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.

SourceResearch connectionFrom yearThrough year

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

At least 1,297 records · Page 72Linked to original sources

PubMed1993

Regenerating axons are not required to induce the formation of a Schwann cell cable in a silicone chamber.

After suture of proximal and distal nerve stumps into the ends of a silicone chamber, a tissue cable forms inside the chamber through which axons regenerate. Schwann cells are a critical cellular component of the cable because in their absence axons fail to regenerate into the cable. In this study, we sought to determine whether axons were needed to induce the formation of a Schwann cell-containing cable. Transected stumps of sciatic nerves of adult rats were sutured into the ends of silicone chambers prefilled with phosphate-buffered saline or dialyzed plasma, leaving a 10-mm interstump gap. In order to eliminate any axonal influence in the chamber, the proximal sciatic nerve was further transected, ligated, and reflected, leaving a 4-mm piece of denervated nerve in the proximal chamber. A tissue cable formed at 4 weeks only in those chambers prefilled with dialyzed plasma. Light and electron microscopy revealed a central core of Schwann cells and fibroblasts within the cable that were collectively surrounded by a circumferential layer of fibroblasts and collagen. Blood vessels were randomly located throughout the cable. The Schwann cells extended numerous processes that were confined within a basal lamina-like membrane. Many of these processes contained microtubules and resembled unmyelinated axons. The ultrastructure of the processes, however, differed from that of axons in that some of the processes were in direct contact with the basal lamina of the Schwann cells and not surrounded by any other cell extensions. However, since these processes neither stained with silver nor disappeared after transection of the nerves entering or leaving the chamber, we conclude that they are not axons but in fact Schwann cell processes. In other animals bearing 4-week cables, the reflected nerve stump was reattached to the nerve piece in the proximal end of the chamber. Four weeks later, all the cables and varying lengths of the distal nerve trunks were filled with numerous myelinated and unmyelinated axons. The Schwann cell cable that forms within a dialyzed plasma prefilled chamber presents a useful system for basic research concerning the molecular mechanisms of Schwann cell or Schwann cell-axonal interactions and for applied research involving the clinical repair of human peripheral nerve injuries. Since a cable formed by our surgical method supports axonal regeneration, it has the potential to eliminate the need for a nerve graft to repair a gap in a nerve that requires delayed surgical intervention.

Animals↗

PubMed2006

An experimental animal model of spinal root compression syndrome: an analysis of morphological changes of myelinated axons during compression radiculopathy and after decompression.

The treatment of radicular pain is mainly empirical because there are only few experimental studies dealing with morphological changes during compression radiculopathy. The goal of the study was to investigate changes in the morphology of myelinated axons during spinal root compression and the influence of decompression in a new rat model. The number of myelinated axons and their diameter were measured at 1, 2, 5, and 8 weeks during compression of the dorsal spinal root. The same approach was applied for 1-week compression followed by decompression for 1 or 2 weeks and compression for 5 weeks followed by 3-week decompression. A decrease in the number of myelinated axons (particularly those of large diameters) occurred after compression for 1 week. Continued compression for up to 8 weeks resulted in centripetal increase in the number of myelinated axons and the persistence of a small fraction of large myelinated axons at the site of compression. After that time, a decreased number of axons and a reduced fraction of large myelinated axons occurred again. Decompression after 1-week compression caused a rapid increase in the number of both small and large myelinated axons within the spinal root including the site of compression. A small fraction of regenerated axons was found after 5-week compression followed by 3-week decompression. Finally, we investigated the time course of the temporary increase in the number of regenerated myelinated axons during dorsal root compression for up to 8 weeks. The efficacy of decompression was superior when applied one week after compression or after regress of the acute phase of aseptic inflammation associated with fragility of spinal root. The results of the study verify the need for early surgical decompression to prevent irreversible damage of the spinal roots.

Animals↗

PubMed1985

Long-term patterns of axon regeneration in the sciatic nerve and its tributaries.

The present study determines the numbers of axons that regenerate after sciatic nerve transection in the rat. The transections are done by removing either 4 mm or 8 mm of the nerve. The axons are counted in the gap and distal stump of the sciatic nerve and in 5 of its tributaries. Survival time is 9 months which we define as long-term to allow comparison with short-term data obtained after a much shorter survival. The first findings is that the numbers of axons in the gap and distal stump are different in the 2 transection paradigms. For the 4 mm paradigm, more axons than normal appear in the gap and only a fraction of these pass into the distal stump. For the 8 mm paradigm, the numbers of axons in the gap are normal and the numbers in the distal stump do not deviate far from these. Thus by changing only the length of the segment of removed nerve, one causes major differences in the numbers of axons that regenerate. Second the numbers of axons that regenerate in tributary nerves that innervate muscle have a different pattern than the numbers that regenerate into cutaneous nerves. Thus the factors control axonal numbers must be different in the 2 types of nerves. Finally, axons that regenerate into tributary nerves do not, by and large, regenerate in concert with those in the distal stump of the parent nerve. Thus the factors that control axonal numbers in the tributary nerves must be different from those that control the numbers in the distal stump of the parent nerve.

Animals↗

PubMed1987

Spinal cord transplants permit the growth of serotonergic axons across the site of neonatal spinal cord transection.

These experiments were designed to determine whether transplants of fetal spinal cord tissue into lesioned spinal cord in newborn rats provide a terrain that supports the growth of serotonergic (5-HT) axons across the site of the lesion. Although descending serotonergic axons can regenerate after chemical lesions in adult animals, they show little regrowth after surgical lesions. In newborn animals, 5-HT axons do not regrow after either chemical or mechanical lesions since the axotomized raphe-spinal neurons die. After partial spinal cord lesions made in developing animals, immature axons can take an aberrant route around the site of the lesion to reach normal target areas. Even these robust, late-growing, uninjured axons, however, are unable to grow through the site of the spinal cord lesion. Immunocytochemical labeling was used to determine if descending serotonergic axons grow into fetal spinal cord transplants, and whether these axons cross the transplant to reach spinal cord levels caudal to the lesion. Spinal cord transection at a mid-thoracic spinal cord level on the day of birth resulted in a dramatic decrease in 5-HT immunoreactivity caudal to the lesion by one day postoperative. 5-HT immunoreactivity caudal to the lesion was abolished by 5 days postoperative and did not return after acute or chronic (6 months) survival periods. When a transplant of fetal spinal cord tissue was placed into the lesion site, 5-HT axons were identified throughout the transplant. At spinal cord levels caudal to the transection and transplant, the serotonergic axons were identified in the host spinal cord in both the white and gray matter. This 5-HT innervation was not confined to spinal cord segments adjacent to the lesion site but extended to spinal cord segments as far as lower lumbar levels. The reinnervation of the host spinal cord caudal to the transection was far less than that seen in unlesioned adult rat spinal cord. Horseradish peroxidase (HRP) injected caudal to the transection and transplant, retrogradely labeled neurons within the medullary raphe nuclei. The HRP and 5-HT results both depended on apposition of the transplant with the rostral and caudal stumps of the host spinal cord; without such apposition, labeling was abolished. These results indicate that the presence of a transplant at the site of the neonatal lesion modifies the environment at the lesion site in such a manner as to support the elongation of identified axons across the site of the lesion and into the host cord caudal to the lesion.

Animals↗

PubMed2006

Chondroitinase applied to peripheral nerve repair averts retrograde axonal regeneration.

Antegrade, target-directed axonal regeneration is the explicit goal of nerve repair. However, aberrant and dysfunctional regrowth is commonly observed as well. At the site of surgical nerve coaptation, axonal sprouts encounter fibrotic connective tissue rich in growth-inhibiting chondroitin sulfate proteoglycan that may contribute to misdirection of axonal regrowth. In the present study, we tested the hypothesis that degradation of chondroitin sulfate proteoglycan by application of chondroitinase at the site of nerve repair can decrease aberrant axonal growth. Adult rats received bilateral sciatic nerve transection and end-to-end repair. One nerve was injected with chondroitinase ABC and the contralateral nerve treated with vehicle alone. After 28 weeks, retrograde axonal regeneration was assessed proximal to the repair by scoring neurofilament-immunopositive axons within the nerve (intrafascicular) and outside the nerve proper (extrafascicular). Intrafascicular retrograde axonal growth was equivalent in both control and chondroitinase treatment conditions. In contrast, chondroitinase treatment caused a pronounced (93%) reduction in extrafascicular retrograde axonal growth. The decrease in axon egress from the nerve was coincident with an increase in antegrade regeneration and improved recovery of motor function. Based on these findings, we conclude that chondroitinase applied at the site of nerve transection repair averts dysfunctional extrafascicular retrograde axonal growth.

Animals↗

PubMed2006

Age-dependent interactive changes in serotonergic and noradrenergic cortical axon terminals in F344 rats.

In the frontal cortex of aging rats, we found an increase in sprouting of the noradrenergic (NA) axons originated from the locus coeruleus (LC). The serotonergic (5-HT) axons originating from the dorsal raphe (DR) share the same cortical area and their age-dependent changes and interactions with NA axons were still unclear. To compare quantitatively the extent of axonal sprouting of DR and LC neurons in the frontal cortex, we extracellularly recorded from both DR and LC neurons in the same animals and antidromically stimulated 32 cortical sites (a pair of stimulating electrodes was moved at 100-mum intervals from 500 to 2000 microm in depth). In addition, to examine the effects of degeneration of 5-HT axons on NA axons, and vice versa, we used specific neurotoxins for 5-HT (PCA) or NA (DSP-4) axons. We also used noradrenaline uptake inhibitor (maprotiline) to verify the effects of NA on degeneration of 5-HT axons. Results suggested that 5-HT axons sprouted between 15 and 17 months of age and noradrenaline accelerated the age-dependent change of 5-HT axons.

Adrenergic Uptake Inhibitors↗

PubMed1998

The ventral motoneurone axon bundle in the CNS--a cordone system?

In the developing CNS neighbouring structures are commonly separated by transient barriers termed cordones, some of which coincide with glial elements. Where ventral motoneuron axons cross the spinal white matter as intramedullary bundles to reach the CNS-PNS transitional zone they are surrounded from early development by a glial sleeve resembling a cordone. This becomes better developed with age and, like some cordones, persists into adult life. This could provide a radial conduit which might underlie the capacity of central segments of mature ventral motoneurone axons to regenerate. It may also provide a pathway for glial migration from the central cord to more superficial levels, including the transitional zone, where they help form the CNS-PNS barrier. Axons in the intramedullary bundle and in the surrounding ventral white column mature at different rates. Glial sleeve cells of the intramedullary bundles are apposed to both. Morphometric analysis of the axon-glial relationships of the two populations indicates that glial development proceeds at a different rate in relation to each axon class and that this is influenced by the degree of axonal maturation, which may in turn be related to target contact. Furthermore, early axon glial relationships differ between the two populations. For ventral motoneurone axons these take place in two stages: firstly, glial segregation of axons (resembling that in the PNS) and secondly, oligodendrocytic contact and ensheathment, which leads on to myelination. Axon-glial relationships in the ventral white column begin with the second of these events, as is more typical of early CNS myelination in general.

Age Factors↗

PubMed1999

Myelin does not influence the choice behaviour of entorhinal axons but strongly inhibits their outgrowth length in vitro.

Myelin is crucial for the stabilization of the entorhinohippocampal projection during late development and is a non-permissive substrate for regrowing axons after lesion in the adult brain. We used two in vitro assays to analyse the impact of myelin on rat entorhinohippocampal projection neurons. A stripe assay was used to study the impact of myelin on the choice behaviour of axons from the entorhinal cortex (EC). Given a choice between alternating hippocampal membrane lanes from developmental stages ranging from early postnatal to adult, EC axons preferred to extend on early postnatal hippocampal membranes. Neither the neutralization of myelin-associated factors by a specific antibody (IN-1) nor the separation of myelin from membranes interfered with the axons' choice behaviour. The entorhinal axons showed no preference in the membrane combination of adult and myelin-free adult hippocampal membranes. These stripe assay experiments demonstrate that support for EC axon choice in the developing hippocampus is maturation-dependent and is not influenced by myelin. The application of IN-1 in the outgrowth assay and the separation of myelin from membranes, enhanced elongation of outgrowing entorhinal axons on adult hippocampal membranes, whereas a control antibody did not. This shows that myelin-associated factors have a strong inhibitory effect on the outgrowth length of entorhinal axons. In conclusion, we suggest that axonal elongation in the entorhinohippocampal system during development is strongly influenced by myelin-associated growth inhibition factors and that specific target finding of entorhinal axons is regulated by a different mechanism.

Age Factors↗

PubMed2002

Mechanical tension can specify axonal fate in hippocampal neurons.

Here we asked whether applied mechanical tension would stimulate undifferentiated minor processes of cultured hippocampal neurons to become axons and whether tension could induce a second axon in an already polarized neuron. Experimental tension applied to minor processes produced extensions that demonstrated axonal character, regardless of the presence of an existing axon. Towed neurites showed a high rate of spontaneous growth cone advance and could continue to grow out for 1-3 d after towing. The developmental course of experimental neurites was found to be similar to that of unmanipulated spontaneous axons. Furthermore, the experimentally elongated neurites showed compartmentation of the axonal markers dephospho-tau and L-1 in towed outgrowth after 24 h. Extension of a second axon from an already polarized neuron does not lead to the loss of the spontaneous axon either immediately or after longer term growth. In addition, we were able to initiate neurites de novo that subsequently acquired axonal character even though spontaneous growth cone advance began while the towed neurite was still no longer than its sibling processes. This suggests that tension rather than the achievement of a critical neurite length determined axonal specification.

Animals↗

PubMed1990

Responses of Regenerating Rat Retinal Ganglion Cell Axons to Contacts with Central Nervous Myelin in vitro.

In order to investigate the responses of neurites to myelin in vitro, retinal explants obtained from adult rats were cultured on poly-L-lysine and laminin. Regenerating adult ganglion cell axons were confronted with rat central myelin which was adsorbed on culture dishes. When the explants were placed directly on the myelin, axons did not grow out. Alternatively, when the explants were placed at a certain distance from the myelin, massive outgrowth of axons was observed. When axonal growth cones encountered the myelin, they displayed various reactions. All single axons observed immediately stopped growing after encountering the myelin border. All of them remained for at least 4 h at the border. Sixteen per cent of them remained in this 'resting state' throughout the time of observation (2 - 5 days). Nineteen per cent of the axons degenerated following contact with the myelin. The majority of axons were able to circumvent the myelin either by backbranching (21%) or by growing in another direction with the leading growth cone (37%). Eight per cent of the axons were observed to enter the myelin. The results indicate that central myelin represents a non-permissive obstacle for growing adult axons. This observation is in conformity with the inability to regenerate that is typical of lesioned optic nerve axons in situ.

Journal Article↗

PubMed1991

Axons Sprout and Microtubules Increase After Local Inhibition of RNA Synthesis, and Microtubules Decrease after Inhibition of Protein Synthesis: A Morphometric Study of Rat Sural Nerves.

Drugs that inhibit RNA or protein synthesis are known to affect some functional properties of axons. In this context, we studied the ultrastructural effects of actinomycin-D, an inhibitor of RNA synthesis, and cycloheximide and emetine, inhibitors of protein synthesis, in rat sural nerves. A silicone sleeve (4 mm long) loaded with drug was placed around the nerves and left for about a week. The ultrastructural alterations of axons and Schwann cells progressed over this period. After cycloheximide and emetine, the cytoplasm of Schwann cells was enlarged and the rough endoplasmic reticulum was prominent. After actinomycin-D, the Schwann cells reached the stage of lysis. Nonmedullated were more affected than myelinated axons. After cycloheximide and emetine, the axoplasmic matrix decreased substantially but reversibly. Microtubules of nonmedullated fibres decreased by about 50%. Actinomycin-D determined sprouting of axons and a rise of axonal microtubules; in nonmedullated axons, the normal inverse correlation between microtubular density and calibre gave way to a high and constant density for all axonal sizes. A few millimetres proximal and distal to the sleeve, the nerve tissue and the axonal microtubular content were close to normal, i.e. the effects of drugs were local. Present results suggest that the local turnover of amino acids in the axon is necessary to maintain the integrity of microtubule and neurofilament proteins. We propose that the Schwann cell down-regulates the axonal cytomatrix.

Journal Article↗

PubMed1991

Presynaptic GABAA and GABAB Receptor-mediated Phasic Modulation in Axons of Spinal Motor Interneurons.

The lamprey spinal cord has been utilized to investigate the role of presynaptic inhibition in the control of the spinal motor system. Axons of the lamprey spinal cord are comparatively large because of their lack of myelination. Axons impaled with microelectrodes demonstrate depolarizing responses to the application of GABAA and GABAB receptor agonists, muscimol and baclofen. These depolarizing effects are counteracted by the specific GABAA and GABAB receptor antagonists, bicuculline and phaclofen. GABAA receptor activation leads to a gating of Cl- channels on the axons. However, the ionic mechanism leading to axonal depolarization following GABAB receptor activation is unknown. After initiation of fictive locomotion, these axons demonstrate oscillations in axonal membrane potential related to the locomotor cycle. During ficitive locomotion they depolarize in phase with the bursting of the ipsilateral ventral root of the same segment. These axonal membrane potential oscillations are due to a phasic GABAA and GABAB receptor-mediated gating of ion channels on the axonal membrane. Fictive locomotion in the lamprey spinal cord is largely unaffected by antagonism of one or other GABA receptor subtype alone, but is severely disrupted by simultaneous antagonism of both subtypes. In conclusions, we demonstrate, for the first time, an agonist-gated depolarization of a vertebrate presynaptic element measured by direct impalement of the axon under study. We also demonstrate that GABA-mediated presynaptic inhibition occurs in axons of spinal interneurons. It is not limited to the primary afferents as has previously been believed.

Journal Article↗

PubMed1985

Relationship among recruitment order, axonal conduction velocity, and muscle-unit properties of type-identified motor units in cat plantaris muscle.

A strict interpretation of the size-principle hypothesis (37, 39-41) is that a muscle's motor units should be recruited in an ascending order according to both the size of their motoneurons and the size of their innervated muscle units (for reviews see Refs. 9, 39, 73). Studies of large mixed muscles in the cat hindlimb, however, have shown that motor axonal conduction velocity and tetanic tension, which are frequently considered indices of motoneuron and muscle-unit size, respectively, are uncorrelated in the fast-twitch (type F) motor-unit subpopulation (12, 13, 23, 24, 30, 32, 63, 71, 79). Attempting to focus on type F units, we compared the recruitment order of 42 pairs of cat plantaris (PL) motor units with both axonal conduction velocity and tetanic tension as well as with other muscle-unit properties. Single PL alpha-motor axons were functionally isolated in intact L7 ventral root filaments of decerebrate cats. Tension responses produced by stimulating each isolated motor axon were used to find the tetanic tension of the muscle unit and to classify the unit (12) as either type S (slow twitch, fatigue resistant), type FR (fast twitch, fatigue resistant), type FI (fast twitch, intermediate fatigability), or type FF (fast twitch, highly fatigable). Conduction velocity of each isolated axon was computed from measurements of axonal conduction time and length. The axon's reflex discharges were recorded from the proximal end of the cut filament and compared with the discharges of another PL axon residing in a different, previously cut filament of the same cat. The recruitment order of each motor-unit pair studied was found during reflexes elicited by homonymous muscle stretch, tendon taps, or single shocks at group I intensity to the PL nerve. If either axon of the pair failed to discharge, as often was the case with the high-threshold type F units, the monosynaptic reflex was facilitated by a 500-pps conditioning train applied proximal to a complete reversible cooling block of the PL nerve. In all 42 pairs studied, the weaker motor unit had the lower functional threshold for recruitment. Recruitment also invariably followed the order S greater than FR greater than FI greater than FF units. The motor unit of a pair with the higher resistance to fatigue thus always had the lower functional threshold. In 21 of the 22 pairs containing at least one type S motor unit, the unit with the slower-conducting motor axon had the lower functional threshold for recruitment.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2003

Mitochondrial movement and positioning in axons: the role of growth factor signaling.

The extreme length of axonal processes requires that aerobic ATP production and Ca(2+) homeostasis are non-uniformly organized in the cytoplasm. As a result, the transport and positioning of mitochondria along axons is essential for neuronal homeostasis. Mitochondria undergo rapid but intermittent transport in both the anterograde and retrograde directions in axons. We have shown that in chick embryonic sensory neurons, the transport of mitochondria responds to physiological changes in the cell and, particularly, to growth cone activity. When an axon is actively elongating, mitochondria move preferentially anterograde and then become stationary, accumulating in the region of the active growth cone. When axonal elongation ceases, mitochondria in the distal axon resume movement but undergo net retrograde transport and become uniformly distributed along the axon. This redistribution of mitochondria is achieved in two ways: there is a transition between motile and stationary mitochondria and a large up- and downregulation of their anterograde, but not retrograde, motor activity. Mitochondrial transport does not respond to the experimentally induced elongation of axons in the absence of an active growth cone, implying that signals from the active growth cone regulate transport. To determine the nature of these signals, we have focally stimulated the shafts of sensory axons in culture with nerve growth factor (NGF) covalently conjugated to polystyrene beads. We find that mitochondria accumulate at regions of focal NGF stimulation. This response is specific to mitochondria and does not result from general disruption of the cytoskeleton in the region of stimulation. Disruption of the phosphoinositide 3-kinase (PI 3-kinase) pathway, one of the signaling pathways downstream from NGF-receptor binding, completely eliminates NGF effects on mitochondrial behavior in axons. We propose that mitochondrial transport and/or docking are regulated in part via NGF/TrkA/PI 3-kinase signaling.

Animals↗

PubMed2004

Axonal defects in mouse models of motoneuron disease.

Human motoneuron disease is characterized by loss of motor endplates, axonal degeneration, and cell death of motoneurons. The identification of the underlying gene defects for familial ALS, spinal muscular atrophy (SMA), and spinal muscular atrophy with respiratory distress (SMARD) has pointed to distinct pathophysiological mechanisms that are responsible for the various forms of the disease. Accumulating evidence from mouse models suggests that enhanced vulnerability and sensitivity to proapoptotic stimuli is only responsible for some but not all forms of motoneuron disease. Mechanisms that modulate microtubule assembly and the axonal transport machinery are defective in several spontaneous and ENU (ethylnitrososurea) mutagenized mouse models but also in patients with mutations in the p150 subunit of dynactin. Recent evidence suggests that axonal growth defects contribute significantly to the pathophysiology of spinal muscular atrophy. Reduced levels of the survival motoneuron protein that are responsible for SMA lead to disturbed RNA processing in motoneurons. This could also affect axonal transport of mRNAs for beta-actin and other proteins that play an essential role in axon growth and synaptic function. The local translation of specific proteins might be affected, because developing motoneurons contain ribosome-like structures in distal axons and growth cones. Altogether, the evidence from these mouse models and the new genetic data from patients suggest that axon growth and maintenance involves a variety of mechanisms, including microtubule assembly and axonal transport of proteins and ribonucleoproteins (RNPs). Thus, defects in axon maintenance could play a leading role in the development of several forms of human motoneuron disease.

Aged↗

PubMed1991

Morphological characterization of rat entorhinal neurons in vivo: soma-dendritic structure and axonal domains.

We used in vivo intracellular labeling with horseradish peroxidase in order to study the soma-dendritic morphology and axonal projections of rat entorhinal neurons. The cells responded to hippocampal stimulation with inhibitory postsynaptic potentials, and thus likely received direct or indirect hippocampal input. All cells (n = 24) showed extensive dendritic domains that extended in some cases for more than 1 mm. The dendrites of layer II neurons were largely restricted to layers I and II or layers I-III, while the dendrites of deeper cells could extend through all cortical layers. Computed 3D rotations showed that the basilar dendrites of deep pyramids extended roughly parallel to the cortical layering, and that they were mostly confined to the layer containing the soma and layers immediately adjacent. Total dendritic lengths averaged 9.8 mm +/- 3.8 (SD), and ranged from 5 mm to more than 18 mm. Axonal processes could be visualized in 21 cells. Most of these showed axonal branching within the entorhinal cortex, sometimes extensive. Efferent axonal domains were reconstructed in detail in 3 layer II stellate cells. All 3 projected axons across the subicular complex to the dentate gyrus. One of these cells showed an extensive net-like axonal domain that also projected to several other structures, including the hippocampus proper, subicular complex, and the amygdalo-piriform transition area. The axons of layer III and IV cells projected to the angular bundle, where they continued in a rostral direction. In contrast to the layer II, III and IV cells, no efferent axonal branches leaving the entorhinal cortex could be visualized in 5 layer V neurons. The data indicate that entorhinal neurons can integrate input from a considerable volume of entorhinal cortex by virtue of their extensive dendritic domains, and provide a further basis for specifying the layers in which cells receive synaptic input. The extensive axonal branching pattern seen in most of the cells would support divergent propagation of their activity.

Animals↗

PubMed1984

Evidence that multiple species of aminoacylated transfer RNA are present in regenerating optic axons of goldfish.

This study reports that 4S RNA present in regenerating optic axons of goldfish is likely to be transfer RNA. Evidence is also presented which indicates that this transfer RNA is similar to transfer RNA found in tectal cells and that its aminocylation is likely to occur both in retinal ganglion cells prior to axonal transport as well as in the axon itself. Fish with regenerating optic nerves received intraocular injections of [3H]uridine followed 4 days later by intracranial injections of [14C]uridine. Radioactive tectal 4S RNA was isolated 6 days after [3H]uridine injections and chromatographed by BD cellulose chromatography. Optical density as well as radioactivity profiles for both [14C]4S RNA (from tectal cells) and [3H]4S RNA (90% of which originated from regenerating optic axons) were found to be similar to E. coli transfer RNA optical density profiles, indicating that the intra-axonal 4S RNA is likely to be transfer RNA. Moreover, comparisons of 3H/14C suggest that intra-axonal and cellular 4S RNAs are composed of similar species of transfer RNA. Results of other experiments indicate that aminoacylation of axonally transported tRNA occurs both in the retina and in optic axons subsequent to axonal transport.

Amino Acids↗

PubMed1986

Structural protein transport in elongating motor axons after sciatic nerve crush. Effect of a conditioning lesion.

In elongating motor axons of the rat sciatic nerve, the maximum outgrowth rate increased from 4.6 to 5.3 mm/d (5.3-6.1 X 10(-8) m/s) when a testing lesion of spinal nerves L4 and L5 was preceded 2 wk earlier by a conditioning lesion of the sciatic nerve. Axonal outgrowth was examined by measuring the transport of 35[S]methionine-labeled structural proteins (tubulin, actin, and neurofilament triplet) from "parent" axon stumps into "daughter" axon sprouts. Since these proteins are conveyed by the slow component of axonal transport at 1-5 mm/d (1.2-6.0 X 10(-8) m/s), the isotope was injected into the spinal cord 1 wk before the testing lesion. Nerves were removed 8 d after the testing lesion, sectioned into 3-mm segments, and homogenized; soluble proteins were separated by polyacrylamide gel electrophoresis. Fluorographs were used as templates to identify gel segments for removal, solubilization, and liquid scintillation counting. Distributions of mean radioactivity for tubulin, actin, and neurofilament triplet were plotted for animals receiving a conditioning vs sham-conditioning lesion. Greater amounts of tubulin and actin were transported into daughter axons in the conditioned group. Tubulin was mainly increased in axon shafts, whereas actin was mainly increased in axon tips. These findings suggest that the axonal transport of tubulin and actin governs the rate of elongation.

Actins↗