Membrane Specializations in Developing Nodes of Ranvier

1980 ◽  
Vol 38 ◽  
pp. 626-627
Author(s):  
J.H. Tao-Cheng ◽  
J. Rosenbluth
Keyword(s):  
Schwann Cell ◽  
Freeze Fracture ◽  
Structural Features ◽  
Nerve Fibers ◽  
Nodes Of Ranvier ◽  
Myelinated Nerve ◽  
Thin Sections ◽  
Frog Tadpole ◽  
Cell Layers ◽  
Mature Node

Mature myelinated nerve fibers exhibit distinctive structural features at nodes of Ranvier and the adjacent paranodal regions. In order to obtain information about the interrelationships between these specializations during development, thin sections and freeze-fracture replicas of immature peripheral nerve fibers from grass frog tadpole hind legs were examined during the period of myelinogenesis. Early in myelination axons are enwrapped individually by a few loose Schwann cell layers whose edges overhang each other forming "terminal loops" against the axolemma. Unlike those of the mature node, these loops are widely sepa-rated and irregularly spaced (Fig.l), and similarly the presumptive nodal region between successive developing myelin segments is usually much longer than adult nodes of Ranvier. The presumptive nodal axolemma may exhibit a cytoplasmic "undercoating." However, the density of this coating is highly variable. Usually it is much lower than at adult nodes, and in some cases the undercoating is not distinguishable. The outermost layers of the Schwann cell are usually the first to form axoglial junctional specializations character¬ized by the presence of "transverse bands" and ER cisternae applied to the junctional Schwann cell membrane. In some instances the outermost layer con¬tacts the axon over an extensive area and forms multiple small junctional specializations at widely separated intervals along the length of the axolemma.

scholarly journals THE ULTRASTRUCTURE OF ADULT VERTEBRATE PERIPHERAL MYELINATED NERVE FIBERS IN RELATION TO MYELINOGENESIS

1955 ◽  
Vol 1 (4) ◽  
pp. 271-278 ◽  
Author(s):  
J. David Robertson
Keyword(s):  
Electron Microscope ◽  
Schwann Cell ◽  
Cell Surface ◽  
Peripheral Nerve ◽  
Myelin Sheath ◽  
Nerve Fibers ◽  
Myelinated Nerve ◽  
Thin Sections ◽  
Double Membrane ◽  
Myelinated Nerve Fibers

Adult chameleon myelinated peripheral nerve fibers have been studied with the electron microscope in thin sections. The outer lamella of the myelin sheath has been found to be connected as a double membrane to the surface of the Schwann cell. The inner lamella is connected as a similar double membrane with the double axon-Schwann membrane. The relations of these double connecting membranes suggest that the layered myelin structure is composed of a double membrane which is closely wound about the axon as a helix. These findings support the new theory of myelinogenesis proposed recently by Geren. The possible significance of these results with respect to cell surface membranes and cytoplasmic double membranes is discussed.

Dedifferentiation of the Axolemma Associated with Demyelination

1981 ◽  
Vol 39 ◽  
pp. 496-497 ◽  
Author(s):  
J. Rosenbluth ◽  
A. Sumner ◽  
T. Saida
Keyword(s):  
Sodium Channels ◽  
Peripheral Nerves ◽  
Freeze Fracture ◽  
Fracture Analysis ◽  
Nerve Fibers ◽  
High Concentration ◽  
Myelinated Nerve ◽  
Spinal Roots ◽  
Myelin Deficient

Freeze-fracture analysis of myelinated nerve fibers has shown that the axolemma has a highly differentiated structure. The node is characterized by a high concentration of intramembranous particles, primarily in the E fracture face, which may represent the sodium channels known to be concentrated there, and the paranodal axolemma is characterized by a distinctive paracrystalline pattern that corresponds to the intercellular junction formed with the terminal “loops” of myelin lamellae. Studies of myelin formation in normal animals and of myelin-deficient mutant animals indicate that the development of these axolemmal specializations is profoundly influenced by the associated myelinforming cells. The present study considers whether or not nodal or paranodal specializations that have already formed persist after demyelination.In order to investigate this question, specimens of peripheral nerves were examined following exposure to an antiserum to galactocerebroside (GC), which is known to cause a predictable series of changes leading to demyelination. Freeze-fracture replicas of rat spinal roots exposed to anti-GC serum in situ for six hours showed marked changes in the paranodal axolemma.

The ultrastructure of Entamoeba sp. (Laredo isolate). Observations on thin sections and freeze-fracture preparations

1979 ◽  
Vol 57 (9) ◽  
pp. 1723-1735 ◽  
Author(s):  
Hampik S. Injeyan ◽  
Erwin Huebner
Keyword(s):  
Particle Density ◽  
Freeze Fracture ◽  
Structural Complexity ◽  
Structural Features ◽  
Nuclear Pore ◽  
Pore Density ◽  
Thin Sections ◽  
Membrane Surfaces ◽  
Intranuclear Microtubules ◽  
First Time

The ultrastructure of Entamoeba sp. (Laredo isolate), seen in thin section and in freeze-fracture preparation, indicates that numerous structural features are common to both this E. histolytica-like amoeba and "regular" strains. In addition, heavy meromyosin (HMM)-binding, actin-like microfilaments and intranuclear microtubules and microfilaments are demonstrated for the first time in Entamoeba. Cytoplasmic microtubules were not detected using two different fixation procedures. Replicas of freeze-fractured membrane surfaces revealed particle size and distribution to be heterogeneous on both fracture faces P and E and suggested a similar structural complexity to that previously described for the HK9 strain of E. histolytica. Particle density was determined in plasma and phagosome membranes, and an enrichment of 4.5-fold and 1.6-fold was estimated for the P and E faces, respectively, of phagosome membranes.Nuclear-pore distribution was heterogenous and pore density was highly variable in log-phase cells probably reflecting different cell-cycle stages. Possible differences in nuclear-pore density and distribution relative to published accounts on "regular" strains of E. histolytica are considered.

scholarly journals Damage and repair of the peripheral myelin sheath and node of Ranvier after treatment with trypsin.

1975 ◽  
Vol 64 (1) ◽  
pp. 1-14 ◽  
Author(s):  
R C Yu ◽  
R P Bunge
Keyword(s):  
Schwann Cell ◽  
Light And Electron Microscopy ◽  
Node Of Ranvier ◽  
Nerve Fibers ◽  
Myelinated Nerve ◽  
Nodal Region ◽  
Fetal Rat ◽  
The Matrix ◽  
Cell Processes

Cultures of whole fetal rat sensory ganglia which had matured and myelinated in culture were treated for 1-3 h with a pulse of 0.2% trypsin. The tissue was observed during the period of treatment and during subsequent weeks using both light and electron microscopy. Within minutes after trypsin addition the matrix of the culture was altered and the nerve fascicles loosened. Progressive changes included the retraction of Schwann cell processes from the nodal region the detachment of the myelin-related paranodal Schwann cell loops from the axon, and lengthening of the nodal region as the axon was bared. The retraction of myelin from nodal stabilized several hours after trypsin withdrawal. Breakdown of the altered myelin segments was rare. There were no discernable changes in neurons or their processes after this exposure to trypsin. The partial repair which occured over a period of several weeks included the reattachment of paranodal Schwann cell loops to the axolemma and the insertion of new myelin segments where a substantial length of axolemma had been bared. The significance of these observations to the characterization of the Schwann cell-axolemmal junctions on myelinated nerve fibers is discussed. The dramatic degree of myelin change that can occur without concomitant myelin breakdown is particularly noted, as is the observation that these altered myelin segments are, in part, repaired.

scholarly journals Myelination of peripheral nerves is controlled by PI4KB through regulation of Schwann cell Golgi function

2020 ◽  
Vol 117 (45) ◽  
pp. 28102-28113 ◽  
Author(s):  
Takashi Baba ◽  
Alejandro Alvarez-Prats ◽  
Yeun Ju Kim ◽  
Daniel Abebe ◽  
Steve Wilson ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerves ◽  
Large Diameter ◽  
Small Diameter ◽  
Nerve Fibers ◽  
Protein Glycosylation ◽  
Mutant Mice ◽  
Nodes Of Ranvier ◽  
Golgi Compartment ◽  
Sciatic Nerves

Better understanding myelination of peripheral nerves would benefit patients affected by peripheral neuropathies, including Charcot–Marie–Tooth disease. Little is known about the role the Golgi compartment plays in Schwann cell (SC) functions. Here, we studied the role of Golgi in myelination of peripheral nerves in mice through SC-specific genetic inactivation of phosphatidylinositol 4-kinase beta (PI4KB), a Golgi-associated lipid kinase. Sciatic nerves of such mice showed thinner myelin of large diameter axons and gross aberrations in myelin organization affecting the nodes of Ranvier, the Schmidt–Lanterman incisures, and Cajal bands. Nonmyelinating SCs showed a striking inability to engulf small diameter nerve fibers. SCs of mutant mice showed a distorted Golgi morphology and disappearance of OSBP at the cis-Golgi compartment, together with a complete loss of GOLPH3 from the entire Golgi. Accordingly, the cholesterol and sphingomyelin contents of sciatic nerves were greatly reduced and so was the number of caveolae observed in SCs. Although the conduction velocity of sciatic nerves of mutant mice showed an 80% decrease, the mice displayed only subtle impairment in their motor functions. Our analysis revealed that Golgi functions supported by PI4KB are critically important for proper myelination through control of lipid metabolism, protein glycosylation, and organization of microvilli in the nodes of Ranvier of peripheral nerves.

scholarly journals The mechanosensitive ion channel TRAAK is localized to the mammalian node of Ranvier

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Stephen G Brohawn ◽  
Weiwei Wang ◽  
Annie Handler ◽  
Ernest B Campbell ◽  
Jürgen R Schwarz ◽  
...  
Keyword(s):  
Action Potential ◽  
Polyclonal Antibodies ◽  
Node Of Ranvier ◽  
Nerve Fibers ◽  
K Channel ◽  
Resting Membrane Potential ◽  
Na Channel ◽  
Nodes Of Ranvier ◽  
Myelinated Nerve ◽  
Myelinated Nerve Fibers

TRAAK is a membrane tension-activated K+ channel that has been associated through behavioral studies to mechanical nociception. We used specific monoclonal antibodies in mice to show that TRAAK is localized exclusively to nodes of Ranvier, the action potential propagating elements of myelinated nerve fibers. Approximately 80 percent of myelinated nerve fibers throughout the central and peripheral nervous system contain TRAAK in what is likely an all-nodes or no-nodes per axon fashion. TRAAK is not observed at the axon initial segment where action potentials are first generated. We used polyclonal antibodies, the TRAAK inhibitor RU2 and node clamp amplifiers to demonstrate the presence and functional properties of TRAAK in rat nerve fibers. TRAAK contributes to the ‘leak’ K+ current in mammalian nerve fiber conduction by hyperpolarizing the resting membrane potential, thereby increasing Na+ channel availability for action potential propagation. We speculate on why nodes of Ranvier contain a mechanosensitive K+ channel.

scholarly journals Methylglyoxal Disrupts Paranodal Axoglial Junctions via Calpain Activation

ASN NEURO ◽  
2018 ◽  
Vol 10 ◽  
pp. 175909141876617 ◽  
Author(s):  
Ryan B. Griggs ◽  
Leonid M. Yermakov ◽  
Domenica E. Drouet ◽  
Duc V.M. Nguyen ◽  
Keiichiro Susuki
Keyword(s):  
Schwann Cell ◽  
Ex Vivo ◽  
Neurological Diseases ◽  
Nerve Fibers ◽  
Exposure Model ◽  
Calpain Inhibitor ◽  
Myelinated Nerve ◽  
Optic Nerves ◽  
Calpain Activation ◽  
Reactive Carbonyl Species

Nodes of Ranvier and associated paranodal and juxtaparanodal domains along myelinated axons are essential for normal function of the peripheral and central nervous systems. Disruption of these domains as well as increases in the reactive carbonyl species methylglyoxal are implicated as a pathophysiology common to a wide variety of neurological diseases. Here, using an ex vivo nerve exposure model, we show that increasing methylglyoxal produces paranodal disruption, evidenced by disorganized immunostaining of axoglial cell-adhesion proteins, in both sciatic and optic nerves from wild-type mice. Consistent with previous studies showing that increase of methylglyoxal can alter intracellular calcium homeostasis, we found upregulated activity of the calcium-activated protease calpain in sciatic nerves after methylglyoxal exposure. Methylglyoxal exposure altered clusters of proteins that are known as calpain substrates: ezrin in Schwann cell microvilli at the perinodal area and zonula occludens 1 in Schwann cell autotypic junctions at paranodes. Finally, treatment with the calpain inhibitor calpeptin ameliorated methylglyoxal-evoked ezrin loss and paranodal disruption in both sciatic and optic nerves. Our findings strongly suggest that elevated methylglyoxal levels and subsequent calpain activation contribute to the disruption of specialized axoglial domains along myelinated nerve fibers in neurological diseases.

Distal Sensorimotor Polyneuropathy in Mature Rottweiler Dogs

1994 ◽  
Vol 31 (3) ◽  
pp. 316-326 ◽  
Author(s):  
K. G. Braund ◽  
M. Toivio-Kinnucan ◽  
J. M. Vallat ◽  
J. R. Mehta ◽  
D. C. Levesque
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerves ◽  
Sensory Neuropathy ◽  
Nerve Fibers ◽  
Nerve Roots ◽  
Myelinated Nerve ◽  
Sensorimotor Polyneuropathy ◽  
Muscle Biopsies ◽  
Ultrastructural Findings ◽  
Dying Back

A polyneuropathy recognized in mature Rottweiler dogs is characterized by paraparesis that progresses to tetraparesis, spinal hyporeflexia and hypotonia, and appendicular muscle atrophy. Although signs may appear acutely, the course tends to be gradually progressive (up to 12 months or longer in some dogs) and may be relapsing. Nerve and muscle biopsies were examined from eight affected Rottweilers (six male and two female) between ages 1.5 and 4 years. Pronounced neurogenic atrophy was present in skeletal muscle samples. Changes in sensory and motor peripheral nerves included loss of myelinated nerve fibers, axonal necrosis, and variable numbers of fibers with inappropriately thin myelin sheaths. Ultrastructural findings included myelinated fibers showing myelinoaxonal necrosis, demyelinated fibers often associated with macrophage infiltration, many axons with myelinlike membranous profiles, increased endoneurial collagen, occasional axonal atrophy, and numerous Büngner bands. Lesions in unmyelinated fibers included increased numbers of Schwann cell profiles and loss of axons in Schwann cell subunits. Morphologic and morphometric studies indicated preferential loss of medium (5.5–8 μm) and large (8.5–12.5 μm) fibers, which was more severe in distal parts of nerves than in more proximal regions and nerve roots. The cause was not determined; however, histopathologic studies suggest this condition is a dying-back distal sensorimotor polyneuropathy that has morphologic and morphometric similarities to hereditary motor and sensory neuropathy (HMSN) type II in humans.

scholarly journals An isoform of ankyrin is localized at nodes of Ranvier in myelinated axons of central and peripheral nerves.

1990 ◽  
Vol 110 (4) ◽  
pp. 1341-1352 ◽  
Author(s):  
E Kordeli ◽  
J Davis ◽  
B Trapp ◽  
V Bennett
Keyword(s):  
Sodium Channel ◽  
Gray Matter ◽  
Peripheral Nerves ◽  
Neuronal Cells ◽  
Specific Interaction ◽  
Nerve Fibers ◽  
Nodes Of Ranvier ◽  
Myelinated Axons ◽  
Myelinated Nerve ◽  
Voltage Dependent

Two variants of ankyrin have been distinguished in rat brain tissue using antibodies: a broadly distributed isoform (ankyrinB) that represents the major form of ankyrin in brain and another isoform with a restricted distribution (ankyrinR) that shares epitopes with erythrocyte ankyrin. The ankyrinR isoform was localized by immunofluorescence in cryosections of rat spinal cord gray matter and myelinated central and peripheral nerves to: (a) perikarya and initial axonal segments of neuron cells, (b) nodes of Ranvier of myelinated nerve with no detectable labeling in other areas of the myelinated axons, and (c) the axolemma of unmyelinated axons. Immunogold EM on ultrathin cryosections of myelinated nerve showed that ankyrinR was localized on the cytoplasmic face of the axolemma and was restricted to the nodal and, in some cases, paranodal area. The major isoform of ankyrin in brain (ankyrinB) displayed a broad distribution on glial and neuronal cells of the gray matter and a mainly glial distribution in central myelinated axons with no significant labeling on the axolemma. These results show that (a) ankyrin isoforms display a differential distribution on glial and neuronal cells of the nervous tissue; (b) an isoform of ankyrin codistributes with the voltage-dependent sodium channel in both myelinated and unmyelinated nerve fibers. Ankyrin interacts in vitro with the voltage-dependent sodium channel (Srinivasan, Y., L. Elmer, J. Davis, V. Bennett, and K. Angelides. 1988. Nature (Lond.). 333:177-180). A specific interaction of an isoform of ankyrin with the sodium channel thus may play an important role in the morphogenesis and/or maintenance of the node of Ranvier.

Gap junctions in the prothoracic glands of the tobacco hornworm, Manduca sexta

1992 ◽  
Vol 50 (1) ◽  
pp. 706-707
Author(s):  
Ji-da Dai ◽  
M. Joseph Costello ◽  
Lawrence I. Gilbert
Keyword(s):  
Gap Junctions ◽  
Small Molecules ◽  
Manduca Sexta ◽  
Freeze Fracture ◽  
Cell Communication ◽  
Cellular Level ◽  
Thin Sections ◽  
Prothoracic Glands ◽  
Polyhydroxylated Steroids ◽  
Stimulation Of

Insect molting and metamorphosis are elicited by a class of polyhydroxylated steroids, ecdysteroids, that originate in the prothoracic glands (PGs). Prothoracicotropic hormone stimulation of steroidogenesis by the PGs at the cellular level involves both calcium and cAMP. Cell-to-cell communication mediated by gap junctions may play a key role in regulating signal transduction by controlling the transmission of small molecules and ions between adjacent cells. This is the first report of gap junctions in the PGs, the evidence obtained by means of SEM, thin sections and freeze-fracture replicas.

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