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Brain Research Jun 1998The involvement of terminal sprouts in neurotransmitter release by in vivo botulinum type-A toxin poisoned motor endings was investigated 15 to 40 days after a single...
The involvement of terminal sprouts in neurotransmitter release by in vivo botulinum type-A toxin poisoned motor endings was investigated 15 to 40 days after a single injection of the toxin onto the levator auris longus muscle of the mouse. Enhanced quantal acetylcholine release was induced by alpha-latrotoxin or La3+ in conditions that prevent endocytosis, and an antibody directed against the lumenal domain of synaptotagmin II (Syt II) was used in the presence or absence of Triton X-100. We showed that, under resting conditions, the intravesicular domain of Syt II requires Triton X-100 to be labelled, whereas it becomes exposed to the outside of the axolemma of both the original terminal arborization and the newly formed sprouts during enhanced exocytosis. These data were taken to indicate that, when sprouting is prominent, the whole modified terminal arborization, including the original branches and the sprouts, possesses the machinery for Ca2+-independent exocytosis.
Topics: Acetylcholine; Animals; Botulinum Toxins, Type A; Exocytosis; Female; Lanthanum; Mice; Motor Neurons; Nerve Endings; Nerve Tissue Proteins; Neuromuscular Junction; Presynaptic Terminals; Spider Venoms; Synaptic Transmission; Synaptotagmin II
PubMed: 9666170
DOI: 10.1016/s0006-8993(98)00475-2 -
Reviews in the Neurosciences 2006The myelinated axon can be divided into three domains: the internodal axon, the paranodal axon and the nodal axon. The internodal axolemma contains high concentrations... (Review)
Review
The myelinated axon can be divided into three domains: the internodal axon, the paranodal axon and the nodal axon. The internodal axolemma contains high concentrations of K+ channels that are enriched in the juxtaparanodal region, whereas Na+ channels cluster in the node. This molecular organization of the myelinated axon membrane is critically important for the rapid and successful transmission of electrical impulses. The juxtaparanodal K+ channels are believed to be electrically inactive in adult peripheral nerves, but experiments with blocking drugs and genetic deletion have shown that they may serve important functions at earlier developmental stages, and during remyelination and regeneration.
Topics: Animals; Nerve Degeneration; Nerve Fibers, Myelinated; Neural Conduction; Shaker Superfamily of Potassium Channels
PubMed: 16878404
DOI: 10.1515/revneuro.2006.17.3.369 -
Brain Research Jul 1984The saturable uptake of tritium-labeled saxitoxin by the rat left cervical sympathetic trunk, which consists almost entirely of unmyelinated fibers, indicates that the...
The saturable uptake of tritium-labeled saxitoxin by the rat left cervical sympathetic trunk, which consists almost entirely of unmyelinated fibers, indicates that the density of sodium channels on the axolemma of these fibers is about 200 channels/microns 2.
Topics: Animals; Axons; Ion Channels; Male; Microscopy, Electron; Rats; Rats, Inbred Strains; Saxitoxin; Sodium; Sympathetic Nervous System
PubMed: 6331604
DOI: 10.1016/0006-8993(84)90442-6 -
Brain and Nerve = Shinkei Kenkyu No... Nov 2015Guillain-Barré syndrome is composed of two distinct clinicopathological entities: acute inflammatory demyelinating polyradiculoneuropathy (AIDP), and acute motor or... (Review)
Review
Guillain-Barré syndrome is composed of two distinct clinicopathological entities: acute inflammatory demyelinating polyradiculoneuropathy (AIDP), and acute motor or motor and sensory axonal neuropathy (AMAN and AMSAN). AIDP is characterized by the patchily distributed demyelinative foci throughout the peripheral nervous system (PNS), whereas in AMAN/AMSAN primary axonal degeneration is observed in the PNS, particularly accentuated at the spinal nerve roots. The aim of this article is to provide an overview of previous findings regarding GBS pathology and thus, to elucidate the pathomechanisms of this life-threatening disorder. The most critical cause for AIDP may be the autoimmune attack on the Schwann cell membrane wrapping the myelinated nerve fibers, and that in AMAN/AMSAN may be an antibody-mediated attack on the axolemma at the nodes of Ranvier.
Topics: Animals; Antibodies; Axons; Guillain-Barre Syndrome; Humans; Myelin Sheath; Peripheral Nervous System; Spinal Nerve Roots
PubMed: 26560948
DOI: 10.11477/mf.1416200303 -
Developmental Biology Jun 1986Axonal and axolemmal development of fibers from rat optic nerves in which gliogenesis was severely delayed by systemic injection of 5-azacytidine (5-AZ) was examined by...
Axonal and axolemmal development of fibers from rat optic nerves in which gliogenesis was severely delayed by systemic injection of 5-azacytidine (5-AZ) was examined by freeze-fracture electron microscopy. In neonatal (0-2 days) rat optic nerves, all fibers lack myelin, whereas in the adult, virtually all axons are myelinated. The axolemma of neonatal premyelinated fibers is relatively undifferentiated. The P-fracture face (P-face) displays a moderate (approximately 550/micron 2) density of intramembranous particles (IMPs), whereas the E-fracture face (E-face) has few IMPs (approximately 125/micron 2) present. By 14 days of age, approximately 25% of the axons within control optic nerves are ensheathed or myelinated, with the remaining axons premyelinated. The ensheathed and myelinated fibers display increased axonal diameter compared to premyelinated axons, and these larger caliber fibers exhibit marked axonal membrane differentiation. Notably, the P-face IMP density of ensheathed and myelinated fibers is substantially increased compared to premyelinated axolemma, and, at nodes of Ranvier, the density of E-face particles is moderately high (approximately 1300/micron 2), in comparison to internodal or premyelinated E-face axolemma. In optic nerves from 14-day-old 5-AZ-treated rats, few oligodendrocytes are present, and the percentage of myelinated fibers is markedly reduced. Despite delayed gliogenesis, some unensheathed axons within 5-AZ-treated optic nerves display an increased axonal diameter compared to premyelinated fibers. Most of these large caliber fibers also exhibit a substantial increase in P-face IMP density. Small (less than 0.4 micron) diameter unensheathed axons within treated optic nerves maintain a P-face IMP density similar to that of control premyelinated fibers. Regions of increased E-face particle density were not observed. The results demonstrate that some aspects of axolemma differentiation continue despite delayed gliogenesis and the absence of glial ensheathment, and suggest that axolemmal ultrastructure is, at least in part, independent of glial cell association.
Topics: Animals; Axons; Azacitidine; Freeze Fracturing; Microscopy, Electron; Myelin Sheath; Neuroglia; Optic Nerve; Rats
PubMed: 2423398
DOI: 10.1016/0012-1606(86)90251-4 -
Expert Review of Neurotherapeutics Jun 2009Guillain-Barré syndrome (GBS) includes demyelinating and axonal subtypes with different immunopathologic mechanisms. In acute inflammatory demyelinating... (Review)
Review
Guillain-Barré syndrome (GBS) includes demyelinating and axonal subtypes with different immunopathologic mechanisms. In acute inflammatory demyelinating polyradiculoneuropathy, segmental demyelination and conduction block are the pathological and electrophysiological correlates of muscle weakness. Slowed conductions and increased temporal dispersion of motor responses are more characteristic of the remyelinative phase and do not affect muscle power. In acute motor axonal neuropathy, muscle weakness has been correlated with an antibody-mediated primary axonal degeneration. Conduction block that recovers without development of increased temporal dispersion or other demyelinating features, however, has been described in some patients with antiganglioside antibodies and related to a physiologic conduction block at the axolemma of the Ranvier node. Severity of axonal damage induced by antiganglioside antibodies may vary from reversible functional impairment of nodal axolemma to complete axonal damage with subsequent Wallerian degeneration. In early GBS, current electrophysiologic criteria are unable to distinguish with certainty different subtypes. Serial electrophysiologic studies are mandatory for identification of GBS subtypes and to elucidate the pathophysiologic mechanisms of muscle weakness among demyelination, axonal degeneration and physiologic conduction block.
Topics: Guillain-Barre Syndrome; Humans; Models, Immunological; Muscle Contraction; Muscle Weakness; Muscle, Skeletal
PubMed: 19496690
DOI: 10.1586/ern.09.43 -
ASN Neuro Mar 2011The ability of an AEF (axolemma-enriched fraction) to influence the proliferation, survival and differentiation of OPC (oligodendrocyte progenitor cells) was evaluated....
The ability of an AEF (axolemma-enriched fraction) to influence the proliferation, survival and differentiation of OPC (oligodendrocyte progenitor cells) was evaluated. Following addition of AEF to cultured OPC, the AEF associated with the outer surface of OPC so that subsequent metabolic events were likely mediated by direct AEF-OPC contact. Addition of AEF to the cultured OPC resulted in a dose- and time-dependent increase in proliferation that was partially dependent on Akt (protein kinase B) and MAPK (mitogen-activated protein kinase) activation. The major mitogen in an AEF-SE (soluble 2.0 M NaCl extract of the AEF) was identified as aFGF (acidic fibroblast growth factor) and accounted for 50% of the mitogenicity. The remaining 50% of the mitogenicity had properties consistent with bFGF (basic fibroblast growth factor) but was not unequivocally identified. Under conditions that limit the survival of OPC in culture, AEF treatment prolonged the survival of the OPC. Antigenic and morphological examination of the AEF-treated OPC indicated that the AEF treatment helped the OPC survive in a more immature state. The potential downstream metabolic pathways potentially activated in OPC by AEF and the consequences of these activated pathways are discussed. The results of these studies are consistent with the view that direct contact of axons with OPC stimulates their proliferation and survival while preventing their differentiation.
Topics: Animals; Animals, Newborn; Cell Count; Cell Differentiation; Cell Proliferation; Cells, Cultured; Cellular Structures; Chromatography, Agarose; Hot Temperature; Mitogen-Activated Protein Kinases; Mitogens; Neurons; Oligodendroglia; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Schwann Cells; Stem Cells; Trypsin
PubMed: 21345173
DOI: 10.1042/AN20100035 -
Proceedings of the Royal Society of... May 1978
Topics: Animals; Axons; Female; Mice; Muscular Dystrophy, Animal; Myelin Sheath; Ranvier's Nodes
PubMed: 27805
DOI: 10.1098/rspb.1978.0047 -
The Journal of General Physiology May 1971The penetration of (14)C-labeled ethylene glycol, erythritol, mannitol, and sucrose was measured in giant axons of various diameters isolated from the hindmost stellar...
The penetration of (14)C-labeled ethylene glycol, erythritol, mannitol, and sucrose was measured in giant axons of various diameters isolated from the hindmost stellar nerves of Doryteuthis plei squid. Axon diameter depends mainly on the age of the squid. The influx of (22)Na, some electrical properties, and the ultrastructure of the axolemma were also studied. The results confirm our previous observation that in medium sized axons of D. plei stimulation causes an increase in the permeability to the penetration of erythritol, mannitol, and sucrose. They also demonstrate that the magnitude of the increase in the penetration of these probing molecules diminishes progressively as the axon diameter increases. The diminution in permeability may be due to a reduction in size of the pathways used by nonelectrolytes to enter the axon. No effect of stimulation on the ethylene glycol permeability is observed. The sodium influx and electrical properties are independent of axon size. The ultrastructural study shows that the axolemma thickness increases with axon diameter. The present experiments indicate that the nonelectrolyte permeability of stimulated axons depends on nerve fiber properties related to axon diameter and on the size of the hydrophilic nonelectrolyte probe.
Topics: Action Potentials; Alcohols; Animals; Axons; Carbon Isotopes; Diffusion; Electrophysiology; Erythritol; Glycols; Mannitol; Membrane Potentials; Mollusca; Permeability; Sodium; Sodium Isotopes; Sucrose
PubMed: 5553105
DOI: 10.1085/jgp.57.5.623 -
Experimental Neurology Jun 2012Serum antibodies to different gangliosides have been identified in some Guillain-Barré (GBS) subtypes and variants. In the January issue of Experimental Neurology... (Review)
Review
Serum antibodies to different gangliosides have been identified in some Guillain-Barré (GBS) subtypes and variants. In the January issue of Experimental Neurology Susuki and colleagues (2012) showed that in experimental neuropathies associated with antibodies to GM1, GD1a and GD1b the common mechanism is a complement mediated dysfunction and disruption of the nodes of Ranvier which causes a pathophysiological continuum from early reversible conduction failure to axonal degeneration. These observations, correlated and integrated with electrophysiological and pathological findings in humans indicate that the GBS subtypes acute motor conduction block neuropathy, acute motor axonal neuropathy, acute motor and sensory neuropathy and acute sensory neuropathy and possibly also a chronic disorder as multifocal motor neuropathy represent a spectrum of the same immunopathologic process. Being the nodal axolemma and the paranode the focus of the nerve injury, these immune mediated neuropathies could be more properly classified as nodo-paranodopathies.
Topics: Animals; Autoantibodies; Gangliosides; Guillain-Barre Syndrome; Humans; Polyneuropathies; Sphingolipid Activator Proteins
PubMed: 22507308
DOI: 10.1016/j.expneurol.2012.03.023