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At least 469 records · Page 26Linked to original sources
PubMed1981

Role of degenerating axon pathways in regeneration of mouse soleus motor axons.

1. The recovery of tension in mouse soleus was assayed 1-5 days after crushing the extramuscular nerve in muscles which had been previously either denervated by nerve crush, partly denervated by spinal nerve root section, or paralysed by I.M. injection of botulinum toxin. Recovery of tension following nerve crush in contralateral control muscles from the same mice was also measured. The muscles were then stained with zinc iodide-osmium and examined in the light microscope. 2. Recovery in control muscles began at about 50 hr after crush and was nearly complete by 5 days. Recovery began at about 50 hr after crush and was nearly complete by 5 days. Recovery began about 10 hr earlier and was more rapid in muscles denervated by crushing the muscle nerve 4 days before recrushing at the same site. 3. Paralysis 12 days earlier by intramuscular injection of botulinum toxin did not enhance recovery after nerve crush. The axons remained following partial denervation 6 days before nerve crush also regenerated at a rate similar to controls. 4. It is concluded that (1) nerves regenerate more quickly down a pre-degenerated pathway, (2) chromatolysis does not significantly enhance reinnervation, and (3) each motor axon regenerating after a crush is constrained to follow its own denervated pathway back into the muscle. 5. Histology was consistent with these conclusions, and also showed that end-plates in control muscles reinnervated after short periods of denervation were normal in appearance and possessed little "escaped' nerve growth. This was in contrast to end-plates which had been regenerated in muscle after a preceding nerve crush, botulinum toxin paralysis or partial denervation. This suggests that growth from nerve terminals is controlled locally within a muscle.

Animals↗
PubMed1980

Fine structure of the axon initial segment and the axon cap of the Mauthner cell in the bullfrog tadpole.

The axonal initial segment of the Mauthner cell of tadpoles of Rana catesbeiana and its surrounding neuropil, the axon cap, were examined by electron microscopy. The initial segment is almost completely covered by numerous synaptic terminals with profuse clear spherical synaptic vesicles. These synaptic terminals are of one uniform type and are found to be extensions of preterminal swellings, which are filled with accumulated mitochondria and glycogen granules in addition to the synaptic vesicles. Some swelling were shown to have two or more terminals. The synaptic terminals as well as the preterminal swelling are occasionally linked by small synaptic junctions. The significance of this structural organization in the inhibitory control of the Mauthner cell activation was discussed.

Animals↗
PubMed1992

Axonal response to traumatic brain injury: reactive axonal change, deafferentation, and neuroplasticity.

Axonal injury appears to be a feature common to all traumatic brain injuries, and has been linked to much of the morbidity seen in head-injured patients. We consider how such axonal injury contributes to morbidity and also sets the stage for CNS reorganization postinjury. Efforts should continue to determine the correlates of such reorganization and to find therapeutic strategies to expedite it.

Animals↗
PubMed1984

Observations on the ultrastructure of the axon hillock and initial axon segments of vestibular ganglion cells in the cat.

The axon hillock and initial axon segments of the vestibular ganglion cells in the cat were studied electron microscopically. The results revealed that the two cell processes are not completely comparable from morphological point of view. One of them is larger, with a more straight course, the axoplasm of the initia segment contains mainly longitudinally arranged neurotubules. The second cell process appears smaller in size, the initial segment have a curved course.

Animals↗
PubMed1989

The morphology of the axons and axon collaterals of rat jaw-elevator motoneurones.

We have made intracellular injections of horseradish peroxidase into the somata of jaw-elevator motoneurones and subsequently reconstructed the axonal morphology of 4 cells. In each case the axons gave off collaterals which were essentially restricted to the ventral portion of the V motor nucleus. This observation provides the first evidence that these motoneurones may exert recurrent synaptic effects.

Action Potentials↗
PubMed1985

AVEC-DIC and electron microscopic analyses of axonally transported particles in cold-blocked squid giant axons.

Anterogradely and retrogradely transported membranous organelles were analysed separately by focally cooling axons (cold-blocking) for 2-4 h. Video-enhanced differential interference contrast light microscopy (AVEC-DIC) and dark field light microscopy showed that particles accumulated in large numbers on both the anterograde and the retrograde sides of the cold-block and that the accumulated particles resumed their transport when the preparation was rewarmed to 18 degrees C. The particles accumulated in files on both sides of the cold-block suggesting that particles move along linear pathways in the axoplasm. Comparisons of the results obtained by AVEC-DIC light microscopy with those obtained by electron microscopy indicate that the AVEC-DIC method is capable of detecting all of the different types of rapidly transported membranous organelles, including the smallest (35-80 nm) vesicles that move anterogradely. Electron microscopic analyses of the transported particles demonstrate that the anterogradely transported organelles are structurally distinct from those that are transported retrogradely. The anterogradely transported particles consisted of normal mitochondria and small (35-80 nm) tubulovesicular profiles. By contrast, the retrogradely transported particles were 150 nm or larger and they often contained complex membranous inclusions. The largest retrogradely transported particles appeared to be degenerating mitochondria. The results are consistent with the hypothesis that the direction of organelle movement is related to the physiological state of the organelle. That is, organelles containing newly synthesized membrane components move primarily anterogradely and organelles that contain transformed and degraded membrane components move retrogradely.

Animals↗
PubMed1994

Neural projections from the frontal cortex to the oculomotor nucleus: an anatomical study using retrograde axonal, anterograde axonal and transneuronal transport of wheat germ agglutinin-conjugated horseradish peroxidase in cats.

Neural projections from the frontal cerebral cortex to the oculomotor nucleus (3N) were investigated in 1- to 2-year-old cats by retrograde and anterograde axonal and transneuronal transport of wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP). Following injection of WGA-HRP into the 3N area and its surrounding tissues, retrogradely labeled cells were observed in the anterior sigmoid gyrus, ventral bank of the cruciate sulcus, medial and lateral walls and base of the presylvian sulcus, gyrus rectus and gyrus proreus. Following injection of WGA-HRP into these frontal cortical areas, anterogradely labeled nerve terminals were observed in the mesencephalic periaqueductal gray matter (PAG) just overlying the 3N. Only a few terminals were observed within the 3N. Following injection of WGA-HRP into the extraocular muscles of 1-month-old kittens, transneuronally labeled small cells were observed in the PAG just overlying the 3N and in the mesencephalic reticular formation, ventrolateral to it. These small cells may represent intercalated neurons of the cortico-oculomotor projections in the cat.

Animals↗
PubMed1985

Axonal transport of cytoskeletal proteins in aluminum toxicity. Aluminum toxicity and axonal transport.

Aluminum administration in certain species results in the accumulation of neurofilament bundles within the neuronal perikaryon and the proximal neuronal processes. The study presented here was designed to investigate how aluminum exerts its effects on the neuronal cytoskeleton. Microinjections of AlCl3 were administered directly to the rabbit lumbar spinal cord; the injections resulted in the accumulation of neurofilament bundles in upwards of 80% of the anterior horn cells. Approximately 7 d later, [35S]methionine was administered to the same region, and exactly 14 d after the radioactive pulse the animals were sacrificed. Sequential 3-mm segments of the sciatic nerves beginning at the root exit zone were processed for gel electrophoresis and fluorography. The counts incorporated into gel bands representing actin, tubulin, and the neurofilament (NF) subunits were determined for each segment, and a distribution curve for the pooled control and pooled aluminum-treated rabbits was constructed. The distribution curves for the two groups, separately analyzed for each cytoskeletal protein, did not significantly differ using an analysis of variance. We conclude that an interruption of slow axonal transport does not occur in this model of aluminum-induced lumbar myelopathy.

Aluminum↗
PubMed1995

Differential synthesis and cytoskeletal deposition of neurofilament subunits before and during axonal outgrowth in NB2a/d1 cells: evidence that segregation of phosphorylated subunits within the axonal cytoskeleton involves selective deposition.

NB2a/d1 cells constitutively express and extensively phosphorylate neurofilament (NF) triplet proteins. However, only hypophosphorylated NFs are observed within the Triton-insoluble perikaryal cytoskeletons of undifferentiated and differentiated cells, while phosphorylated NF isoforms accumulate exclusively within the axonal neurites elaborated following treatment with dbcAMP. We examined NF synthesis and distribution of newly synthesized subunits by immunoprecipitation from 35S-methionine-radiolabeled undifferentiated and dbcAMP-treated differentiated cells. Following a 15 min pulse radiolabeling, NF-H isoforms migrating from approximately 160-200 kDa, NF-M isoforms migrating from approximately 97 k-145 Da, and a single 70 kDa NF-L isoform were readily detectable within Triton-soluble fractions from both undifferentiated and differentiated cells. During chase analyses in the absence of radiolabel, the entire spectrum of isoforms was present in Triton-soluble and -insoluble fractions from both undifferentiated and differentiated cells. However, differentiated cells displayed a significant increase in radiolabel associated with each subunit and isoform. Normalization of their NF synthesis levels to those of undifferentiated cells revealed that differentiated cells deposited 10-fold more radiolabeled subunits into the Triton-insoluble cytoskeleton as compared to undifferentiated cells. Similar levels of radiolabeled subunits were observed throughout the 2 hr period in dbcAMP-treated cells. By contrast, radiolabeled subunits and isoforms increased in undifferentiated cytoskeletons during the chase period, although final levels remained substantially lower than those observed in cytoskeletons of dbcAMP-treated cells. These data were considered with respect to potential mechanisms by which the phosphorylated NFs are normally excluded from perikaryal cytoskeletons. The presence of extensively phosphorylated subunits within perikarya indicates the presence of necessary NF kinases.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Axonal microtubules necessary for generation of sodium current in squid giant axons: II. Effect of colchicine upon asymmetrical displacement current.

Effect of internal colchicine on asymmetrical displacement currents was studied by internally perfusing squid giant axons with a solution containing colchicine. It was found that (1) asymmetrical displacement currents were composed of two parts; colchicine-sensitive and colchicine-resistant; that (2) the colchicine-sensitive part had a definite rising phase while the colchicine-resistant one showed an instantaneous jump, followed by exponential decay; and that (3) the colchicine-sensitive part related to normal Na channels.

Animals↗
PubMed1985

Axonal transport of beta-receptors during the response to axonal injury and repair in locus coeruleus neurons.

Injections of the catecholamine neurotoxin, 6-hydroxydopamine, were placed in the ascending locus coeruleus (LC) pathway in the right cerebral cortex of rats partially destroying the noradrenergic projection to the somatosensory cortex. Norepinephrine (NE) levels fell to a nadir of 49% of control over the first 14 days, associated with a 40% increase in the number of beta-adrenoreceptor binding sites (labeled with [3H]dihydroalprenolol; [3H]DHA) in the denervated cortex. Both NE levels and cortical beta-receptor binding returned to control levels by 28 days. Similar changes, of lesser magnitude, also occurred in the unlesioned, left somatosensory cortex. Catecholamine histofluorescence studies supported these findings of denervation and reinnervation of the right cortex over a 3-month period. Anterograde axonal transport of beta-receptors was assessed by measuring the accumulation of beta-receptor binding sites ([3H]DHA) behind a second lesion placed in the more proximal portion of the ipsilateral LC pathway. Anterograde transport was completely blocked at 4 days, during the initial fall of NE levels, then was increased to 200% of control at 14-21 days, when recovery of cortical NE levels was beginning, and then returned towards control levels by 2-3 months when normal NE levels had been restored.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Relations between axon length and axon caliber. "Is maximum conduction velocity the factor controlling the evolution of nerve structure"?

A search was made for any existent relationship between the length of a nerve fiber and the caliber of its axon. This was done in the hope of defining morphological parameters useful for assessing conduction time. Four fiber populations were examined: (1) phrenic fibers in rat and rabbit during different phases of body growth; (2) phrenic fibers of mature animals of greatly different body size including mouse and cow; (3) rat intercostal nerves which vary in length by a factor exceeding 5 due to the funnel-shape of the thorax; and (4) ventral root fibers of the cow. In all of these fiber populations, there was no evidence for a direct relationship between the length of a fiber and its caliber. Rather, a tendency was noted for fiber caliber to approach certain ceilings independent of length. These data, seen in conjunction with other information on fiber structure, cast serious doubt on the widely accepted concept that maximum conduction velocity is the factor controlling nerve structure. A much more likely factor controlling the structure of myelinated nerve fibers is the capacity to modulate information by frequency coding of impulses.

Aging↗
PubMed1988

Studies of axon-glial cell interactions and periaxonal K- homeostasis--I. The influence of Na+, K+, Cl- and cholinergic agents on the membrane potential of the adaxonal glia of the crayfish medial giant axon.

The ionic basis for the low (-40 mV) resting membrane potential of glial cells surrounding the giant axons of the crayfish and their hyperpolarization by cholinergic agents (to -55 mV) was studied using standard electrophysiological techniques, ionic substitutions and pharmacological agents. The resting membrane potential of the glial cell was depolarized by increasing [K+]o, but the response was not Nernstian. Na+ depletion caused a small depolarization of the glial resting membrane potential, whereas Cl- depletion resulted in a hyperpolarization comparable to that seen with carbachol at various [K+]o. Both furosemide (1 mM) and bumetanide (0.1 mM) produced an 8-10 mV hyperpolarization as compared to 15-17 mV seen with Cl- depletion or carbachol. Carbachol has no further effect on the potential following furosemide treatment or Cl- depletion. After carbachol administration or Cl- depletion the resting membrane potential of the glial cell responded to [K+]o in a more Nernstian manner. The data indicate that the low resting membrane potential of glial cells is due to a combination of a low [K+]i and an outwardly-directed (depolarizing) Cl- electrochemical gradient. Carbachol acts to decrease Cl- conductance, resulting in the hyperpolarization of the glial cell membrane and a decrease in the outwardly-directed K+ electrochemical gradient by approximately two-thirds. We hypothesize that this mechanism for modulation of the glial cell membrane potential and the K+ electrochemical gradient serves to enhance the uptake of K+ by the glial cell transport system.

Animals↗
PubMed1998

Axon guidance: GTPases help axons reach their targets.

During development and regeneration of the nervous system, axons must correctly navigate to their specific targets through a complex molecular environment. Recent work has shed light on how GTPases of the Ras family are involved in transducing extracellular signals into responses that lead to directed neurite outgrowth.

Animals↗
PubMed2005

Mild early onset axonal Charcot-Marie-Tooth disease not linked to other axonal Charcot-Marie-Tooth loci.

Autosomal dominant axonal Charcot-Marie-Tooth disease type 2 (CMT2) is a heterogeneous group of disorders with seven chromosomal loci mapped in the uncomplicated forms of CMT2. The authors report clinical, electrophysiologic, and genetic analysis of a Polish CMT2 family. Nine known CMT2 gene loci and one MPZ gene locus have been excluded. The authors' findings suggest that this family represents a novel form of CMT2 disease.

Action Potentials↗
PubMed2001

Functional implications of neurotransmitter expression during axonal regeneration: serotonin, but not peptides, auto-regulate axon growth of an identified central neuron.

We studied the regenerative properties of one of two electrically coupled molluscan neurons, the serotonergic cerebral giant cells (CGCs) of Lymnaea stagnalis, after axotomy. The CGCs play a crucial role in feeding behavior, and when both cells are disconnected from their target neurons, animals no longer feed. When one CGC was permanently disconnected from its targets and the other was reversibly damaged by a nerve crush, the latter one regenerated over a period of 2 weeks to reform functional synapses with specific target neurons. At the same time, recovery of the feeding behavior was observed. After the crush, neuropeptide gene expression in the CGC was downregulated to approximately 50%. Serotonin synthesis, on the other hand, remained unaffected, suggesting that serotonin might have an active role in regeneration. In primary neuron culture, CGCs failed to extend neurites in the presence of serotonin; in cells that extended neurites in the absence of serotonin, focally applied serotonin, but not neuropeptides, induced growth cone collapse. Using serotonin-sensitive sniffer cells, we show that CGC neurites and growth cones release serotonin in culture. Finally, both the spontaneous and stimulation-induced release of serotonin from CGCs in culture resulted in growth cone collapse responses that could be blocked by the serotonin receptor antagonist methysergide. Our data suggest that auto-released serotonin is inhibitory to CGC neurite outgrowth in vitro. During regeneration in vivo, serotonin release might fine-tune axon guidance and branching by inducing local collapse responses in extending neurites.

Animals↗
PubMed1992

Axonal and non-axonal immunolocalization of cytosolic aspartate aminotransferase (cAATase), GABA and glutamic acid decarboxylase (GAD) in the rat cochlear nucleus.

The localization of both cAATase activity, by histoenzymological method, and the immunoreactivity against cAATase, were investigated in the cochlear nucleus of rats. The immunohistochemical determination of cAATase was carried out using the PAP method, with an antiserum obtained from rabbits immunized with porcine cAATase. It was also studied both the immunolocalization of GABA-like and GAD-like substances. Our observations, with light microscope, revealed weak cAATase activity in the small neurons, and a more intense one in the fibers surrounding neuronal bodies. The large neurons presented a very weakly activity within their neuronal bodies and dendrites, but it was strongly found in granulations that surround the perikaryon and dendrites. cAATase immunoreactivity presents the same distribution as the enzymological activity. In the same way, we have investigated the pattern of distribution of both GABA- and GAD-like substances. Immunolocalization of these substances was similar to that found for cAATase. In the control sections incubated with Gostatin (0.05 mM), cAATase activity was absent. The immunoreactivity was also negative in every immunohistochemical control sections. These facts suggest that aspartate could intervene as a co-neurotransmitter or neuromodulator in the rat cochlear nucleus, and that axonic endings could contain cAATase, GABA and GAD. It was also found immunoreactivity against cAATase, GABA and GAD, in neuronal bodies, dendrites and glial processes, in close association with capillary wall. These observations have led us to suggest the possible co-localization and co-release of both GABA and aspartate from synaptic and non-synaptic sites in the cochlear nucleus.

Animals↗
PubMed1989

Ultrastructural identification of synaptic terminals from cortical axons and from collateral axons of geniculo-cortical relay cells in the perigeniculate nucleus of the cat.

Electron microscopic analysis of sections of the perigeniculate nucleus (PGN) of the cat processed with horseradish peroxidase (HRP) histochemistry after massive injections of this enzyme in the visual cortex showed two types of synaptic terminals labeled with HRP reaction products. One type (RLD terminals) is characterized by round synaptic vesicles, large size, dark mitochondria and asymmetrical synaptic contacts with somata and dendrites. The second type (RSD terminals) is characterized by round synaptic vesicles, small size, dark mitochondria and asymmetrical synaptic contacts with dendrites. The HRP+ RSD terminals, which were also found in the dorsal lateral geniculate nucleus (LGN), are interpreted as terminals of cortical origin both in the PGN and LGN, since previous studies have identified cortical terminals as being of RSD type in the LGN and in other thalamic nuclei. The HRP+ RLD terminals are interpreted as synaptic terminals of collaterals axons of geniculocortical relay cells in the PGN labeled by retrograde transport of HRP from the cortex. In addition, in semithin and ultrathin sections somata in the PGN were never found labeled with HRP products indicating the absence of a PGN projection to the visual cortex.

Animals↗