuse necrotic phenotype. These data support the hypothesis that, during cell-mediated demyelination, iNOS may influence Schwann cell-axon relationship causing axonal damage and regulating endoneurial cell life and death.
Animals↗
Two novel mammalian Nogo receptor homologs differentially expressed in the central and peripheral nervous systems.
The regenerative capacity of the adult mammalian central nervous system is restricted by the myelinating oligodendrocytes that form a nonpermissive environment for axonal growth. Currently only the Nogo receptor (NgR), in complex with p75(NTR) neurotrophin receptor is known to be involved in this inhibitory signalling in neurons. NgR is a common receptor for the three inhibitory myelin proteins Nogo-A, OMgp, and MAG. Here we describe two novel Nogo receptor gene homologs named NGRL2 and NGRL3 from human and mouse that, like NGR, encode putative leucine-rich repeat containing GPI-anchored proteins. We show by in situ hybridisation and by RT-PCR that NGRL mRNAs are predominantly expressed in the neurons of the embryonic and adult central and peripheral nervous systems, and that they together with NGR possess distinct and partially nonoverlapping expression patterns. We also show that all four members of the reticulon family, including Nogo-A, are widely expressed in the nervous system, and therefore are possible ligands for the NgRLs.
Amino Acid Sequence↗
Considerations on neurotrophic relations in the central and peripheral nervous system.
The evidence for the existence of neurotrophic (non-impulse) influences is reviewed especially with respect to choice of adequate parameters and of differentiation of neurotrophic influences from other mechanisms affecting intercellular relations. The importance of growth processes in neurotrophic control is stressed, the mechanisms being apparently similar in the central and peripheral nervous system. Collateral sprouting as a compensatory response of the neuron on one hand and the old age changes at neuromuscular synapses resulting in "silent" synapses and later "silent" terminals present phenomena indicating mechanisms of growth and arrest of growth processes in neurotrophic control.
Aging↗