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PubMed1987

Tangled masses of central axons (central axonomas) in the brain stem: anatomical evidence for the regenerative growth of human central axons.

Eight additional cases of tangled masses of unmyelinated fine axons occurring in the brain stem in association with cystic infarcts or traumatic cysts are described. Because they are solely composed of bare axons and because of their consistent association with old, destructive lesions, they are called axonomas in lieu of the previous designation as non-myelinated neuromas. Axonomas were located at the border of the associated lesions exclusively in or near the central tegmental tract of the midbrain, pons or medulla. Their occurrence in the restricted region is considered as the reason for their rarity and for the failure to observe them in the past. The discrete, compact, mass formation, the occurrence of a large number in groups, the exclusive occurrence in specific regions of the central nervous system (CNS), and the consistent association with old axonal injury are presented as circumstantial evidence that axonomas represent regenerative growths of central axons. Based on the restricted site of predilection, it is inferred that axonomas originate from a special group or groups of CNS neurons which may have an exceptionally high capacity to regenerate. In other words, certain central neurons in man are not only capable of abundant regenerative sprouting but also are able to sustain the newly formed sprouts in the form of axonomas for years or perhaps permanently, but the specific neurons are not yet identified.

Adult↗
PubMed1990

Computerized quantification of immunofluorescence-labeled axon terminals and analysis of co-localization of neurochemicals in axon terminals with a confocal scanning laser microscope.

The confocal scanning laser microscope (CSLM) offers improved optical resolution and contrast, high photometric precision, and the ability to make optical sections. These benefits were explored for use in quantitative analysis of immunofluorescence-labeled axon terminals. Guidelines were obtained for adjustments of the CSLM parameters. In the present applications, bleaching of the fluorescence did not represent a serious obstacle to analysis with the CSLM. A method was developed to distinguish the background fluorescence from the specific fluorescence labeling. This procedure made way for the development of automated quantification of immunolabeled axon terminals. The automated procedures substantially reduced the man-hour expenditure for analysis and provided highly reproducible quantifications compared with manual methods. The increased resolution and contrast of the CSLM allowed measurements of the fluorescence signal strength of individual axon terminals. The CSLM also allowed detection of co-localized neurochemicals in axon terminals.

Animals↗
PubMed2004

Immunoglobulin improves a model of acute motor axonal neuropathy by preventing axonal degeneration.

BACKGROUND: The action mechanism of IV immunoglobulin (IVIg) for Guillain-Barré syndrome has yet to be clarified. OBJECTIVE: To evaluate clinical, histologic, and immunologic effects in a disease model of acute motor axonal neuropathy (AMAN) treated by IVIg. METHODS: Rabbits were sensitized with gangliosides including GM1 and divided randomly into two groups at disease onset. One group received IV homologous gamma-globulin (400 mg/kg/day) for 5 days (n = 15), and the other received saline (n = 15). Disease severity was scored (0 to 13 points) daily. Sixty days after onset, anti-GM1 antibodies were tested by ELISA, and the number of degenerative axons was counted in spinal anterior roots. RESULTS: Between both groups at onset, there was no difference in any characteristics including clinical score. The IVIg group had faster recovery than the saline group (p = 0.03). The percentage of rabbits that improved by a score of < or =4 was higher in the IVIg (53%) than in the saline (13%) group 60 days after onset (p = 0.03). Anti-GM1 IgG titers 60 days after onset did not differ between the groups. The anterior roots of rabbits surviving 60 days after onset showed lower frequency of axonal degeneration in the IVIg-treated (n = 11; mean 4.5%) than in the saline-treated (n = 8; mean 11.1%) rabbits (p = 0.01). CONCLUSIONS: The therapeutic efficacy of IVIg in an AMAN model was confirmed. IVIg may not affect the production or catabolism of anti-GM1 IgG, but it may prevent axonal degeneration of motor nerves.

Animals↗
PubMed1976

"Giant axonal neuropathy" caused by industrial chemicals: neurofilamentous axonal masses in man.

Symmetrical polyneuropathy developed in two patients after they had been in contact with acrylamide and methyl n-butyl ketone, respectively. In sural nerve biopsy material from both patients, electron microscopy showed frequent focal axonal swellings containing masses of neurofilaments. Some axons undergoing axonal degeneration also were seen. These morphologic features are identical to those produced in experimental animals after exposure to these chemicals and are similar to those found in n-hexane neuropathy and in the three reported cases of giant axonal neuropathy. Sural nerve biopsy is an important diagnostic test in identifying cases of peripheral neuropathy caused by these chemicals.

Acrylamides↗
PubMed2001

RET signaling is essential for migration, axonal growth and axon guidance of developing sympathetic neurons.

Sympathetic axons use blood vessels as an intermediate path to reach their final target tissues. The initial contact between differentiating sympathetic neurons and blood vessels occurs following the primary sympathetic chain formation, where precursors of sympathetic neurons migrate and project axons along or toward blood vessels. We demonstrate that, in Ret-deficient mice, neuronal precursors throughout the entire sympathetic nervous system fail to migrate and project axons properly. These primary deficits lead to mis-routing of sympathetic nerve trunks and accelerated cell death of sympathetic neurons later in development. Artemin is expressed in blood vessels during periods of early sympathetic differentiation, and can promote and attract axonal growth of the sympathetic ganglion in vitro. This analysis identifies RET and artemin as central regulators of early sympathetic innervation.

Animals↗
PubMedDate not supplied

Substance P immunoreactive sensory axons as a subset of the total axonal population in the maxillary sinus of the rabbit: a characterization of normal and infected mucosa.

Substance P (SP), one of the neuropeptides released from sensory nerves, is thought to mediate neurogenic inflammation. Although SP immunoreactive axons have been described in the sinus mucosa, no attempt has been made to characterize SP fibers as a subset of all axons present in the sinus mucosa. In addition, no study to date has characterized the changes in infected sinus mucosa. The maxillary sinus mucosa of New Zealand white rabbits was harvested from control animals and in animals with induced maxillary sinusitis. Immunohistochemical staining of the sinus mucosa for both Protein Gene Product 9.5 (PGP), a nonspecific marker for all nerves, and for SP was performed on 11 animals: 3 controls and 8 infected. In sinus mucosa from the control rabbits, <50% of all axons labeled by PGP were immunoreactive for SP. In infected mucosa, the absolute number of axons found by PGP staining decreased and nearly all of these remaining fibers were also immunoreactive for SP. We conclude that the phenotypical labeling of nerve fibers seen in normal mucosa is altered by bacterial-induced infection.

Animals↗
PubMed2001

Exacerbation of traumatically induced axonal injury by rapid posthypothermic rewarming and attenuation of axonal change by cyclosporin A.

OBJECT: Although considerable attention has been focused on the use of posttraumatic hypothermia, little consideration has been given to the issue of posthypothermic rewarming and its potentially damaging consequences. In this communication, the authors examine the issue of rapid posthypothermic rewarming compared with gradual rewarming while exploring the potential utility of cyclosporin A (CsA) administration for attenuating any rapid rewarming-induced axonal change. METHODS: Male Sprague-Dawley rats were subjected to impact-acceleration injury and then their body temperature was lowered to 32 degrees C for 1 hour postinjury. After hypothermia, rewarming to normothermic levels was accomplished either within a 20-minute period (rapid rewarming) or over a 90-minute period (slow rewarming). Some animals in the rapid rewarming group received intrathecal infusion of either CsA or its vehicle, whereas the rats in the slow rewarming group received vehicle alone. Both the CsA and its vehicle were administered immediately before initiation of rewarming. Twenty-four hours postinjury the animals' brains were processed for visualization of amyloid precursor protein (APP), a marker of traumatic axonal injury. The APP-positive axonal density in the gradually rewarmed group receiving vehicle was statistically significantly reduced in comparison with the rapidly rewarmed, vehicle-treated group. For the group undergoing rapid rewarming and treatment with CsA, a statistically significant reduction was also found in the density of the APP profiles compared with the rapidly rewarmed, vehicle-treated group. CONCLUSIONS: The results of this study show that rapid rewarming exacerbates traumatically induced axonal injury, which can be significantly attenuated by administering CsA.

Amyloid beta-Protein Precursor↗
PubMed2000

A model of high-frequency ripples in the hippocampus based on synaptic coupling plus axon-axon gap junctions between pyramidal neurons.

So-called 200 Hz ripples occur as transient EEG oscillations superimposed on physiological sharp waves in a number of limbic regions of the rat, either awake or anesthetized. In CA1, ripples have maximum amplitude in stratum pyramidale. Many pyramidal cells fail to fire during a ripple, or fire infrequently, superimposed on the sharp wave-associated depolarization, whereas interneurons can fire at high frequencies, possibly as fast as the ripple itself. Recently, we have predicted that networks of pyramidal cells, interconnected by axon-axon gap junctions and without interconnecting chemical synapses, can generate coherent population oscillations at >100 Hz. Here, we show that such networks, to which interneurons have been added along with chemical synaptic interactions between respective cell types, can generate population ripples superimposed on afferent input-induced intracellular depolarizations. During simulated ripples, interneurons fire at high rates, whereas pyramidal cells fire at lower rates. The model oscillation is generated by the electrically coupled pyramidal cell axons, which then phasically excite interneurons at ripple frequency. The oscillation occurs transiently because rippling can express itself only when axons and cells are sufficiently depolarized. Our model predicts the occurrence of spikelets (fast prepotentials) in some pyramidal cells during sharp waves.

Action Potentials↗
PubMed2000

Effects of acute and chronic gonadectomy on the catecholamine innervation of the cerebral cortex in adult male rats: insensitivity of axons immunoreactive for dopamine-beta-hydroxylase to gonadal steroids, and differential sensitivity of axons immunoreactive for tyrosine hydroxylase to ovarian and testicular hormones.

Previous studies have shown that gonadectomy in adult male rats induces a complex series of region- and time-specific changes in the density of presumed cerebral cortical dopamine axons that are immunoreactive for tyrosine hydroxylase. The present study asked whether noradrenergic cortical afferents also show hormone sensitivity by assaying axons immunoreactive for the enzyme dopamine-beta-hydroxylase in representative areas of acutely and chronically gonadectomized and sham-operated adult male rats. Catecholamine afferents (both tyrosine hydroxylase-immunoreactive and dopamine-beta-hydroxylase-immunoreactive) were also quantified in gonadectomized rats supplemented with testosterone propionate, with 17-beta-estradiol, or with 5-alpha-dihydrotestosterone. Analyses of noradrenergic (dopamine-beta-hydroxylase) afferents revealed no differences in axon appearance or density among the hormonally intact and hormonally manipulated groups. However, analyses of tyrosine hydroxylase immunoreactivity revealed an unexpected division of labor among ovarian and testicular hormones in ameliorating the effects of acute verses chronic hormone deprivation on these afferents. Estradiol replacement attenuated the decreases in immunoreactivity induced by acute gonadectomy, but was ineffective in suppressing changes in immunoreactivity stimulated by chronic gonadectomy. In contrast, supplementing gonadectomized animals with dihydrotestosterone provided no protection from acute decreases in innervation, but fully attenuated both the supragranular decreases and infragranular increases in tyrosine hydroxylase-immunoreactive axon density that mark the association cortices of chronically gonadectomized rats. Together these findings indicate both long- and short-term effects of gonadectomy on cortical catecholamines, principally target dopamine afferents, and that chronic gonadectomy, which selectively disturbs dopamine innervation in the prefrontal cortices, involves a compromise in androgen signaling pathways.

Afferent Pathways↗
PubMed1996

Axonal action-potential initiation and Na+ channel densities in the soma and axon initial segment of subicular pyramidal neurons.

A long-standing hypothesis is that action potentials initiate first in the axon hillock/initial segment (AH-IS) region because of a locally high density of Na+ channels. We tested this idea in subicular pyramidal neurons by using patch-clamp recordings in hippocampal slices. Simultaneous recordings from the soma and IS confirmed that orthodromic action potentials initiated in the axon and then invaded the soma. However, blocking Na+ channels in the AH-IS with locally applied tetrodotoxin (TTX) did not raise the somatic threshold membrane potential for orthodromic spikes. TTX applied to the axon beyond the AH-IS (30-60 microm from the soma) raised the apparent somatic threshold by approximately 8 mV. We estimated the Na+ current density in the AH-IS and somatic membranes by using cell-attached patch-clamp recordings and found similar magnitudes (3-4 pA/microm2). Thus, the present results suggest that orthodromic action potentials initiate in the axon beyond the AH-IS and that the minimum threshold for spike initiation of the neuron is not determined by a high density of Na+ channels in the AH-IS region.

Action Potentials↗
PubMed1999

Acute motor axonal neuropathy and acute motor-sensory axonal neuropathy share a common immunological profile.

Griffin and colleagues (Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, Mishu B, Cornblath DR, Macko C, McKhann GM, Asbury AK. Pathology of motor-sensory axonal Guillain-Barré syndrome. Ann Neurol 1996;39:17-28 [4]) proposed that acute motor axonal neuropathy (AMAN) and acute motor-sensory axonal neuropathy (AMSAN) are part of the spectrum of a single type of immune attack on the axon. In contrast, IgG anti-GM1 antibody is associated closely with AMAN, but whether other IgG anti-ganglioside antibodies are associated with this neuropathy is not clear. We investigated whether IgG anti-ganglioside antibodies can be used as immunological markers to differentiate AMAN from acute inflammatory demyelinating polyneuropathy (AIDP) and whether these autoantibodies are present in AMSAN. The frequencies of anti-GM1, anti-GM1b, and anti-GD1a IgG antibodies in 21 AMAN patients were significantly higher than in 19 AIDP patients. Anti-GM1b and anti-GD1a IgG, as well as anti-GM1 IgG antibodies, therefore are immunological markers for AMAN. The patients with AMSAN had anti-GM1, anti-GM1b, and anti-GD1a IgG antibodies, indicative that AMAN and AMSAN share a common immunological profile.

Adolescent↗
PubMed1994

Retrograde axonal transport of locally synthesized proteins, e.g., actin and heat shock protein 70, in regenerating adult frog sciatic sensory axons.

The local synthesis and subsequent retrograde axonal transport of [35S]methionine-labelled proteins was studied in the in vitro regenerating adult frog sciatic sensory axons. By the use of a three compartment culture system, proteins in the outgrowth region were selectively labelled. After 2 days in culture a rise in TCA-insoluble radioactivity was detected in the dorsal root ganglia, which could be prevented by the addition of vinblastine or 2,4-dinitrophenol to the nerve proximal to the crush site. Two-dimensional polyacrylamide gel electrophoresis of ganglionic proteins revealed a pattern of 35 labelled polypeptides with apparent molecular masses (Mm) ranging from < 15 to 95 kDa and with isoelectric points (pI) ranging from 4.5 to 6.5. The major ones, representing about 75% of the activity in a gel, were of Mm/pI 47/5.4, 48/6.1,. 57/6.0, 62/5.2, 65/4.9-5.0, 65/5.2, and 81/5.4 respectively. One of these polypeptides (47/5.4) was identified as actin and another (81/5.4) as a member of the heat shock protein 70 family. The spots at 65/4.9-5.0 were tubulin isoforms. There was a striking similarity between transported proteins on one hand, and proteins synthesized in the injured nerve on the other, with respect to the Mm/pI of at least 14 protein species. The results suggest that a selected set of proteins, synthesized by non-neuronal cells, e.g., Schwann cells, is transferred to the ganglionic cell bodies by retrograde axonal transport.

Actins↗
PubMed2001

Calcium/calmodulin-dependent protein kinase IIalpha in optic axons moves with slow axonal transport and undergoes posttranslational modification.

In neurons, the mRNA for calcium/calmodulin-dependent protein kinase II alpha (CKIIalpha) is known to be targeted to dendrites-where the enzyme is synthesized and supports postsynaptic functions. We are interested in knowing how neuronal proteins enter axons from the nerve cell body, and the mechanism for protein transport to terminals. Because CKIIalpha immunofluorescence can be demonstrated in over 80% of retinal ganglion cells, we asked whether this regulatory protein is being transported into optic axons. Using Sprague-Dawley rats, [(35)S] methionine was injected into the vitreous humor of the eye. Four days later, the optic nerves, tracts, lateral geniculate ganglia, and superior colliculi were removed and processed for 2D-PAGE and Western blotting. Radiolabeled CKIIalpha appears to move with slow component b (SCb) of axonal transport, as is the case in rodent sciatic motor neurons. In addition, the radiolabeled CKIIalpha isoform that enters the optic nerve is found to be 4 kDa heavier (in SDS-PAGE molecular mass) than the isoform in the optic tract, superior colliculus, and lateral geniculate nucleus. This reduction is likely the result of dephosphorylation, which is a mechanism used to regulate the enzyme's activity.

Animals↗
PubMed1996

Effects of nerve growth factor on axonal retrograde transport after axonal injury of motoneurons.

In this experimental study we coupled nerve growth factor (NGF) with notatin by dicyclohexylcarbodiimide to label NGF and observed the effects of NGF on axonal retrograde transport after axonal injury of motoneurons with the aid of notatin chemiluminescence system. The results showed that NGF could be transported through axon not only to sensory neurons in dorsal root ganglia but also to motoneurons in spinal cord ventral horn.

Animals↗
PubMed1996

The axonal transport of beta III-tubulin is altered in both branches of sensory axons after injury of the rat sciatic nerve.

We have analyzed the axonal transport of beta III-tubulin in the central (dorsal root) and peripheral (sciatic nerve) branches of sensory axons after injury of the sciatic nerve. Our finding that the relative amount of beta III-tubulin transported in slow component b (SCb) is increased in both axonal branches does not support the generally accepted hypothesis that the transport of cytoskeletal proteins is altered in the peripheral, but not the central branch after injury of the sciatic nerve.

Animals↗
PubMed1987

Differential growth of the branches of a regenerating bifurcate axon is associated with differential axonal transport of organelles.

Axonal trees display differential growth during development or regeneration; that is, some branches stop growing and often retract while other branches continue to grow and form stable synaptic connections. In this study, an in vitro model of differential growth is examined to identify the intracellular events responsible for this phenomenon. When the giant cerebral neuron of Aplysia californica is placed in culture, vigorous growth occurs from the ends of both branches of its bifurcate axon. If an appropriate target neuron is placed next to one branch, growth from that branch is unabated while growth from the other branch is suppressed. The bidirectional fast transport of membranous organelles was examined in the two branches by the use of high-resolution video microscopy. Transport was similar in the branches in the absence of a target cell but was much greater in the growing than in the nongrowing branch when a target was present. Electron microscopic examination of fixed specimens confirmed these findings. Differential growth may be initiated or sustained by a diversion from certain branches of materials used in growth which are supplied by fast axonal transport.

Animals↗
PubMed1985

Localization of axonally transported [125I]wheat germ agglutinin in rat abducens motoneuron axons and terminals after intracisternal injection.

Iodinated wheat germ agglutinin (WGA) was taken up and transported by rat abducens motoneurons to nerve terminals in the lateral rectus muscle. Five days after intracisternal injection of lectin, axon terminals wee found to be the most radioactive source, based on the density of labeling. In axons the radioactive label was concentrated in an annular region about 1.26 microns wide beneath the plasma membrane. We hypothesize that the WGA was associated with smooth vesicular and tubular structures in the axoplasm but not limited to organelles immediately beneath the axon plasma membrane. No evidence of intercellular transfer to muscle cells was found.

Abducens Nerve↗
PubMed1991

Retrograde axonal transport of the GTP-binding protein Gi alpha: a potential neurotrophic intra-axonal messenger.

When a neuronal target is to provide information to the nucleus of the neurone innervating it, it faces the problem of getting its message up the long length of axon separating the cell body from the site of receptor activation at the terminal. The retrograde axonal transport of the neurotrophic molecule, nerve growth factor (NGF), provided one possible mechanism for this information transfer in the sympathetic nervous system. However, some neurotrophic molecules are not retrogradely transported, indicating the message is carried back by a different mechanism. In this paper, we examined such a novel mechanism mediated by the retrograde axonal transport of the alpha subunit of the second messenger protein, Gi. It is proposed that some non-transported neurotrophic molecules may produce a stable second messenger that is itself transported to the nucleus to convey the target derived information for survival.

Animals↗