Axon diameter distributions across the monkey's optic nerve

The distribution of axons according to diameter has been examined in the optic nerve of old world monkeys. Axon diameters were measured from electron micrographs, and histograms were constructed at regular intervals across a section through the optic nerve to reveal the local axon diameter distribution. The total axon diameter distribution was also estimated. Fine-calibre optic axons (less than 2.0 micron in diameter) are found at all locations across the optic nerve. They are most frequent centrotemporally, where very few coarse optic axons can be found, but also make up the majority at the optic nerve's periphery. Coarse optic axons (greater than 2.0 microns in diameter) are increasingly common at progressively peripheral positions in the nerve. Around the nerve's circumference, these coarse optic axons are least numerous temporally, and most common dorsonasally. The axon diameter distribution peaks around 1.25 microns at most locations across the optic nerve, but there are more, slightly larger (1.5-2.0 microns), optic axons dorsally than ventrally. The estimated total axon diameter distribution is unimodal, peaking at 1.0-1.25 microns, with an extended tail towards larger diameters. This centroperipheral gradient of increasing axon diameters across the optic nerve is not substantial enough to account for the partial segregation of axons by size in the monkey's optic tract: there, coarse optic axons form a conspicuously greater proportion of the local axon diameter distribution along the tract's superficial (sub-pial) border, and fine optic axons are the only axons present near the tract's deep border. Hence, the fibre distribution in the optic tract cannot be formed by a simple combination of the fibre distributions of the two respective half-nerves, as described in the classic neuro-ophthalmologic literature. Rather, the present results, in conjunction with previous results from the optic tract, demonstrate that there must be a reorganization of axons by size in or near the optic chiasm.     

Distribution, size and number of axons in the optic pathway of ground squirrels

The present study has examined the distribution of axons of differing sizes in the optic pathway of the ground squirrel. Axon diameters were measured from electron micrographs at various locations across sections of the optic nerve and tract, and total distributions and numbers were estimated. In both the nerve and tract, roughly 1.2 million optic axons were present. The population of optic axons had a unimodal size distribution, peaking at 0.9 μm in diameter and having an extended tail toward larger diameters. Local axon diameter distributions in the optic tract indicated distinct (though partially overlapping) axon diameter classes, including one of fine sizes peaking at 0.8–0.9 μm, a second of medium sizes peaking around 1.7–1.8 μm, and a third composed of the larger fibers with diameters up to 4.8 μm. The fine-caliber axons were found at all locations in the tract, and were the only axons present immediately adjacent to the pia, while the medium- and coarse-caliber axons were found at deeper locations. Curiously, the larger axons were found primarily in the medial parts of the tract, where axons from the dorsal retina normally course. A similarly restricted distribution of the larger axons was observed in the dorsotemporal parts of the optic nerve, suggesting that this difference in the tract may relate to an asymmetric distribution of ganglion cells on the retina giving rise to these axons. Measurements of axonal size taken within the optic fiber layer in dorsal and ventral parts of the retina confirmed this asymmetry, consistent with previous demonstrations of soma size differences in the dorsal versus ventral retina. The partial segregation of axons by size in the optic tract of the ground squirrel then reflects both the asymmetric distribution of retinal ganglion cell classes and the chronotopic reordering of optic axons that occurs within the chiasmatic region. Received: 14 March 1997 / Accepted: 30 June 1997     

Conduction velocity, size and distribution of optic nerve axons in the turtle, Pseudemys scripta elegans

Electrophysiological and morphological techniques have been used to characterize optic nerve axons in the red-eared turtle. Three distinct groups of axons are identified on the basis of conduction velocity and axon diameter. The first group (T1) is a small population of axons with large diameters (2.8-4.5 microns) and mean conduction velocities of 13 m/sec. The second group (T2) is a large population of axons with medium diameters (0.4-2.8 microns) and mean conduction velocities of 3 m/sec. The third group (T3) is a medium sized population of small diameter (0.2-0.6 micron), mostly unmyelinated axons with mean conduction velocities of 1 m/sec. There is a significant regional variation in the size, density and myelination of axons in the optic nerve. Large axons are found dorsally and ventrally, while smaller axons and the majority of unmyelinated fibers are found along a dorsotemporal to ventronasal axis through the nerve. Fink-Heimer techniques were used to trace the trajectories of axons of different sizes from the retina to the brain. Large diameter axons can be traced along the dorsal and ventral portions of the optic tract, with a dorsal group leaving the tract in the pretectum and a ventral group entering the basal optic tract. These observations suggest that the distribution of axons within the optic nerve reflects in part the distribution of ganglion cell somata in the retina. However, there is also some segregation of axons of different sizes according to their various central targets.     

Fiber order in the opossum's optic tract

Summary The distribution of axons by size in the optic tract of the South American opossum, Didelphis marsupialis was studied. Thin and semi-thin sections were examined, and measurements of axonal diameter were made on electron micrographs taken from various locations across the optic tract of normal opossums. In order to determine the contributions of the different axon diameter classes to the crossed and uncrossed retinofugal pathways, measurements were also made from the tracts of opossums in which one eye had been enucleated 5 weeks previously. Within the opossum's optic tract, the axons are partially segregated by their size: the deepest parts of the tract contain only fine and medium-sized axons, whereas coarse axons are also present superficially. In the middle of the tract, all three size classes are present. At increasingly superficial positions, there is a steady reduction in the proportion of medium-diameter axons, and an increase in the number of the finest axons. Medium and coarse axons contribute to both the crossed and uncrossed pathways, and the uncrossed component is displaced superficially relative to the crossed component. The fine axons in the deeper parts of the tract arise from both retinae, while those in the superficial parts of the tract, near the pial surface, are virtually all crossed. The opossum's optic tract thus displays the segregation of axons by size found in placental mammals, and follows a pattern reminiscent of that found in carnivores. Such a common organizational plan, particularly the similarities between the didelphids and carnivores, is suggestive of an early acquisition of parallel visual pathways in mammalian phylogeny. Since the fiber order in the optic tract of eutherians is a chronological map of axonal arrival during development, these results suggest that a conserved developmental mechanism has led to a common organizational plan.     

睫状神经营养因子对视神经损伤的修复作用

视神经损伤后,视网膜神经节细胞进行性损害,轴突变性坏死,再生困难。睫状神经营养因子是一种非靶源性神经营养因子,在视网膜神经节细胞的生长发育中起重要调控作用,主要表现在对损伤的视网膜神经节细胞有促进存活及轴突再生的作用。     

Dendritic invagination of developing optic tract axons in the hamster

Summary Between E15 and P4 in the hamster, axons of retinal ganglion cells in the optic tract over the dorsal lateral geniculate nucleus, are invaginated by, and make synaptic contacts with, small processes interpreted as tips or appendages of geniculate dendrites. In some cases a branch-like protrusion emerges from the axon at or close to the invagination. We hypothesize that the invaginations may be part of the mechanism by which retinocollicular axons are induced to branch and establish the retinogeniculate pathway.     

Anatomical correlations of intrinsic axon repair after partial optic nerve crush in rats.

About 15% of retinal ganglion cells survive diffuse axonal injury of the optic nerve in adult rats. Following initial blindness, discrimination of visual stimuli in behavioral tests recovers within three weeks. To investigate the mechanisms promoting this functional recovery the axonal transport and the neurofilaments were studied. Intraocularly applied MiniRuby is transported until the place of crush and accumulated in enlarged axon terminals. Three weeks after lesion the anterograde transport of MiniRuby recovers distal to the place of crush. At the same point in time the retrograde transport of surviving retinal ganglion cells is restored which was visualized by horseradish peroxidase injected into the superior colliculus. The heavy neurofilament was stained immunohistochemically and analyzed statistically up to three weeks after optic nerve crush. The stained filaments in the axon fibers of retinal ganglion cells appear wavelike and/or fragmented up to day 8, but first signs of heavy neurofilament restitution in the fibers of the optic nerve are seen at day 12 after axonal injury. Because these results cannot be explained by longlasting axon regeneration, the present results provide convincing evidence for intrinsic axon repair soon after diffuse axonal injury that correlates in time with recovery of vision.     

Binocular interaction in the fetal cat regulates the size of the ganglion cell population

During fetal development of the cat's visual system there is a marked overproliferation of optic nerve axons. In utero binocular interaction contributes to the severity of fiber loss since removal of an eye during gestation attenuates axon loss in the remaining optic nerve. The purpose of the present study was to determine whether this reduced loss of optic nerve fibers is due to a failure of retraction by supernumerary axon branches or to a reduction in ganglion cell death. To resolve this issue, we compared the number of ganglion cells and optic nerve fibers in adult cats which had one eye removed at known gestational ages. Retinal ganglion cells were backfilled with horseradish peroxidase and counts were made from retinal wholemounts. The axon complement was assessed with an electron microscopic assay. In the retinas of a normal cat we estimated 151,000 and 152,000 ganglion cells. The optic nerves of two other normal cats contained approximately 158,000 and 159,000 axons. In comparison, an animal enucleated on embryonic day 42 had 180,000 ganglion cells and 178,000 optic nerve fibers, while in an animal enucleated on embryonic day 51 the corresponding estimates were 182,000 and 190,000. The close agreement between cell and fiber counts indicates that axonal bifurcation does not contribute appreciably to the axon surplus in the optic nerve of prenatally enucleated cats. These results demonstrate that prenatal binocular interaction regulates the size of the mature retinal ganglion cell population.     

Electron microscopic study of the interaction of axons and glia at the site of anastomosis between the optic nerve and cellular or acellular sciatic nerve grafts

Summary The interactions between retinal ganglion cell (RGC) axons and glia at the site of optic nerve section and at the junctional zone between optic nerve and cellular or acellular peripheral nerve (PN) grafts have been studied electron microscopically. After transection, RGC axons, accompanied by processes of astrocyte cytoplasm, grew out from the proximal optic nerve stump into the scar tissue that developed between proximal and distal stumps. However, axons failed to cross the scar, and none entered the distal stump. By 3 days post lesion (DPL), bundles of RGC axons, accompanied by astrocytes and oligodendrocytes, grew out from the proximal optic nerve stump into the junctional zone between optic nerve and either type of PN graft. The bundles of RGC axons and growth cones that grew towards acellular PN grafts degenerated within 10–20 DPL; by 30 DPL a small number of axons persisted within the end of the proximal optic nerve stump. No axons were seen within the acellular PN grafts. These results suggest that reactive axonal sprouting, axon outgrowth and glial migration from the proximal optic nerve stump are events that occur during an acute response to injury, and that they are independent of the presence of Schwann cells. However, it would appear that few axons entered either scar or junctional zone unless accompanied by glia. There was little evidence that axon outgrowth was laminin-dependent.The bundles that grew towards cellular PN grafts encountered cells that we have identified as Schwann cells within the junctional zone: the axons in these bundles survived and entered the cellular grafts. Schwann cells migrated into the junctional zone from the cellular PN graft. It is probable that Schwann cells facilitated RGC axon entry into the graft directly by both cell contact and the secretion of neuronotrophic factors, and indirectly by modifying the CNS glia in the junctional zone.     

Peripheral nerve explants grafted into the vitreous body of the eye promote the regeneration of retinal ganglion cell axons severed in the optic nerve

Summary We have conducted experiments in the adult rat visual system to assess the relative importance of an absence of trophic factors versus the presence of putative growth inhibitory molecules for the failure of regeneration of CNS axons after injury. The experiments comprised three groups of animals in which all optic nerves were crushed intra-orbitally: an optic nerve crush group had a sham implant-operation on the eye; the other two groups had peripheral nerve tissue introduced into the vitreous body; in an acellular peripheral nerve group, a frozen/thawed teased sciatic nerve segment was grafted, and in a cellular peripheral nerve group, a predegenerate teased segment of sciatic nerve was implanted. The rats were left for 20 days and their optic nerves and retinae prepared for immunohistochemical examination of both the reaction to injury of axons and glia in the nerve and also the viability of Schwann cells in the grafts. Anterograde axon tracing with rhodamine-B provided unequivocal qualitative evidence of regeneration in each group, and retrograde HRP tracing gave a measure of the numbers of axons growing across the lesion by counting HRP filled retinal ganglion cells in retinal whole mounts after HRP injection into the optic nerve distal to the lesion. No fibres crossed the lesion in the optic nerve crush group and dense scar tissue was formed in the wound site. GAP-43-positive and rhodamine-B filled axons in the acellular peripheral nerve and cellular peripheral nerve groups traversed the lesion and grew distally. There were greater numbers of regenerating fibres in the cellular peripheral nerve compared to the acellular peripheral nerve group. In the former, 0.6–10% of the retinal ganglion cell population regenerated axons at least 3–4 mm into the distal segment. In both the acellular peripheral nerve and cellular peripheral nerve groups, no basal lamina was deposited in the wound. Thus, although astrocyte processes were stacked around the lesion edge, a glia limitans was not formed. These observations suggest that regenerating fibres may interfere with scarring. Viable Schwann cells were found in the vitreal grafts in the cellular peripheral nerve group only, supporting the proposition that Schwann cell derived trophic molecules secreted into the vitreous stimulated retinal ganglion cell axon growth in the severed optic nerve. The regenerative response of acellular peripheral nerve-transplanted animals was probably promoted by residual amounts of these molecules present in the transplants after freezing and thawing. In the optic nerves of all groups the astrocyte, microglia and macrophage reactions were similar. Moreover, oligodendrocytes and myelin debris were also uniformly distributed throughout all nerves. Our results suggest either that none of the above elements inhibit CNS regeneration after perineuronal neurotrophin delivery, or that the latter, in addition to mobilising and maintaining regeneration, also down regulates the expression of axonal growth cone-located receptors, which normally mediate growth arrest by engaging putative growth inhibitory molecules of the CNS neuropil.     

The conditioning effect of optic nerve injury upon axonal regrowth from adult rat retinal ganglion cells explanted in vitro

An in vitro assay was used to determine the effects of conditioning nerve lesions on the regeneration of adult rat retinal ganglion cell (RGC) axons from retinal explants. Following the conditioning lesion (CL) of unilateral optic nerve transection, maximal regrowth was seen from RGC explanted from ipsilateral retinae 10 days post-CL. Explants from this group initiated axonal regrowth earlier and a greater percentage regrew axons when compared with explants from normal rats. Axonal regrowth from explants of retinae contralateral to CL was also seen earlier than normal. In further experiments, the effects of both exposure of the optic nerve sheath in the orbit and the incision of the dura without injury to optic nerve axons were studied. The conditioning effect of a dural incision was found to be the same as that of optic nerve transection, whilst exposure of the optic nerve sheath had no conditioning effect on RGC axonal regrowth in vitro.     

The guidance of optic axons in the developing and adult mouse retina

Previous studies in chick embryos (Goldberg, '77) indicated that unidirectional guidance of retinal axons toward the optic nerve is restricted to the vitread portion of the ganglion cell fiber layer (GCFL) of the retina; random fiber growth was noted after deflection of the optic axons sclerad to the GCFL. The present study on mice confirms these observations. Silver-stained flat mounts of retinal colobomas were examined. Many optic axons in colobomas do not exit normally from the eye, but travel randomly when deflected sclerad to the GCFL. Newborn mouse axons grew around retinal lesions in a highly directed manner. Such axons were always situated in the vitread portion of the GCFL. The unidirectional guidance found in newborn mice was absent in adults. Deflected adult axons traveled randomly regardless of their level within the GCFL. We propose that defective guidance largely accounts for failure of axonal regeneration in the adult mouse retina. The inability of the adult axons to fasciculate (adhere to one another and form fiber bundles) suggests that impaired cellular adhesivity may be part of the mechanism of regenerative failure.     

The guidance of optic axons in the developing and adult mouse retina.

Previous studies in chick embryos (Goldberg, '77) indicated that unidirectional guidance of retinal axons toward the optic nerve is restricted to the vitread portion of the ganglion cell fiber layer (GCFL) of the retina; random fiber growth was noted after deflection of the optic axons sclerad to the GCFL. The present study on mice confirms these observations. Silver-stained flat mounts of retinal colobomas were examined. Many optic axons in colobomas do not exit normally from the eye, but travel randomly when deflected sclerad to the GCFL. Newborn mouse axons grew around retinal lesions in a highly directed manner. Such axons were always situated in the vitread portion of the GCFL. The unidirectional guidance found in newborn mice was absent in adults. Deflected adult axons traveled randomly regardless of their level within the GCFL. We propose that defective guidance largely accounts for failure of axonal regeneration in the adult mouse retina. The inability of the adult axons to fasciculate (adhere to one another and form fiber bundles) suggests that impaired cellular adhesivity may be part of the mechanism of regenerative failure.     

Regrowth of retinal ganglion cell axons into a peripheral nerve graft in the adult hamster is enhanced by a concurrent optic nerve crush

Summary Transplantation of a segment of peripheral nerve to the retina of the adult hamster resulted in regrowth of damaged ganglion cell axons into the graft, with the fastest regenerating axons extending at 2 mm/day after an initial delay of 4.5 days (Cho and So 1987b). In this study, the effect of making 2 lesions on the same axon (the conditioning lesion effect) on the regrowth of ganglion cell axons into the peripheral nerve graft was examined. When a conditioning lesion (first lesion) was made by crushing the optic nerve 7 or 14 days before the peripheral nerve grafting (the second lesion) to the retina, the distance of regrowth achieved by the fastest regenerating axons in the graft, measured at the 7th post-grafting day, was lower than in animals with a peripheral nerve grafted to a normal eye. This indicated that in contrast to the situation in peripheral nerve axons (Forman et al. 1980) and goldfish optic axons (Edwards et al. 1981), the conditioning lesion was unable to enhance the regrowth of mammalian retinal ganglion cell axons. However, when crushing of the optic nerve was followed immediately by peripheral nerve grafting, an enhancement in axonal regrowth could be observed. The initial delay time before the axons extended into the peripheral nerve graft was reduced by 1 day while the rate of elongation of the fastest regrowing axons in the graft apparently remained unchanged. Moreover, the shortening of the initial delay could still be observed even when the sequence of performing the 2 lesions was reversed. From these data, it was concluded that the classical conditioning lesion effect was not responsible for the enhancement observed. Rather it was suggested that changes in the intra-retinal environment brought about by crushing of the optic nerve might account for it.     

The retinal axon's pathfinding to the optic disk

Retinal ganglion cell (RGC) axons travel in radial routes unerringly toward the optic disk, their first intermediate target in the center of the eye. The path of the RGC growth cone is restricted to a narrow zone subjacent to the endfeet of Müller glial cells and the vitreal basal lamina. The present survey indicates that RGC growth cones are guided by many molecular cues along their pathway which are recognized by receptors on their surface. Growth-promoting molecules on Müller glial endfeet and in the basal lamina assist growth cones in maintaining contact with these elements. The repellant character of deeper retinal laminae discourages them from escaping the RGC axon layer. Cell adhesion/recognition proteins enable growth cones to fasciculate with preformed axons in their vicinity. It is still unclear whether the optic disk emits long range guidance components which enable the growth cones to steer toward it. Recent evidence in fish indicates the existence of an axonal receptor (neurolin) for a guidance component of unknown identity. Receptor blockade causes RGC axons to course in aberrant routes before they reach the disk. At the disk, axons receive signals to exit the retina. Contact with netrin-1 at the optic disk/nerve head encourages growth cones to turn into the nerve. This response requires the axonal netrin receptor DCC, laminin-1, beta-integrin and most likely the UNC5H netrin receptors which convert the growth encouraging signal into a repulsive one which drives growth cones into the nerve.     

Xenopus sonic hedgehog guides retinal axons along the optic tract

The role of classic morphogens such as Sonic hedgehog (Shh) as axon guidance cues has been reported in a variety of vertebrate organisms (Charron and Tessier‐Lavigne [ 2005 ] Development 132:2251–2262). In this work, we provide the first evidence that Xenopus sonic hedgehog (Xshh) signaling is involved in guiding retinal ganglion cell (RGC) axons along the optic tract. Xshh is expressed in the brain during retinal axon extension, adjacent to these axons in the ventral diencephalon. Retinal axons themselves express Patched 1 and Smoothened co‐receptors during RGC axon growth. Blocking Shh signaling causes abnormal ventral pathfinding, and targeting errors at the optic tectum. Misexpression of exogenous N‐Shh peptide in vivo also causes pathfinding errors. Retinal axons grown in culture respond to N‐Shh in a dose‐dependent manner, either by decreasing extension at lower concentrations, or retracting axons in the presence of higher doses. These data suggest that Shh signaling is required for normal RGC axon pathfinding and tectal targeting in the developing visual system of Xenopus. We propose that Shh serves as a ventral optic tract repellent that helps to define the caudal boundary for retinal axons in the diencephalon, and that this signaling is also required for initial target recognition at the optic tectum. Developmental Dynamics 239:2921–2932, 2010. © 2010 Wiley‐Liss, Inc.     

The amount of slow axonal transport is proportional to the radial dimensions of the axon

Summary Axons are fundamentally cylindrical and their geometry is defined by two basic parameters, i.e. diameter and length. The average cross-sectional diameter of an axon is determined primarily by the number and density of cytoskeletal structures (i.e. microtubules and neurofilaments) in the axon. The proteins that constitute these structures are synthesized in the nerve cell body and are conveyed through the axon by slow axonal transport. In particular, slow component a (SCa) supplies all of the axonal neurofilament proteins and most of the microtubule proteins to the axon. To study the relationship between slow axonal transport and axonal diameter, the slowly transported proteins were radiolabelled in rat dorsal root ganglion (DRG) cells. The amount of radiolabelled SCa proteins transported in individual unmyelinated and myelinated DRG axons was measured by the electron microscopic autoradiographic method. We found that the amount of SCa transported in the axons is proportional to axonal cross-sectional area. These results indicate that slow axonal transport of microtubules and neurofilaments is a primary determinant of axonal diameter.     

Regrowth of PNS axons through grafts of the optic nerve of the Browman-Wyse (BW) mutant rat

Summary We have examined the behaviourin vivo of regenerating PNS axons in the presence of grafts of optic nerve taken from the Browman-Wyse mutant rat. Browman-Wyse optic nerves are unusual because a 2–4 mm length of the proximal (retinal) end of the nerve lacks oligodendrocytes and CNS myelin and therefore retinal ganglion cell axons lying within the proximal segment are unmyelinated and ensheathed by processes of astrocyte cytoplasm. Schwann cells may also be present within some proximal segments. Distally, Browman-Wyse optic nerves are morphologically and immunohistochemically indistinguishable from control optic nerves.When we grafted intact Browman-Wyse optic nerves or triplets consisting of proximal, junctional and distal segments of Browman-Wyse optic nerve between the stumps of freshly transected sciatic nerves, we found that regenerating axons avoided all the grafts which did not contain Schwann cells, i.e., proximal segments which contained only astrocytes; regions of Schwann cell-bearing proximal segments which did not contain Schwann cells; junctional and distal segments (which contained astrocytes, oligodendrocytes and CNS myelin debris). However, axons did enter and grow through proximal segments which contained Schwann cells in addition to astrocytes. Schwann cells were seen within grafts even after mitomycin C pretreatment of sciatic proximal nerve stumps had delayed outgrowth of Schwann cells from the host nerves; we therefore conclude that the Schwann cells which became associated with regenerating axons within the grafts of Browman-Wyse optic nerve were derived from an endogenous population. Our findings indicate that astrocytes may be capable of supporting axonal regeneration in the presence of Schwann cells.     

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.