Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Axons”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 397 records · Page 22Linked to original sources
PubMed1995

Direct measurement of fast axonal transport rates in corticospinal axons of the adult rat.

The bi-directional movement of proteins from the soma to the axon terminal is called axonal transport. Fast anterograde transport moves organelles and membrane-bound proteins distally. Fast transport rates were measured in corticospinal tract axons of male Sprague-Dawley rats by microinjection of tritiated proline into the sensorimotor cortex. Animals were killed after 3-5 h and the tract cut into 1 mm segments. A bimodal wave of radiolabeled proteins was evident, with the first peak at the spino-medullary junction and the second peak in cervical spinal segments. The fast transport rate was calculated at the leading edge of the distal wave, and found to be 303 +/- 44 mm/day.

Animals↗
PubMed1972

Neuronal dynamics and axonal flow: axonal peristalsis.

By time-lapse, phase-contrast cinemicrography of sensory nerve fibers of young mice, isolated with their originating spinal ganglia in nutrient solution, the postulated peristaltic surface drive of the cellulifugal propulsion of the semisolid axonal column at a rate of the order of 1 mm/day (1 mum/min) could be verified and quantitatively analyzed. The pulse waves follow each other at about 30-min intervals, regardless of whether the continuity of the axon is preserved or disrupted by degenerative fragmentation. Even when the axonal flow is obstructed, surface peristalsis continues.

Animals↗
PubMed1981

Changes in axonally transported proteins during axon regeneration in toad retinal ganglion cells.

In an effort to understand the regulation of the transition of a mature neuron to the growth, or regenerating, state we have analyzed the composition of the axonally transported proteins in the retinal ganglion cells of the toad Bufo marinus after inducing axon regeneration by crushing the optic nerve. At increasing intervals after axotomy, we labeled the retinal ganglion cells with [35S]methionine and subsequently analyzed the labeled transported polypeptides in the crushed optic nerve by means of one- and two-dimensional electrophoretic techniques. The most significant conclusion from these experiments is that, while the transition from the mature to the regenerating state does not require a gross qualitative alteration in the composition of axonally transported proteins, the relative labeling of a small subset of rapidly transported proteins is altered dramatically (changes of more than 20-fold) and reproducibly (more than 30 animals) by axotomy. One of these growth-associated proteins (GAPs) was soluble in an aqueous buffer, while three were associated with a crude membrane fraction. The labeling of all three of the membrane-associated GAPs increased during the first 8 d after axotomy, and they continued to be labeled for at least 4 wk. The modulation of these proteins after axotomy is consistent with the possibility that they are involve in growth-specific functions and that the altered expression of a small number of genes is a crucial regulatory event in the transition of a mature neuron to a growth state. In addition to these selective changes in rapidly transported proteins, we observed the following more general metabolic correlates of the regeneration process: The total radioactive label associated with the most rapidly transported proteins (groups I and II) increased three to fourfold during the first 8 d after the nerve was crushed, while the total label associated with more slowly moving proteins (group IV) increased about 10-fold during this same period. Among these more slowly transported polypeptides, five were observed whose labeling increased much more than the average. Three of these five polypeptides resemble actin and alpha- and beta-tubulin in their electrophoretic properties.

Animals↗
PubMed1982

Fast axonal transport in squid giant axon.

Video-enhanced contrast-differential interference contrast microscopy has revealed new features of axonal transport in the giant axon of the squid, where no movement had been detected previously by conventional microscopy. The newly discovered dominant feature is vast numbers of "submicroscopic" particles, probably 30- to 50-nanometer vesicles and other tubulovesicular elements, moving parallel to linear elements, primarily in the orthograde direction but also in a retrograde direction, at a range of steady velocities up to +/- 5 micrometers per second. Medium (0.2 to 0.6 micrometer) and large (0.8 micrometer) particles move more slowly and more intermittently with a tendency at times to exhibit elastic recoil. The behavior of the smallest particles and the larger particles during actual translocation suggests that the fundamental processes in the mechanisms of organelle movement in axonal transport are not saltatory but continuous.

Animals↗
PubMedDate not supplied

[The demonstration of recurrent motor axon collaterals in the chick embryo by using horseradish peroxidase axonal transport].

Motoneurons were labelled by retrograde axonal transport of HRP applied to transected spinal nerves in 9-11-day chick embryos in the in vitro spinal cord preparation. Recurrent motor axon collaterals were revealed in 17 of 48 motor axons which could be followed in the edge regions of labelled motoneuronal pools. The results, coupled with author's earlier electrophysiological data, provide further evidence for the presence of the Renshaw inhibition in the avian spinal cord.

Animals↗
PubMed1998

Molecular gradient along the axon pathway is not required for directional axon growth.

We show that axon guidance of embryonic hippocampal neurons is promoted by pathways of a decapeptide (RDIAEIIKDI) derived from a neurite outgrowth domain of the gamma1 chain of laminin-1. This guidance is directly dependent on: (1) a concentration difference of the decapeptide between the peptide pathway and its surrounding areas, and (2) the optimal surface geometry of the decapeptide pathway. These results indicate that axon guidance of central neurons may proceed along a preferred substratum pathway without a concentration gradient of the guiding molecule along this pathway, or without a repulsive molecule next to the axon pathway.

Animals↗
PubMed1987

Remodelling of early axonal projections through the selective elimination of neurons and long axon collaterals.

Studies using neuroanatomical techniques have shown that the connections characteristic of the mature vertebrate brain are brought about by a considerable refinement of the projections initially established during development. The selective loss of neurons and long axon collaterals plays a major role in this remodeling process as illustrated in the development of the retina and cortex of the rat. In the retina, two-thirds of the initial population of ganglion cells (RGCs) die early. This loss serves to remove selectively RGCs that make erroneous axonal projections, including those which project to an incorrect target, to an inappropriate part of a correct target, or to the wrong side of the brain. Studies using the sodium channel blocker, tetrodotoxin, suggest that in rats the selective elimination of erroneously projecting RGCs is based, in part, on patterns of impulse activity. In the cortex a different mechanism is illustrated. All neocortical areas initially give rise to callosal and pyramidal tract axons but through a process of selective collateral elimination not involving cell death these projections assume the limited distributions seen in adult rats. Manipulations resulting in the maintenance of such long collaterals suggest that their removal is functionally and locally determined. In contrast to error elimination, this phenomenon of collateral elimination may be a developmental strategy for generating connectional diversity while limiting the amount of information required for the regional specification of the cortex.

Animals↗
PubMed2003

Acute motor axonal neuropathy rabbit model: immune attack on nerve root axons.

Macrophages in the periaxonal space and surrounding intact myelin sheath are the most prominent pathological feature of acute motor axonal neuropathy (AMAN). We describe this characteristic in nerve roots from paralyzed rabbits immunized with bovine brain ganglioside or GM1. IgG was deposited on nerve root axons. Distal nerve conduction was preserved, and late F wave components were absent during the acute phase. Initial lesions were located mainly on nerve root axons, as in human AMAN. This study thus provides supportive evidence that the rabbits constitute a model of AMAN.

Action Potentials↗
PubMed1990

Transmembrane cytoskeletal modulation in preterminal growing axons: I. Arrest of bulk and organelle transport in goldfish retinal ganglion cell axons regenerating in vitro by lectins binding to sialoglycoconjugates.

Goldfish retinal ganglion cell (RGC) axons regenerating in vitro exhibit a novel mode of axoplasmic transport that entails a rapid bidirectional bulk redistribution of axoplasm, "packaged" as protruding varicosities and non-protruding phase-dense inclusions (Koenig et al.: J. Neurosci. 5:715-729, 1985; Edmonds and Koenig Brain Res. 406:288-293, 1987). We have used phase-contrast video microscopy to study transmembrane effects of surface-binding lectins on bulk transport and transport of single visible organelles in RGC axons. Our findings show that certain lectins which crosslink sialoglycoconjugates, such as wheat germ agglutinin (WGA) and the more specific sialic acid-binding lectin Limax flavus agglutinin (LFA), induce a rapid inhibition of transport activity. The LFA-induced inhibition of transport can be reversed by appropriate simple sugar haptens, and can also be antagonized by pretreatment with cytochalasin D. One of the consequences of LFA binding is an increase in RITC-conjugated phalloidin fluorescence staining of preterminal axons. The latter observation in conjunction with the antagonistic action of cytochalasin D suggests that one possible explanation for the transmembrane arrest of transport induced by crosslinking of surface sialoglycoconjugates may involve a polymerization and/or reorganization of the actin filament network which hinders translocation of mobile axoplasmic components.

Animals↗
PubMed2003

GABAergic and glutamatergic axons innervate the axon initial segment and organize GABA(A) receptor clusters of cultured hippocampal pyramidal cells.

We have studied gamma-aminobutyric acid (GABA)(A) receptor (GABA(A)R) clustering within the axon initial segment (AIS) in low-density cultures of hippocampal pyramidal cells following GABAergic and glutamatergic innervation of the AIS. Large, intensely fluorescent, and postsynaptic GABA(A)R clusters were present in the AIS. More than 95% of these clusters colocalized with presynaptic GABAergic or glutamatergic terminals, forming matched or mismatched synapses, respectively. Less than 5% of the GABA(A)R clusters of the AIS did not colocalize with GABAergic or glutamatergic terminals, suggesting that GABA(A)Rs normally do not form clusters unless the AIS received GABAergic or glutamatergic innervation. Few or no clusters of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors or the postsynaptic density-95 protein (PSD-95) were found in the AIS, even when the AIS was innervated by glutamatergic axons. Glutamatergic innervation of the AIS that formed mismatched synapses with postsynaptic GABA(A)R clusters mainly occurred when the AIS did not receive GABAergic innervation. However, when the AIS was innervated by GABAergic axons, the formation of matched GABAergic synapses predominated and coincided with large reductions in both the density of glutamatergic terminals from the AIS and the mismatching of GABA(A)R clusters. A similar effect was observed at axo-dendritic synapses, where GABAergic innervation also led to a large decrease in mismatched GABA(A)R clusters and a smaller, but significant, decrease in glutamatergic terminal density in dendrites that received GABAergic innervation. We hypothesize that competition between GABAergic and glutamatergic innervation of the AIS in the intact hippocampus leads to the exclusive presence of GABAergic inhibitory synapses in the AIS of pyramidal cells.

Animals↗
PubMed2004

Myelin-, reactive glia-, and scar-derived CNS axon growth inhibitors: expression, receptor signaling, and correlation with axon regeneration.

Axon regeneration is arrested in the injured central nervous system (CNS) by axon growth-inhibitory ligands expressed in oligodendrocytes/myelin, NG2-glia, and reactive astrocytes in the lesion and degenerating tracts, and by fibroblasts in scar tissue. Growth cone receptors (Rc) bind inhibitory ligands, activating a Rho-family GTPase intracellular signaling pathway that disrupts the actin cytoskeleton inducing growth cone collapse/repulsion. The known inhibitory ligands include the chondroitin sulfate proteoglycans (CSPG) Neurocan, Brevican, Phosphacan, Tenascin, and NG2, as either membrane-bound or secreted molecules; Ephrins expressed on astrocyte/fibroblast membranes; the myelin/oligodendrocyte-derived growth inhibitors Nogo, MAG, and OMgp; and membrane-bound semaphorins (Sema) produced by meningeal fibroblasts invading the scar. No definitive CSPG Rc have been identified, although intracellular signaling through the Rho family of G-proteins is probably common to all the inhibitory ligands. Ephrins bind to signalling Ephs. The ligand-binding Rc for all the myelin inhibitors is NgR and requires p75(NTR) for transmembrane signaling. The neuropilin (NP)/plexin (Plex) Rc complex binds Sema. Strategies for promoting axon growth after CNS injury are thwarted by the plethora of inhibitory ligands and the ligand promiscuity of some of their Rc. There is also paradoxical reciprocal expression of many of the inhibitory ligands/Rc in normal and damaged neurons, and NgR expression is restricted to a limited number of neuronal populations. All these factors, together with an incomplete understanding of the normal functions of many of these molecules in the intact CNS, presently confound interpretive acumen in regenerative studies.

Animals↗
PubMed2005

An 8.5-kb segment of the PMP22 promoter responds to loss of axon signals during Wallerian degeneration, but does not respond to specific axonal signals during nerve regeneration.

Altered expression of the PMP22 gene causes Charcot-Marie-Tooth disease type 1A (CMT1A) and hereditary neuropathy with liability to pressure palsies (HNPP). We have examined the promoter activity of 8.5 kb upstream of the first coding exon of the rat peripheral myelin protein-22 (rPmp22) gene in transgenic mice. We found that the -8.5 kb rPmp22/chloramphenicol acetyl transferase (CAT)/beta-galactosidase (lacZ) construct directs reporter gene expression in a weakly developmental and tissue-specific pattern, consistent with the expression pattern of the endogenous Pmp22 gene. The -8.5 kb rPmp22/CAT/lacZ transgene responds to loss of axonal signals during Wallerian degeneration but unlike the endogenous Pmp22 gene, the transgene fails to respond to axonal signals during nerve regeneration after a sciatic nerve crush injury. In conclusion, the function of the -8.5 kb rPmp22/CAT/lacZ transgene suggests that there are separable regulatory elements in the rPmp22 gene that respond differently to axonal signals received by Schwann cells during nerve development, and during remyelination.

Animals↗
PubMed2002

Axonal hyperpolarization associated with acute hypokalemia: multiple excitability measurements as indicators of the membrane potential of human axons.

Multiple nerve excitability measurements have been proposed for clinical testing of nerve function, and an important determinant of excitability is membrane potential. We report a patient with acquired hypokalemic paralysis in whom multiple excitability indices (stimulus-response curve, strength-duration properties, threshold electrotonus, recovery cycle) were measured during and after an acute hypokalemic attack (serum K(+) level, 2.1 mEq/L and 4.5 mEq/L, respectively). During hypokalemia, there was a shift of the stimulus-response curve to the right, a decrease in strength-duration time constant, a "fanning-out" of responses during threshold electrotonus, a reduction in relative refractory period, and an increase in superexcitability; all of these indicate axonal hyperpolarization, presumably due to the K(+) equilibrium potential being more negative. These indices returned to normal 20 h later, associated with normalization of the serum K(+) level. These results demonstrate that the changes associated with hypokalemic paralysis are not confined to muscle and that axons undergo hyperpolarization in vivo. Multiple excitability measurements can be used as a tool to identify changes in membrane potential of human axons.

Action Potentials↗
PubMed1987

Morphological and electrophysiological characteristics of somatosensory thalamocortical axons studied with intra-axonal staining and recording in the cat.

The intracortical arborizations of thalamocortical fibers arising from the ventroposterolateral (VPL) nucleus in the cat were studied following intra-axonal injections of horseradish peroxidase (HRP). The axons were impaled 1.5 to 3 mm below the surface of the cortex, identified electrophysiologically by stimulating the VPL nucleus and functionally by stimulating the somatic receptive field with natural stimuli. Many of the results obtained in a previous study using similar techniques (Landry and Deschênes 1981) were confirmed by the present experiments. Fibers activated by cutaneous stimulation arborized either in area 3b or 1 but some did send branches to both areas. Also, the intracortical arborization of a rapidly adapting cutaneous afferent fiber in area 2 is described. The size and tangential extent of the fiber in area 2 are similar to those arborizing in other areas of the primary somatosensory cortex and consist of multiple patches separated by uninvaded gaps. One fiber activated by stimulation of deep tissue receptors gave rise to two bushes that arborized along a rostrocaudal axis exclusively in area 3b. Terminal boutons and varicosities were found mostly in layers VI, IV, the bottom third of III and the upper portion of V, but some fibers did send a few collateral branches to layer II and the bottom part of layer I. The results suggest that in the forebrain representation, the same modality and submodality can be recorded in more that one cytoarchitectonic area but that areas 3b, 1 and 2 should not be considered as a single functionally homogeneous area. Counts of terminals suggest that a single fiber arborizing in area 1 makes as many as 3 times the number of synapses made in area 2 or 3b. Since fibers appear to be modality and submodality specific, if convergence of modality, submodality and/or body areas occur in the cortex, then this must be preferentially, but not exclusively, done by thalamic fibers of different functions which arborize in the same cytoarchitectonic area and synapse upon a shared postsynaptic target. In the same experiments intra-axonal recordings revealed the presence of two hyperpolarizing after potentials elicited by a preceding action potential. The first after potential was associated with a decrease in excitability of the fiber and an increase in membrane resistance.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2005

Morphological and molecular features of the mammalian olfactory sensory neuron axons: What makes these axons so special?

The main organization and gross morphology of the mammalian olfactory primary pathway, from the olfactory epithelium to the olfactory bulb, has been initially characterized using classical anatomical and ultrastructural approaches. During the last fifteen years, essentially thanks to the cloning of the odorant receptor genes, and to the characterization of a number of molecules expressed by the olfactory sensory neuron axons and their environment, significant new insights have been gained into the understanding of the development and adult functioning of this system. In the course of these genetic, biochemical and neuroanatomical studies, however, several molecular and structural features were uncovered that appear somehow to be unique to these axons. For example, these axons express odorant receptors in their terminal segment, and transport several mRNA species and at least two transcription factors. In the present paper, we review these unusual structural and molecular features and speculate about their possible functions in the development and maintenance of the olfactory system.

Animals↗
PubMed1982

Intra-axonal recordings in rat dorsal column axons: membrane hyperpolarization and decreased excitability precede the primary afferent depolarization.

Intra-axonal recordings were obtained in the dorsal columns of the rat lumbosacral spinal cord. Dorsal root or dorsal column stimulation at levels subthreshold for the impaled axon elicited a prolonged depolarization corresponding to the primary afferent depolarization (PAD). The depolarization was preceded by a brief hyperpolarizing potential during which excitability was decreased. The hyperpolarization corresponds temporally to the extracellularly recorded DRP IV component of the dorsal root potential described by Lloyd and McIntyre, and may represent the intracellular correlate of this potential. Possible mechanisms for this hyperpolarization include electrical interactions between neuronal elements, a biphasic GABA response, or attenuation of background afferent axonal depolarization.

Afferent Pathways↗
PubMed1992

Growth cones of regenerating adult sciatic sensory axons release axonally transported proteins.

Labelled, rapidly transported axonal proteins were shown to be released from adult frog sciatic sensory neurons, regenerating in vitro after a crush injury. The spatial distribution of the transported, released proteins could accurately be resolved by culturing the nerve on nitrocellulose paper, which trapped the released proteins. The release was located to the crush and to the entire outgrowth region. When regeneration was inhibited by adenosine, the release was limited to the crush site, implying that the release was linked to the growing axons. Other experiments suggested that the release emanated from growth cones. Furthermore, two-dimensional electrophoretical analysis of both fast axonally transported and of released proteins showed that the latter represented a selection of the transported protein species.

Adenosine↗
PubMed1993

Demonstration of axon terminals of projection fibers from the periaqueductal gray onto neurons in the nucleus raphe magnus which send their axons to the trigeminal sensory nuclei.

Axon terminals of projection fibers from the periaqueductal gray (PAG) onto neurons in the nucleus raphe magnus (NRM) sending their axons to the principal sensory trigeminal nucleus (Vp) or caudal spinal trigeminal nucleus (Vc) were demonstrated light microscopically: In the rats which were injected with Phaseolus vulgaris leucoagglutinin (PHA-L) and wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) respectively into the PAG and trigeminal sensory complex (Vp or Vc), presumed axon terminals labeled anterogradely with PHA-L appeared to make synaptic contacts with NRM neurons labeled retrogradely with WGA-HRP.

Animals↗