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PubMed1981

Nodal axon diameter correlates linearly with internodal axon diameter in spinal roots of the cat.

Nodal and internodal axon diameters of individual myelinated nerve fibres were measured electron microscopically in fibre samples from serially sectioned L7 ventral and dorsal spinal root of young adult cats. Axon cross-sectional area at the node of Ranvier in axons more than 4 micrometer in diameter was reduced to less than 20% of its internodal value. Internodal and nodal axon diameters showed a rectilinear distribution and linear regression analysis gave coefficients of correlation between 0.93 and 0.99. An individual nodal diameter value could be fitted to an internodal axon diameter value in a 95% prediction interval of +/- 1.06-2.41 micrometer.

Animals↗

PubMed1988

Studies of axon-glial cell interactions and periaxonal K+ homeostasis--III. The effect of anisosmotic media and potassium on the relationship between the resistance in series with the axon membrane and glial cell volume.

The effect of anisosmotic physiological solutions and [K+]o on the resistance in series with the axon membrane were studied in medial giant axons of the crayfish, Procambarus clarkii, to determine if changes in series resistance are correlated with changes in glial cell volume and volume regulatory responses. Series resistance was estimated from computer analysed voltage waveforms generated by constant current and space clamp techniques using piggy-back axial wire current passing and glass pipette recording electrodes. Axons subjected to anisosmotic physiological solution in the range of 23 to 175% of isosmolar solution demonstrated that the series resistance of axons changes in a manner similar to that expected for a volume change in isolated cells. In hyperosmotic solution the series resistance changes biphasically, initially decreasing followed by a recovery of the series resistance, similar to the regulatory volume increase described for glial cells in culture. The increase in series resistance following the initial decrease is inhibited by bumetanide (0.1 mM). Ouabain (1 mM), an inhibitor of the volume decreasing Na-K pump, causes the series resistance to increase significantly above that seen for the no-drug control. Bumetanide, an inhibitor of the volume increasing Na-K-Cl cotransporter, inhibits the volume regulatory response to anisosmotic media. Treating the axon with three times normal external [K+] causes the series resistance to decrease approximately 15% while five times normal [K+] leads to a 15% increase in series resistance. Both ouabain and d-tubocurare (10(-p8) M) prevent the three-fold [K+]-induced decrease in series resistance while carbachol (10(-7) M) and bumetanide have little effect. On the other hand, ouabain enhances the five-fold [K+]-induced increase in series resistance while carbachol and bumetanide cause the five-fold [K+] response to be in a decreasing direction. d-Tubocurare has little effect on the five-fold [K+]-induced increase in series resistance. The study demonstrates that under the conditions of these experiments changes in series resistance are a reflection of changes in cell volume modulated by ouabain- and bumetanide-sensitive K+ uptake mechanisms. The effects of carbachol and d-tubocurare on the series resistance suggest that their effects are modulated through their actions on the glial cell membrane potential and the electrochemical gradient for K+, which in turn controls the amount of K+ that appears in the periaxonal space.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1987

Axonal maturation in development--I. Characterization of monoclonal antibodies reacting with axon-specific neurofilament epitopes.

Monoclonal antibodies reacting with the high molecular weight neurofilament polypeptides (NF 150K and NF 200K) were obtained upon immunization with NF 150K and NF 200K isolated from bovine spinal cord by anion exchange chromatography. The five monoclonal antibodies obtained with NF 200K stained only axons. With three monoclonals the reactivity was abolished by digestion with phosphatase and by dilution of the supernatants in sodium potassium phosphate. The nine monoclonal antibodies obtained upon immunization with NF 150K stained both high molecular weight neurofilament polypeptides on immunoblots of bovine and rat spinal cord extracts with the exception of one monoclonal only reacting with the homologous antigen. The antibodies could be divided into two groups, axon-specific and conventional. Conventional antibodies decorated neurofilaments regardless of their location, i.e. axons, perikarya and dendrites. With all these antibodies the immunostaining was not affected by phosphatase digestion of neurofilament protein nor by dilution of the supernatants in sodium potassium phosphate. Axon-specific antibodies reacting with both NF 150K and NF 200K in rat spinal cord only stained the heterologous antigen (NF 200K) in rat optic nerve and sciatic nerve extracts. We suggest that some axon-specific neurofilament antibodies recognize neurofilament modifications other than phosphorylation; or, alternatively that they react with phosphorylated epitopes not accessible to phosphate or to exogenous phosphatases. Furthermore, we suggest that some neurofilament modifications do not occur uniformly throughout the nervous system.

Animals↗

PubMed2004

Axonal heparan sulfate proteoglycans regulate the distribution and efficiency of the repellent slit during midline axon guidance.

The presentation of secreted axon guidance factors plays a major role in shaping central nervous system (CNS) connectivity. Recent work suggests that heparan sulfate (HS) regulates guidance factor activity; however, the in vivo axon guidance roles of its carrier proteins (heparan sulfate proteoglycans, or HSPGs) are largely unknown. Here we demonstrate through genetic analysis in vivo that the HSPG Syndecan (Sdc) is critical for the fidelity of Slit repellent signaling at the midline of the Drosophila CNS, consistent with the localization of Sdc to CNS axons. sdc mutants exhibit consistent defects in midline axon guidance, plus potent and specific genetic interactions supporting a model in which HSPGs improve the efficiency of Slit localization and/or signaling. To test this hypothesis, we show that Slit distribution is altered in sdc mutants and that Slit and its receptor bind to Sdc. However, when we compare the function of the transmembrane Sdc to a different class of HSPG that localizes to CNS axons (Dallylike), we find functional redundancy, suggesting that these proteoglycans act as spatially specific carriers of common HS structures that enable growth cones to interact with and perceive Slit as it diffuses away from its source at the CNS midline.

Animals↗

PubMed2006

Retroviral misexpression of cVax disturbs retinal ganglion cell axon fasciculation and intraretinal pathfinding in vivo and guidance of nasal ganglion cell axons in vivo.

The transcription factor cVax (Vax2) is expressed in the ventral neural retina and restricted expression is a prerequisite for at least three prominent aspects of retinal dorsal-ventral patterning: polarized expression of EphB/B-ephrin molecules, the retinotectal projection and the distribution of rod photoreceptors across the retina. In the chick retina, the fasciculation pattern of ganglion cell axons also differs between the dorsal and ventral eye. To investigate the molecular mechanisms involved, the nerve fiber layer was analyzed after retroviral misexpression of several factors known to regulate the positional specification of retinal ganglion cells. Forced cVax expression ventralized the fasciculation pattern and caused axon pathfinding errors near the optic disc. Ectopic expression of different ephrin molecules indicated that axon fasciculation is, at least in part, mediated by the EphB system. Finally, we report that retroviral misexpression of cVax increased the pool of EphA4 receptors phosphorylated on tyrosine residues and altered the guidance preference of nasal axons in vitro. These results identify novel functions for cVax in intraretinal axon fasciculation and pathfinding as well as suggest a mechanism to explain how restricted cVax expression may influence map formation along the dorso-ventral and antero-posterior axes of the optic tectum.

Animals↗

PubMed2001

Inflammation with no axonal damage of the rat saphenous nerve trunk induces ectopic discharge and mechanosensitivity in myelinated axons.

Inflammation along a nerve trunk with no frank axonal nerve damage produced by complete Freund's adjuvant (CFA) or Carrageenan is known to induce a painful peripheral neuropathy. In the present study, we examined the electrophysiological properties of myelinated axons (spontaneous discharge and mechanical sensitivity) at the inflamed nerve site. The rat saphenous nerves were exposed at mid-thigh level and wrapped in 2 mm wide bands of haemostatic oxidized cellulose (Oxycel) that were saturated with undiluted CFA. In the control rats the Oxycel) was saturated with saline. At postoperative days (PODs) 2-5 and 6-10, fine axon bundles were teased from the nerve, and electrophysiological recordings performed. At both time points spontaneous activity at the site of the application in CFA rats (PODs 2-5=9.9+/-2.5%: PODs 6-10=6.1+/-1.4%) was significantly higher than in the control animals (PODs 2-5=2.9+/-1.1%: PODs 6-10=1.6+/-1.4%: P=0.03, P=0.02, respectively). Mechanical sensitivity at both time points was significantly higher in CFA rats (PODs 2-5=12.6+/-3.1%: PODs 6-10=10.3+/-3.1%) than in saline rats (PODs 2-5=3.4+/-2.91%: PODs 6-10=0.8+/-1.0%: P=0.03, P=0.04, respectively). This study clearly shows that perineural inflammation with no axonal nerve damage induced by CFA application around the nerve trunk elevates spontaneous activity and induces mechanosensitivity in myelinated axons.

Action Potentials↗

PubMed1998

Axon-glial relations during regeneration of axons in the adult rat anterior medullary velum.

The anterior medullary velum (AMV) of adult Wistar rats was lesioned in the midsagittal plane, transecting all decussating axons including those of the central projection of the IVth nerve. At selected times up to 200 days after transection, the degenerative and regenerative responses of axons and glia were analyzed using transmission and scanning electron microscopy and immunohistochemistry. In particular, both the capacity of oligodendrocytes to remyelinate regenerated fibers and the stability of the CNS/PNS junctional zone of the IVth nerve rootlet were documented. Transected central AMV axons exhibited four patterns of fiber regeneration in which fibers grew: rostrocaudally in the reactive paralesion neuropil (Group 1); randomly within the AMV (Group 2); into the ipsilateral IVth nerve rootlet, after turning at the lesion edge and growing recurrently through the old degenerated contralateral central trochlear nerve trajectory (Group 3); and ectopically through paralesion tears in the ependyma onto the surface of the IVth ventricle (Group 4). Group 1-3 axons regenerated unperturbed through degenerating central myelin, reactive astrocytes, oligodendrocytes, microglia, and large accumulations of hematogenous macrophages. Only Group 3 axons survived long term in significant numbers, and all became myelinated by oligodendrocytes, ultimately establishing thin sheaths with relatively normal nodal gaps and intersegmental myelin sheath lengths. Schwann cells at the CNS/PNS junction of the IVth nerve rootlet did not invade the CNS, but astrocyte processes grew across the junction into the PNS portion of the IVth nerve. The basal lamina of the junctional glia limitans remained stable throughout the experimental period.

Animals↗

PubMed1982

Microinjection into an identified axon to study the mechanism of fast axonal transport.

Microinjection into an axon of an identified invertebrate neuron is shown to be a useful technique for analyzing the mechanisms of fast axonal transport. It permits direct assessment of the effect of agents that cannot permeate the plasma membrane on the translocation of material in the axon. The actin filament depolymerizer DNase I, when injected into the axon of the Aplysia neuron R2, caused a local block of fast transport of [3H]glycoprotein. Two agents that should interfere with the functioning of actin filaments without causing extensive depolymerization, tne N-ethylmaleimide-modified nuclease S1 fragment of myosin (injected) and dihydrocytochalasin B (applied externally). had no effect. Together these results suggest that actin plays a structural role in the axonal cytoskeleton rather than a role in transport force generation, the effect of DNase I being mediated by structural disordering of the axoplasm. Experiments were also done with inhibitors of dynein, the microtubule-associated ATPase. erythro-9-[3-(2-Hydroxynonyl)]adenine blocked transport but vanadate was ineffective.

Actins↗

PubMed1984

Axonal tubulin and axonal microtubules: biochemical evidence for cold stability.

Nerve extracts containing tubulin labeled by axonal transport were analyzed by electrophoresis and differential extraction. We found that a substantial fraction of the tubulin in the axons of the retinal ganglion cell of guinea pigs is not solubilized by conventional methods for preparation of microtubules from whole brain. In two-dimensional polyacrylamide gel electrophoresis this cold-insoluble tubulin was biochemically distinct from tubulin obtained from whole brain microtubules prepared by cold cycling. Cleveland peptide maps also indicated some differences between the cold-extractable and cold-insoluble tubulins. The demonstration of cold-insoluble tubulin that is specifically axonal in origin permits consideration of the physiological role of cold-insoluble tubulin in a specific cellular structure. It appears likely that much of this material is in the form of cold-stable microtubules. We propose that the physiological role of cold-insoluble tubulin in the axon may be associated with the regulation of the axonal microtubule complexes in neurons.

Animals↗

PubMed2005

Axonal oscillations in developing mammalian nerve axons.

We study neuronal spike propagation in a developing myelinated axon in various stages of its development through detailed computational modeling. Recently, a form of bursting (axonal bursting), has been reported in axons in developing nerves in the absence of potassium channels. We present a computational study using a detailed model for a myelinated nerve in development to explore under what circumstances such an effect can be expected. It is shown that axonal oscillation may be caused by backfiring between the nodes of Ranvier or through backfiring from internodal sodium channels or by reducing the thickness of the myelin wrapping the axon between the nodes of Ranvier.

Action Potentials↗

PubMed1986

Axonal transport of synapsin I- and cholinergic synaptic vesicle-like material; further immunohistochemical evidence for transport of axonal cholinergic transmitter vesicles in motor neurons.

The axonal transport of organelles in motor axons in the sympathectomized rat sciatic has been studied using two antisera which recognize specific components of synaptic vesicles. Anti-synapsin I recognizes synapsin I (SYN I) which is affiliated with the external membrane of synaptic vesicles, while rabbit-anti-synaptic vesicle antiserum (RASVA) recognizes integral membrane glycoproteins in cholinergic synaptic vesicles. Immunofluorescence studies, including cytofluorimetric scanning, show that immunoreactive (IR) material recognized by both antisera: rapidly accumulate proximal to a crush; the material has a granular appearance in the microscope; is redistributed in an isolated segment, and that the transport of the material is sensitive to vinblastine. Thus the proximodistal transport has the characteristics of fast axonal transport. Furthermore, recycling organelles, accumulating on the distal side of a crush are recognized by RASVA, but carry only very little SYN I-IR. The results give further support to the hypothesis that motor cholinergic axons transport axonal cholinergic vesicles towards the motor endplates.

Animals↗

PubMed1990

Vasopressinergic axon collaterals and axon terminals in the magnocellular neurosecretory nuclei of the rat hypothalamus.

Axon collaterals emerging from the vasopressinergic neurons of the supraoptic (SON) and paraventricular (PVN) nuclei and recurving back towards their respective nuclei have been previously reported. Since such axon collaterals can play a role in the neuromodulation of SON and PVN, these nuclei have been further investigated immunohistochemically under the light and electron microscope. The PAP technique, using a commercial antibody, was employed. Vasopressin-positive axon collaterals were seen to recurve towards their nuclei of origin. In the latter, vasopressinergic intrinsic neurons were also observed. Under the electron microscope, axon terminals containing vasopressin-immunoreactive neurosecretory granules were noted. Such terminals presumably arise from the vasopressin-positive recurrent axon collaterals or from the intrinsic neurons for the purpose of neuromodulation within the SON and PVN.

Animals↗

PubMed2001

Neurofilaments consist of distinct populations that can be distinguished by C-terminal phosphorylation, bundling, and axonal transport rate in growing axonal neurites.

We examined the steady-state distribution and axonal transport of neurofilament (NF) subunits within growing axonal neurites of NB2a/d1 cells. Ultrastructural analyses demonstrated a longitudinally oriented "bundle" of closely apposed NFs that was surrounded by more widely spaced individual NFs. NF bundles were recovered during fractionation and could be isolated from individual NFs by sedimentation through sucrose. Immunoreactivity toward the restrictive C-terminal phospho-dependent antibody RT97 was significantly more prominent on bundled than on individual NFs. Microinjected biotinylated NF subunits, GFP-tagged NF subunits expressed after transfection, and radiolabeled endogenous subunits all associated with individual NFs before they associated with bundled NFs. Biotinylated and GFP-tagged NF subunits did not accumulate uniformly along bundled NFs; they initially appeared within the proximal portion of the NF bundle and only subsequently were observed along the entire length of bundled NFs. These findings demonstrate that axonal NFs are not homogeneous but, rather, consist of distinct populations. One of these is characterized by less extensive C-terminal phosphorylation and a relative lack of NF-NF interactions. The other is characterized by more extensive C-terminal NF phosphorylation and increased NF-NF interactions and either undergoes markedly slower axonal transport or does not transport and undergoes turnover via subunit and/or filament exchange with individual NFs. Inhibition of phosphatase activities increased NF-NF interactions within living cells. These findings collectively suggest that C-terminal phosphorylation and NF-NF interactions are responsible for slowing NF axonal transport.

Amoxicillin-Potassium Clavulanate Combination↗

PubMed2003

Cytoskeletal and morphological alterations underlying axonal sprouting after localized transection of cortical neuron axons in vitro.

We examined the cytoskeletal dynamics that characterize neurite sprouting after axonal injury to cortical neurons maintained in culture for several weeks and compared these with initial neurite development. Cultured neocortical neurons, derived from embryonic day 18 rats, were examined at 3 d in vitro (DIV) and at various time points after axotomy at 21 DIV. The postinjury neuritic response was highly dynamic, progressing through an initial phase of retraction, followed by substantial axonal sprouting within 4-6 hr. Postinjury sprouts were motile and slender with expanded growth cone-like end structures. Microtubule markers were localized to sprout shafts and the proximal regions of putative growth cones and filamentous actin was distributed throughout growth cones, whereas neurofilament proteins were restricted to sprout shafts. A similar distribution of cytoskeletal proteins was present in developing neurites at 3 DIV. Exposure of developing and mature, injured cultures to the microtubule stabilizing agent taxol (10 microg/ml) caused growth inhibition, process distension, the transformation of growth cones into bulbous structures, and abnormal neurite directionality. Microtubule and neurofilament segregation occurred after taxol exposure in developing neurites and postinjury sprouts. Exposure to the microtubule destabilizing agent nocodazole (100 microg/ml) resulted in substantial morphological alteration of developing neurons and inhibited neurite growth and postinjury axonal sprouting. Our results indicate that the axons of cortical neurons have an intrinsic ability to sprout after transection, and similar cytoskeletal dynamics underlie neurite development and postinjury axonal sprouting.

Animals↗

PubMed1983

Altered axons and axon terminals in the nucleus gracilis of the dog.

Altered axons and axon terminals in the nucleus gracilis o the dogs were followed by means of electron microscopy. The axon terminals with characteristic ultrastructure were accompanied by synapses with altered presynaptic part. The changes of the presynaptic part were expressed by the evident decrease in synaptic vesicle number, hyperplasia of smooth endoplasmic reticulum and by abnormal mitochondrial figures. The altered axons measuring 14,6 micrometers in average contained hyperplastic and quite often dilated smooth endoplasmic reticulum as well as multiplied microtubular profiles. The mitochondria of the altered axons were characterized by the different degree of degeneration. The above mentioned structures in synapses as well as in axoplasma of the nucleus gracilis were found in the dogs of both sexes.

Afferent Pathways↗

PubMed1985

Neuroanatomical tracing by use of Phaseolus vulgaris-leucoagglutinin (PHA-L): electron microscopy of PHA-L-filled neuronal somata, dendrites, axons and axon terminals.

Following iontophoretic application of the plant lectin Phaseolus vulgaris-leucoagglutinin (PHA-L) to brain areas of rats, and subsequent immunohistochemistry, reaction product can be observed with the light microscope to fill neurons completely, including their somata, dendrites, dendritic appendages and axons. Moreover, axons often show profuse collateralization and indications of termination, including numerous en passant and terminal varicosities. The present report describes a protocol for combining light microscopic examination of PHA-L-stained neurons and electron microscopy of details of their processes, including the axonal varicosities. The results support the hypothesis that axonal varicosities are the light microscopic representations of synaptic axon terminals seen in electron microscopic preparations.

Agglutinins↗

PubMed2005

Integration of engrafted Schwann cells into injured peripheral nerve: axonal association and nodal formation on regenerated axons.

Transplantation of myelin-forming cells can remyelinate axons, but little is known of the sodium channel organization of axons myelinated by donor cells. Sciatic nerve axons of female wild type mice were transected by a crush injury and Schwann cells (SCs) from green fluorescence protein (GFP)-expressing male mice were transplanted adjacent to the crush site. The male donor cells were identified by GFP fluorescence and fluorescence in situ hybridization (FISH) for Y chromosome. In nerves of GFP-expressing mice, GFP was observed in the axoplasm and in the cytoplasmic compartments of the Schwann cells, but not in the myelin. Following transplantation of GFP-SCs into crushed nerve of wild type mice, immuno-electron microscopic analysis indicated that GFP was observed in the cytoplasmic compartments of engrafted Schwann cells which formed myelin. Nodal and paranodal regions of the axons myelinated by the GFP-SCs were identified by Na(v)1.6 sodium channel and Caspr immunostaining, respectively. Nuclear identification of the Y chromosome by FISH confirmed the donor origin of the myelin-forming cells. These results indicate that engrafted GFP-SCs participate in myelination of regenerated peripheral nerve fibers and that Na(v)1.6 sodium channel, which is the dominant sodium channel at normal nodes, is reconstituted on the regenerated axons.

Animals↗

PubMed1995

Concentric lamellar bodies in axon terminals and preterminal axons of cerebellar Purkinje cells in groggy mutant rat: acid phosphatase cytochemistry.

The process of formation and degeneration of concentric lamellar bodies (CLBs) in axon terminals and preterminal axons of Purkinje cells were examined by acid phosphatase (ACPase) cytochemistry. In myelinated axons, tubular structures measuring 20-50 nm in diameter contained ACPase reaction products. In altered axon terminals and preterminal axons of Purkinje cells, elongated saccular structures contained numerous reaction products. These saccular structures were arranged concentrically and enclosed cytoplasmic organelles. In the CLBs displaying degenerative profiles, ACPase reaction products were dispersed in the degenerating materials. The nature of the tubular structures and their roles in the transport of ACPase and the formation of CLBs are discussed.

Acid Phosphatase↗