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PubMed1988

Biochemical composition and dynamics of the axonal cytoskeleton in the corticospinal system of the adult hamster.

The corticospinal system is an important central nervous system (CNS) pathway that is implicated in debilitating diseases such as amyotrophic lateral sclerosis and in traumatic injuries to the spinal cord. This study characterizes some of the fundamental biochemical and kinetic properties of normal corticospinal axons, establishing an important reference for studies that aim to elucidate the cellular modifications that result during pathological conditions of these axons. Slow axonal transport which conveys the axonal cytoskeleton as well as cytomatrix constituents, such as many of the metabolic enzymes and regulatory proteins, has been examined. For these studies, [35S]methionine was injected into the sensorimotor cortex of adult male Golden hamsters, and labeled, transported proteins present in corticospinal axons at 1-42 days after injection were assessed using one- and two-dimensional gel electrophoresis/fluorography. The complex group of slow component b (SCb) proteins (including clathrin, actin, enolase, creatine phosphokinase, and many others) was observed to move at a rate of approximately 2 mm/day in adult corticospinal axons. The slow component a (SCa) proteins (tubulins, neurofilament proteins, and actin) were transported at a substantially slower rate of approximately 0.4 mm/day. The biochemical and kinetic properties of slow transport in corticospinal axons were very similar to those previously described in another CNS pathway, axons of retinal ganglion cells, and substantially different from those documented in large, peripheral sensory or motor axons. These findings suggest that some of the basic properties of axonal transport which determine many of the structural and functional properties of axons may be different in the CNS compared to the peripheral nervous system.

Animals↗
PubMed1980

Early stages of axonal regeneration in the goldfish optic tract: an electron microscopic study.

Two hours after the goldfish optic tract was cut, the severed axons in the retinal stump of the tract showed ballooning of the axoplasm and myelin sheath in the region of the cut, with accumulation in the swollen axon of various organelles, including dense cored vesicles. By day 1 the myelin sheath had degenerated back to a node of Ranvier and the tip of the severed axon had formed a myelin-free terminal bulb with a well-organized core of 9-10 nm filaments. By 2 days, such terminal bulbs were often seen to be extended on a neck of cytoplasm a few micrometers in length, presumably indicating axonal outgrowth. In addition, occasional small bundles of axon sprouts were first seen at this time. The sprouts had a diameter of about 2 micrometers and contained a central core of 9-10 nm filaments surrounded by a mantle of cell organelles (smooth endoplasmic reticulum, mitochondria and diverse vesicles), with few if any microtubules. Sprouts within a bundle were separated by fairly uniform 10-15 nm spaces. Beginning at 3 days, significant numbers of microtubules appeared in the sprouts, and there was an increasing proportion of small diameter (greater than or equal to 0.3 micrometer) sprouts. Thus it was not until 3 days that the sprouts took on the appearance usually considered to be typical of regenerating axons. By 6 days a dense layer of glial cells or macrophages formed a cap over the cut surface of the tract. Penetrating this layer were bundles containing up to 20-30 axon sprouts and also single axons which may have been serving as 'pioneering' fibres to which later-emerging axons would attach. There was no evidence that the regenerating axons were guided by the glial cells. At 6 days astroglia began to separate individual axons within the bundles but oligodendrocytes were still inactive at this time.

Animals↗
PubMed1996

Expression of ubiquitin-like immunoreactivity in axons after compression trauma to rat spinal cord.

The ubiquitin-mediated proteolytic pathway is an important mode of protein degradation in various tissues. Since breakdown of proteins may occur in axons after injury we evaluated the presence of ubiquitin-like immunoreactive material in rat spinal cord following compression injury of mild, moderate and severe degrees at T8-9 level, resulting in no neurological deficit, reversible paraparesis and paraplegia of the hind limbs, respectively. Rats with mild to severe compression injury surviving 1-4 days showed numerous, intensely immunoreactive expanded axons at the site of compression. The labelled axons were randomly distributed in the longitudinal tracts but they were never found in the corticospinal tracts. No labelling was detected by 9 days after injury. In addition, the presence of labelled axons was investigated in the T7 and the T10 segments from rats with moderate compression. No labelling was seen in T7, but in T10 segments many immunoreactive axons were present. Control rats did not show immunoreactive axons in the spinal cord. Neurons of dorsal root ganglia, trigeminal ganglia and of the grey matter of the spinal cord were immunoreactive. Cerebral cortical neurons did not show ubiquitin expression. Thus, compression of the rat spinal cord causes a transient accumulation of ubiquitin-like immunoreactive material in axonal swellings. Even though the dynamics of ubiquitin conjugates are not fully understood, the observed axonal accumulation presumably reflects arrested anterograde axonal transport of protein chiefly derived from neurons of dorsal root ganglia and the local neurons of the spinal cord. The presence of ubiquitin in damaged axons is one prerequisite for degradation of abnormal proteins by the ubiquitin-mediated proteolytic pathway, which may be activated in reactive axonal swellings.

Animals↗
PubMed2002

Cell surface carbohydrates reveal heterogeneity in olfactory receptor cell axons in the mouse.

Cell surface carbohydrates, both in the olfactory system and elsewhere, have been proposed to play critical roles in axon guidance and targeting. Recent studies have used plant lectins to study the heterogeneous distribution of carbohydrates in the olfactory system. One lectin, Dolichos biflorus agglutinin (DBA), heterogeneously labels subsets of glomeruli. In the olfactory epithelium DBA labeled a subset of olfactory sensory neurons (OSNs) including their cilia, dendrites, and somata. OSN axons were also labeled and readily observed in the olfactory nerve and bulb. The patterns of glomerular innervation by DBA labeled (DBA(+)) axons were diverse; some glomeruli contained many labeled axons, while others contained few or no labeled axons. To characterize the heterogeneous innervation of glomeruli, we double labeled olfactory bulbs with DBA and an antibody to olfactory marker protein (OMP). OMP colocalized in most, but not all, DBA(+) axons. To determine if those axons that did not express OMP were immature, we double labeled olfactory bulbs with DBA and anti-GAP-43. GAP-43 rarely colocalized with DBA, suggesting that DBA(+) axons are not, as a population, immature. Triple labeling with all three markers revealed a small subset of DBA(+) axons which did not express either OMP or GAP-43. Electron microscopy established that DBA labels axons in the olfactory nerve and DBA-labeled axons form typical glomerular axodendritic synapses.

Animals↗
PubMed2006

The sorting behaviour of olfactory and vomeronasal axons during regeneration.

In order to begin to understand how primary olfactory and vomeronasal organ (VNO) axons target specific regions of the olfactory bulb, we examined the sorting behaviour of these axons following neonatal unilateral olfactory bulbectomy. Bulbectomy induced widespread ipsilateral death of the primary olfactory and VNO neurons. After 4 weeks, many new sensory axons had re-grown into the cranial cavity and established a prominent plexus with evidence of dense tufts that were similar in gross appearance to glomeruli. Axons expressing the cell adhesion molecule OCAM, which normally innervate the ventrolateral and rostral halves of the main and accessory olfactory bulbs, respectively, sorted out and segregated from those axons not expressing this molecule within the plexus. In addition, VNO axons formed large discrete bundles that segregated from main olfactory axons within the plexus. Thus, VNO and primary olfactory axons as well as discrete subpopulations of both are able to sort out and remain segregated in the absence of the olfactory bulb. Sorting and convergence of axons therefore occur independently of the olfactory bulb and are probably attributable either to inherent properties of the axons themselves or to interactions between the axons and accompanying glial ensheathing cells.

Animals↗
PubMed2005

Axon reactive B cells clonally expanded in the cerebrospinal fluid of patients with multiple sclerosis.

Demyelination and axonal loss have been described as the histological hallmarks of inflammatory lesions of multiple sclerosis (MS) and are the pathological correlates of persistent disability. However, the immune mechanisms underlying axonal damage in MS remain unknown. Here, we report the use of single chain-variable domain fragments (scFv) from clonally expanded cerebrospinal fluid (CSF) B cells to show the role of an anti-axon immune response in the central nervous system (CNS) in MS. The cellular and subcellular distribution of the antigen(s) recognized by these CSF-derived clonal scFv antibodies (CSFC-scFv Abs) was studied by immunochemical staining of brain tissues obtained at autopsy from patients with MS. Immunochemistry showed specific binding of CSFC-scFv Abs to axons in acute MS lesions. The stained axons showed three major types of axonal pathological changes: 1) linear axons, axonal ovoid formation, and axonal transection were seen in the myelinated white matter adjacent to the lesion; 2) accumulation of axonal ovoid formations and Wallerian degeneration were seen at the border between demyelinated lesions and the adjacent white matter; and 3) Wallerian degeneration occurred at the center and edge of acute demyelinated lesions. These findings suggest a B cell axonal specific immune response in the CNS in MS.

Antigens↗
PubMed1984

Regeneration of axons in tributary nerves.

The present study tests 2 hypotheses: (1) that the numbers of axons that regenerate into a tributary nerve are in part dependent on the type of lesion used to transect the axons in the parent nerve; and (2) that the numbers of axons that regenerate will be different in different tributary nerves. Axons were counted in the sural nerve and the nerve to the medial gastrocnemius muscle 8 weeks following crush, simple transection, transection with removal of 4 mm and transection with removal of 8 mm of the sciatic nerve in the rat. The counts of myelinated and unmyelinated axons are presented in the text. If axon numbers in the 2 nerves are normalized, the proportion of regenerated to normal myelinated axon numbers are approximately the same in the 2 nerves, with more regenerated axons than normal following crush, simple transection, or 4 mm gap transection and fewer following 8 mm gap transection. The unmyelinated axons behave differently. In the nerve to the medial gastrocnemius muscle, the numbers of unmyelinated axons are greater than or equal to the normal numbers following our various surgical paradigms whereas in the sural nerve there are always fewer unmyelinated axons than normal. These findings indicate that the above hypotheses are correct for the nerves tested in the rat.

Animals↗
PubMed1985

Axon terminals of GABAergic chandelier cells are lost at epileptic foci.

Axon terminals of chandelier cells were analyzed in monkeys with cortical focal epilepsy produced by alumina gel to determine if this type of GABAergic terminal is lost at epileptic foci. These terminals form a dense plexus with the axon initial segments of pyramidal neurons, especially those in layers II and III. Axon initial segments of pyramidal neurons were traced for at least 40 micron in serial thin sections and beyond this point were observed to become myelinated. In single sections, 10-15 axon terminals were found to form symmetric synapses throughout the entire length of the axon initial segments from nonepileptic preparations and were observed to synapse with only these structures and not adjacent dendrites or spines. In epileptic cortex, the axon initial segments of pyramidal neurons were apposed by glial profiles that contained clusters of filaments typical of reactive astrocytes. Only a few, small axon terminals were observed to form symmetric synapses with these axon initial segments. Thus, the chandelier cell axons appeared to degenerate in epileptic cortex. The highly strategic site of GABAergic inhibitory synapses on axon initial segments suggests that they exert a strong influence on the output of pyramidal cells. The near absence of these chandelier cell axons in epileptic foci most likely contributes to the hyperexcitability of neurons.

Animals↗
PubMed1985

Numbers of regenerating axons in parent and tributary peripheral nerves in the rat.

This study is concerned with numerical parameters of axonal regeneration in peripheral nerves. Our first finding is that the number of axons that regenerate into the distal stump of a somatic nerve at a particular time after transection is partially dependent on the type of lesion used to interrupt the axons. The second question concerns the proportion of axons that regenerate into the distal stump of a parent nerve compared to the proportions that regenerate into tributary nerves that arise from the parent. The proportions of regenerated myelinated axons in the nerve to the medial gastrocnemius muscle and myelinated and unmyelinated axons in the sural nerve are the same as the proportions of myelinated and unmyelinated axons that regenerate into the distal stump of the sciatic nerve for the crush, 0 and 4 mm gap transections. Proportionally fewer axons regenerate into the tributary nerves following the 8 mm gap transection, however. This implies that the length of the gap has an influence on whether or not axons in tributary nerves regenerate in concert with axons in the distal stump of the parent nerve. The unmyelinated fibers in the nerve to the medial gastrocnemius muscle are different because they do not regenerate in proportion to those in the distal stump of the sciatic nerve. We also provide evidence to indicate that myelinated axons branch whereas unmyelinated fibers end blindly when they enter the distal stump after crossing a sciatic nerve transection. Finally the normal arrangement of perineurial cells seems to be disrupted after the sciatic nerve regenerates across a gap.

Animals↗
PubMed1988

Three-dimensional analysis of the whole axonal arbors originating from single CA2 pyramidal neurons in the rat hippocampus with the aid of a computer graphic technique.

The axonal arborization of single pyramidal neurons in field CA2 and the rostral adjacent area of the rat hippocampus was studied with intracellular staining following the pressure microinjection of horseradish peroxidase (HRP) in combination with the immunoperoxidase technique, and was analyzed three-dimensionally with the aid of a computer system. The axonal arbors were composed of two types of axon branches, which were distinguished as the primary and secondary axon branches on the basis of morphological criteria. The axon branches in the ipsilateral hippocampus exhibited almost the contour of the dorsal hippocampus. The large amount of axon branches labeled with HRP in the stratum (str.) oriens of field CA1 was comparable to that in the str. radiatum of the field. The labeled axon branches in the dorsal hippocampus were not distributed uniformly in terminal regions but were focused on the caudolateral CA1a-b subfields. Most primary axon branches ran to a focus along the alvear fibers. The lamellar organization in the CA2 pyramidal neurons may be composed of axon branches running caudally and terminal branches forming a focus. The dense association fibers along the septotemporal axis may connect the lamellar organized circuits to each other. Axon branches in the septal nuclei of each hemisphere formed a rather flat plane. The commissural fibers of the CA2 pyramidal neurons seemed to form a symmetrical projection field in the contralateral side against the median plane. The axonal arbors and dendritic expansion of the pyramidal neurons shown in this study appeared to reveal the whole image of the single CA2 pyramidal neuron.

Animals↗
PubMed1988

Unmyelinated and myelinated axon membrane from rat corpus callosum: differences in macromolecular structure.

The macromolecular structure of unmyelinated and myelinated internodal axon membrane was examined with freeze-fracture electron microscopy. Unmyelinated axons exhibited a gradient of axonal diameters, generally ranging from 0.1 to 0.5 micron, with some unmyelinated axons of up to 0.7 micron diameter. Myelinated fibers also displayed a range of axonal diameters, with axons generally 0.3-1.0 micron. The overlap in diameters, between unmyelinated and myelinated fibers, permitted a comparison of membrane structure in myelinated and unmyelinated axons of the same diameter. Small (less than 0.5 micron) diameter unmyelinated axons exhibited a moderate density (approximately 700/micron2) of P-face intramembranous particles (IMPs), while large (greater than or equal to 0.5 micron) caliber unmyelinated axons displayed a significantly greater P-face IMP density (approximately 1100/micron2). Internodal membrane of both small (less than 0.5 micron) and large (greater than or equal to 0.5 micron) diameter myelinated fibers exhibited densities of P-face particles (approximately 1400/micron2) that were similar to each other, but significantly different from unmyelinated fibers. These results demonstrate that there are differences in membrane structure between unmyelinated and myelinated axons of similar diameter. These findings also demonstrate that membrane structure of unmyelinated axons is not invariant for all unmyelinated fibers within a given CNS tract but, on the contrary, is related to diameter.

Animals↗
PubMed1988

Electrophysiological determination of the axonal projections of single dorsal respiratory group neurons to the cervical spinal cord of cat.

Antidromic microstimulation and orthodromic extracellular spike-triggered averaging were used to determine the axonal positions, divergence and terminations of 16 axons arising from bulbospinal, inspiratory (I) neurons. Activity from these neurons was recorded in the dorsal respiratory groups (DRG) of 12 cats. Systematic tracking was done both transversely and longitudinally in the contralateral fifth and sixth cervical segments of the spinal cord. Axonal position was determined by antidromically activating axons and by recording axonal field potentials. Thirteen axons were located in the lateral funiculus, two in the ventrolateral funiculus and one in the ventral funiculus. Axonal conduction velocity (CV) was calculated from conduction distance and conduction time, the latter defined as the interval of time from the recorded action potential in the medulla to the recorded averaged axonal potential in the spinal cord. Average (+/- S.D.) axonal CV was 52 +/- 15 m/s. Terminal potentials were recorded for 13 of these axons and were coincident with the location of evoked field potentials resulting from antidromic stimulation of phrenic motoneurons. In addition, terminal potentials from single I cells were recorded at multiple sites along the longitudinal axis of the phrenic motor column. These data indicate that axons of spontaneously active, DRG bulbospinal I cells descend predominantly in the lateral columns and diverge and terminate extensively within the phrenic motor column.

Action Potentials↗
PubMed1989

Time- and frequency-dependent effects of potassium channel blockers on large and medium diameter optic tract axons.

Compound action potential recording techniques were used to investigate the time- and frequency-dependent effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA) on large diameter, fast conducting (t1) and medium diameter, middle conducting (t2) optic tract axons in anesthetized hooded rats. Single-pulse studies show 4-AP causes a rapid decrease in t1 and t2 response amplitude with larger decreases and longer lasting effects in t2 axons. In both axons, 4-AP leads to waveform broadening which is accounted for by increases in fall time since rise time and conduction velocity are unaffected by 4-AP. Strength-duration curves reveal 4-AP increases rheobase and decreases chronaxie in both axons with larger increases occurring in t1. T1, but not t2, axons also display some TEA-sensitivity. The absolute and relative refractory periods, determined with paired-pulse recovery functions, are increased by 4-AP to a greater degree in t1 than t2 axons. These axons, however, display equal sensitivity to TEA. In contrast, 4-AP and TEA decrease frequency following in both axons with larger effects observed in t2. Based on our data, and that of others, we speculate that t1 axons exhibit 4-AP and TEA sensitivity at nodal/paranodal regions and not at internodal regions, while t2 axons exhibit 4-AP sensitivity at nodal/paranodal and internodal regions and TEA sensitivity only at internodal regions of the axolemma. The possible relevance of these findings to the distribution of 4-AP- and TEA-sensitive potassium channels on t1 and t2 axons and the coding of visual spatial and temporal information remains to be determined.

4-Aminopyridine↗
PubMed1993

Protection of the axonal cytoskeleton in anoxic optic nerve by decreased extracellular calcium.

Since CNS white matter tracts contain axons, oligodendrocytes and astrocytes but not synapses, it is likely that anoxic injury of white matter is mediated by cellular mechanisms that do not involve synapses. In order to test the hypothesis, that anoxic injury of white matter is mediated by an influx of Ca2+ into the intracellular compartment of axons, we compared the ultrastructure of axons in rat optic nerve exposed to 60 min of anoxia in artificial cerebrospinal fluid (aCSF) containing normal (2 mM) Ca2+, and in aCSF containing zero-Ca2+ together with 5 mM EGTA. Optic nerves fixed at the end of 60 min of anoxia in 2 mM Ca2+ exhibit extensive ultrastructural alterations including disruption of microtubules and neurofilaments within the axonal cytoskeleton, development of membranous profiles and empty spaces between the axon and the ensheathing myelin, and swelling of mitochondria with loss of cristae. Bathing the nerves in zero-Ca2+ aCSF during anoxia protected the axons from cytoskeletal changes; after 60 min of anoxia, optic nerve axons retained normal-appearing microtubules and neurofilaments. Membranous profiles were rare, and empty spaces between axons and myelin did not develop in anoxic optic nerves bathed in zero-Ca2+ aCSF. Disorganization of cristae in axonal mitochondria was observed in anoxic optic nerves even when Ca2+ was omitted from the medium. Because Ca(2+)-mediated injury is known to disrupt the axonal cytoskeleton, these results support the hypothesis that anoxia triggers an abnormal influx of Ca2+ into myelinated axons in CNS white matter.

Animals↗
PubMed1991

Relationship of glia to GnRH axonal outgrowth from third ventricular grafts in hpg hosts.

The homozygous mutant hypogonadal (hpg) mouse lacks a functional gene for the neuropeptide gonadotropin releasing hormone (GnRH). The consequence of this defect is an infantile reproductive tract in adulthood. This condition can be reversed by the implantation of normal fetal preoptic area tissue that contains GnRH neurons. Reversal is always preceded by the outgrowth of GnRH axons into the host target tissue, the median eminence, by a stereotyped pathway. In the current experiments we investigated the cellular nature of the path taken by early emerging GnRH axons focusing on their relationship with astrocytic components and with the specialized ependymal population of this area, the tanycytes. In control tissue glial fibrillary acid protein (GFAP) immunoreactivity was confined to the exterior of cerebral blood vessels and glial limitans. Both GFAP and vimentin, another intermediate filament protein, marked the specialized ependymal cells of this region, the tanycytes. There was a robust reactive astrocytic response to the injury of transplantation in both the donor and host tissue within 5 days of implantation and the reactive astrocytes persisted for 60 days. These cells were GFAP-positive and were present in many areas of the host along the cannula tract and not confined to the area of GnRH axonal outgrowth. Vimentin, another intermediate filament, marked only the specialized ependymal cells of this region, the tanycytes, in both control and grafted tissue. Despite the profound reactive gliosis, GnRH axons were shown to exit the implant as early as 5 days after grafting suggesting that the gliotic process did not constitute a barrier to this phenomenon. At the light microscopic level, double label immunocytochemical studies did not reveal any specific association between GFAP or vimentin-positive cellular processes and these pioneer GnRH fibers. However, since normal GnRH axons had been reported to travel in tanycytic channels through the medial basal hypothalamus we reinvestigated the pattern of early emerging GnRH axons at the ultrastructural level. With this higher resolution, GnRH axons were found adjacent to glial elements along their entire traverse from the graft-host interface, through the host basal hypothalamus to their termination on the hypophysial portal capillaries. At the interface, GnRH-positive axons appeared to exit via glial channels similar to those described in other developing and regenerating systems. In the host, GnRH immunoreactive axonal profiles were surrounded by glial processes though the latter could not be further defined as tanycytic or astroglial. Other, immunonegative, axons were frequently seen in axonal bundles or fascicles and not necessarily in contact with glia.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Frequency analysis of catecholamine axonal morphology in human brain. II. Alzheimer's disease and hippocampal sympathetic ingrowth.

We have examined the various diverse morphologies of catecholamine axons in the brains of patients with Alzheimer's disease. Alzheimer's disease and aged control brain tissue were obtained by a rapid autopsy protocol (mean postmortem delay < 1 h). Tissue blocks from the superior frontal cortex (Brodmann area 9), the hippocampal gyrus, and the calcarine cortex (Brodmann area 17) were processed for identification of catecholamine axons using tyrosine hydroxylase immunocytochemistry. A total of 1275 tyrosine hydroxylase immunoreactive axons were randomly sampled from coded sections and classified into one of six distinct axon-type categories. The axon classification from patients with Alzheimer's disease significantly differed from those of an age-matched control population in the hippocampus. The Alzheimer's disease brains were decreased in the frequency of very long, thin, tyrosine hydroxylase immunoreactive axons (type 1) and had an increased frequency of shorter, tortuous, axons (type 3). These selective quantitative shifts in hippocampal catecholaminergic axon morphology are consistent with the hypothesis that sympathetic noradrenergic axons invade the hippocampus of patients with Alzheimer's disease. Multivariate modeling of the frequency sampling data found that the axon type classification scheme successfully predicted the presence of Alzheimer's disease. In particular, the use of quantitative neuroanatomical measures of the catecholaminergic system in human brain tissue was found to have errorless predictive ability with respect to late onset (> 75 years) Alzheimer's disease. In summary, the use of quantitative neuroanatomical measures of catecholamine axonal morphologies in Alzheimer's disease brain tissue identified a specific frequency shift which may represent hippocampal sympathetic ingrowth and this unique measure was found to have predictive utility with respect to Alzheimer's disease.

Aged↗
PubMed1996

Competitive exclusion between axons dependent on a single trophic substance: a mathematical analysis.

A mathematical model is presented of competition between axons for a trophic substance, such as is believed to occur particularly during development. The model is biologically realistic. The growth-stimulating activity of the trophic molecules is assumed to result from their binding to high-affinity receptors on neurons and their axons, but the model also incorporates uptake by nonneuronal cells possessing only lower affinity receptors. Plausible and fairly general assumptions are made concerning the kinetics of binding and internalization and the effects on axonal growth. The model takes into account the possibility that trophic factor production may be regulated by the afferent axons or autoregulated. The variables specified are the "axonal vigor" of each axon, representing the ability of each axon to take up trophic molecules, and the concentration of trophic molecules in the extracellular space of the axonal target region. Of the several parameters introduced, the most important turns out to be the "zero vigor-growth parameter," which is defined as the concentration of trophic molecules that gives zero growth of the vigor of a given axon. By means of a Lyapunov function, it is shown that the system will approach asymptotically to a stable equilibrium characterized by the survival of only the axon whose zero-growth parameter is lowest. Or, if several axons share the same lowest zero-growth parameter, these will all survive. The model may be particularly relevant to the elimination of polyneuronal innervation from developing muscle fibers and from autonomic ganglion cells.

Animals↗
PubMed1988

Intraretinal axons of ganglion cells in the Japanese monkey (Macaca fuscata): conduction velocity and diameter distribution.

In anesthetized and immobilized Japanese monkeys (Macaca fuscata), intraretinal conduction velocities of the ganglion cell axons were measured. The field potentials elicited by optic chiasm shocks consisted of fast and slow components with estimated conduction velocities of 1.19 and 0.72 m/s in recordings from the optic nerve fiber layer, and 1.65 and 1.00 m/s in recordings from the ganglion cell layer. Single cell recordings verified that the time course of the fast component corresponded to the antidromic spike latencies of Y-like cells, whereas that of the slow component covered the latency range of both X-like and W-like cells. In an electron microscopic study of the cross-sections of the intraretinal optic nerve fiber bundles, the axon diameter histograms of large samples (n = 3000-6000) all showed a unimodal distribution with a sharp peak at 0.3-0.6 micron and a long tail extending to 2-3 micron. The mean diameter was largest in the ventral and nasal bundles, smallest in the papillomacular bundle and intermediate in the dorsal, upper arcuate and lower arcuate bundles. However, diameter histograms of a small number of regional axons (n = 255-300) showed a broad tail distinct from the peak at 0.3-0.6 micron, enabling us to segregate a group of larger axons from the medium-sized to small axons. From such regional axon diameter histograms we estimated the mean relative occurrences of the larger axons (7.1-11.3%) and their mean diameters (0.9-1.3 micron). We further applied this relative frequency to the unimodal distribution of the histograms with larger samples in the upper and lower arcuate bundles and estimated the mean axon diameter of the large axons (1.1 micron) and that of the medium-sized to small axons (slightly below 0.5 micron). Finally, in studying the relation between axon diameter and conduction velocity in the two arcuate fiber bundles, we found it to be somewhat different from that previously reported for the cat retina.

Animals↗