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PubMed1995

Morphology of physiologically identified retinal X and Y axons in the cat's thalamus and midbrain as revealed by intraaxonal injection of biocytin.

Prior morphological studies of individual retinal X and Y axon arbors based on intraaxonal labeling with horseradish peroxidase have been limited by restricted diffusion or transport of the label. We used biocytin instead as the intraaxonal label, and this completely delineated each of our six X and 14 Y axons, including both thalamic and midbrain arbors. Arbors in the lateral geniculate nucleus appeared generally as has been well documented previously. Interestingly, all of the labeled axons projected a branch beyond thalamus to the midbrain. Each X axon formed a terminal arbor in the pretectum, but none continued to the superior colliculus. In contrast, 11 of 14 Y axons innervated both the pretectum and the superior colliculus, one innervated only the pretectum, and two innervated only the superior colliculus. Two of the Y axons were quite unusual in that their receptive fields were located well into the hemifield ipsilateral with respect to the hemisphere into which they were injected. These axons exhibited remarkable arbors in the lateral geniculate nucleus, diffusely innervating the C-laminae and medial interlaminar nucleus, but, unlike all other X and Y arbors, they did not innervate the A-laminae at all. In addition to these qualitative observations, we analyzed a number of quantitative features of these axons in terms of numbers and distributions of terminal boutons. We found that Y arbors contained more boutons than did X arbors in both thalamus and midbrain. Also, for axons with receptive fields in the contralateral hemifield (all X and all but two Y axons), 90-95% of their boutons terminated in the lateral geniculate nucleus; the other two Y axons had more of their arbors located in midbrain.

Animals↗
PubMed1995

The increase in B-50/GAP-43 in regenerating rat sciatic nerve occurs predominantly in unmyelinated axon shafts: a quantitative ultrastructural study.

The growth-associated protein B-50/GAP-43 is thought to play a crucial role in axonal growth. We investigated, by quantitative immunoelectron microscopy, whether there are differences in the subcellular distribution of B-50 in unmyelinated and myelinated axons of intact and regenerating sciatic nerves. Adult rats received an unilateral sciatic nerve crush and were euthanized 8 days later. Nerve pieces proximal from the crush site were embedded, and B-50 was visualized by specific B-50 antibodies and immunogold detection in ultrathin sections. The density of B-50 at the plasma membrane of unmyelinated axon shafts was significantly increased in the ipsilateral regenerating nerve in comparison to that of the contralateral intact nerve. In contrast, there was no significant difference in the B-50 density at the axolemma of myelinated regenerating and intact axon shafts. In the contralateral intact nerve, more B-50 was associated with the axolemma of unmyelinated axons than with the plasma membrane of myelinated axons. The density of axoplasmic B-50 was similar in intact unmyelinated and myelinated axon shafts, but was higher in regenerating nerve than in intact nerve. This suggests that enhanced axonal transport of B-50 occurs during axon outgrowth. Our study demonstrates a differential subcellular distribution of B-50 in unmyelinated and myelinated axon shafts in both the intact and regenerating sciatic nerve, indicating a differential inducible capacity for remodeling of the axon shafts.

Animals↗
PubMed1995

The guidance molecule semaphorin III is expressed in regions of spinal cord and periphery avoided by growing sensory axons.

The protein collapsin was purified from chick brain on the basis of its ability to inhibit sensory neuron growth cones, implicating this molecule in sensory axon guidance (Luo et al. [1993] Cell 75:217-227). To examine the relationship between collapsin and sensory axon growth, we examined the pattern of mRNA expression of collapsin's mammalian paralogue, Semaphorin III (Sema III), and compared it to dorsal root ganglion (DRG) axon pathways in the developing rat embryo. Centrally, DRG axons enter the spinal cord by embryonic (E) 11 and branch into the gray matter by E15 in brachial and thoracic regions. Laminar specific targets are reached by E17. Between E13 and E17, Sema III mRNA is expressed at high levels in the entire ventral half of the spinal cord except the floor plate. This pattern suggests that Sema III may inhibit non-proprioceptive sensory axons from penetrating the ventral spinal cord. Peripherally, sensory axons have entered the anterior sclerotome by E11 at all rostrocaudal levels. At this age, Sema III mRNA is already expressed in the dermamyotome and ventral aspect of the posterior sclerotome, areas which axons pass between but do not penetrate en route to their peripheral targets. From E12 to E15, the axons lengthen and branch into smaller fascicles which extend toward peripheral targets. During this time, Sema III mRNA is expressed by many mesodermal structures surrounding the axon fascicles, with highest levels observed in the dermamyotome, perinotochordal mesenchyme, pelvic girdle, and limb. As development proceeds, Sema III mRNA expression is quickly downregulated before disappearing by birth. Taken together, our results demonstrate that the gene for Sema III is expressed in central and peripheral regions which are avoided by growing DRG axons. These findings are consistent with the idea that Sema III inhibits growth and branching of axons into inappropriate areas during development.

Animals↗
PubMed1994

Transplants of immature astrocytes promote axonal regeneration in the adult rat brain.

To study beneficial effects of immature astrocytes on axonal regeneration in the injured adult mammalian brain, we have stereotactically implanted cultured astrocytes from embryonic (E 14-16) rat cerebral cortex into the lesion site following transection of the postcommissural fornix. The spatio-temporal pattern of axonal degeneration and regrowth in the proximal fornix stump was investigated using wheat germ agglutinin-horseradish peroxidase tracing techniques and quantitative analysis of myelinated axon profiles. Transection of the postcommissural fornix tract caused disintegration of the axons in the distal stump as well as rapid and pronounced retrograde axonal degeneration up to 800-1,200 microns proximal to the lesion site. While a small bundle of subicular fibers spontaneously extended to the lesion site within 4 weeks after injury, axonal regeneration was markedly stimulated in those animals that had received an astroglial implant. Following the former pathway, regenerating axons sprouted towards the implant but did not penetrate the graft. Instead, the axons elongated over the surface of the transplant, avoiding growth into the surrounding neuropil or into the distal fornix segment. In grafted animals we further observed a substantial increase in the number of myelinated axons of approximately 31.5% (at the level of 800 microns) and approximately 40% (at the 400 microns level) compared with the injured tract lacking a transplant. Our results indicate the capacity of juvenile astrocytes to stimulate axonal regeneration after injury of the post-commissural fornix tract in the adult rat brain. We further demonstrate myelination of the regenerated axons.

Animals↗
PubMed2005

Early profiles of axonal growth and astroglial response after spinal cord hemisection and implantation of Schwann cell-seeded guidance channels in adult rats.

We previously demonstrated that transplantation of Schwann cell-seeded channels promoted the regrowth of injured axons in the adult spinal cord. It is not clear, however, whether injured axons recapitulate the developmental scenarios to accomplish regeneration. In the present study, we investigated the early events associated with axonal regrowth after spinal cord hemisection at the eighth thoracic level and implantation of a Schwann cell-seeded minichannel in adult rats. Animals were sacrificed at postoperative days (PO) 2, 4, 7, and 14. Anterograde tracing with fluoro-ruby showed that regenerating axons grew into the graft prior to PO2 and reached the distal end of the channel at PO7. These axons expressed both embryonic neural cell adhesion molecule (E-NCAM) and growth associated protein-43 (GAP-43). Although the expression of E-NCAM decreased by PO7, that of GAP-43 remained high throughout the first 2 weeks after implantation. A close relation of vimentin-positive astroglia to the growing axons in the host tissue suggested a contact-mediated role of these cells in axon guidance. Aggregation of glial fibrillary acidic protein (GFAP)-positive astrocytes together with the increased expression of chondroitin sulfate proteoglycans (CSPGs) starting at PO7 appeared to inhibit axonal growth at the host-graft interface. Thus, adult regenerating axons and astroglia do express developmentally related molecules that may facilitate axonal growth into a permissive graft at the early phase of injury and regeneration. These results suggest that molecules and astroglia essential to development are both important in influencing axonal regrowth in the adult spinal cord.

Animals↗
PubMed2006

Alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid-mediated excitotoxic axonal damage is attenuated in the absence of myelin proteolipid protein.

In vivo and in vitro studies have shown that alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-receptor-mediated excitotoxicity causes cytoskeletal damage to axons. AMPA/kainate receptors are present on oligodendrocytes and myelin, but currently there is no evidence to suggest that axon cylinders contain AMPA receptors. Proteolipid protein (PLP) and DM20 are integral membrane proteins expressed by CNS oligodendrocytes and located in compact myelin. Humans and mice lacking normal PLP/DM20 develop axonal swellings and degeneration, suggesting that local interactions between axons and the oligodendrocyte/myelin unit are important for the normal functioning of axons and that PLP/DM20 is involved in this process. To determine whether perturbed glial-axonal interaction affects AMPA-receptor-mediated axonal damage, AMPA (1.5 nmol) was injected into the caudate nucleus of anesthetized Plp knockout and wild-type male mice (n = 13). Twenty-four hours later, axonal damage was detected by using neurofilament 200 (NF 200) immunohistochemistry and neuronal damage detected via histology. AMPA-induced axonal damage, assessed with NF 200 immunohistochemistry, was significantly reduced in Plp knockout mice compared with wild-type mice (P = 0.015). There was no significant difference in the levels of neuronal perikaryal damage between the Plp knockout and wild-type mice. In addition, there was no significant difference in the levels of glutamate receptor subunits GluR1-4 or KA2 in Plp knockout compared with wild-type littermates. The present study suggests that PLP-mediated interactions among oligodendrocytes, myelin, and axons may be involved in AMPA-mediated axonal damage.

Animals↗
PubMed1985

Barium action potentials in regenerating axons of the lamprey spinal cord.

Intracellular recordings were obtained from growing tips of regenerating giant axons in the lamprey spinal cord, the recording sites verified by Lucifer yellow injection. In the presence of extracellular Ba++ (3-6 mM), tetraethylammonium (10-15 mM), and 4-aminopyridine (4-6 mM), action potentials showed prolonged plateaus. The fast initial phase of the action potential, but not the plateau (Ba++-spike), was blocked by tetrodotoxin (10(-6) gm/ml). The Ba++ spike was associated with increased membrane conductance and could be terminated with hyperpolarizing current pulses. Normal axons did not generate similar Ba++ spikes. However, TTX-resistant, voltage-dependant conductance changes could be elicited in normal axons if much higher concentrations of Ba++ (18-30 mM) were used. Their rate of rise was slower than in regenerating axons (0.6 V/sec vs 3.2 V/sec; n = 5), and the response did not outlast the current pulse. The Ba++ responses in normal and regenerating axons were blocked by ions known to block voltage-gated Ca++ conductances (Co++, Ni++, or Cd++). Therefore, these spikes probably represent Ba++ entry through voltage-dependent Ca++ channels, suggesting the presence of a higher-than-average voltage-dependent Ca++ conductance in the growing axon. However, Ca++-dependent spikes could not be obtained under any conditions in either normal or regenerating axons. Simultaneous intracellular recordings from growth cones and axons indicated that the Ba++ spike was initiated, in most cases, at the growth cone. The Ba++ spikes were recorded in regenerating axons for as long as 50 days following cord transection and were not correlatable with the "dying-back" phenomenon in cut axons, which usually is over before day 6. The concept of a higher-than-average voltage-dependent Ca++ conductance in growing tips of regenerating axons is in agreement with the hypothesis that Ca++ is important in regeneration and that regeneration may be related to the process of chemical synaptic transmission.

4-Aminopyridine↗
PubMed1991

Tyrosinated and detyrosinated microtubules in axonal processes of cerebellar macroneurons grown in culture.

We have used the monoclonal antibody YL 1/2 (Tyr) specific for tyrosinated tubulin, and a polyclonal antibody (Glu) specific for detyrosinated tubulin to visualize the distribution of microtubules and microtubule assembly sites during axonal outgrowth. Cerebellar macroneurons growing in culture initially extend several short and thin neurites which have the potential to differentiate either as axons or dendrites (Ferreira and Caceres: Developmental Brain Research 49:205-213, 1989). At the onset of axonal outgrowth the Tyr antibody labels the minor neurites, the axon, and its growth cone, while the Glu antibody only shows immunoreactivity in the axonal shaft. After nocodazole treatment, the Tyr staining disappears, whereas that produced by the Glu antibody remains practically unchanged. When nocodazole was removed, tyrosinated microtubules reappeared first at the tip of the axon, in a more distal region than that occupied by detyrosinated microtubules; another focal site of tyrosinated tubulin incorporation was detected in the cell body. Incorporation of tyrosinated tubulin into growing axons was also studied after taxol treatment. After long incubation periods in the presence of taxol, the Tyr staining disappeared from the axon but remained in the cell body; however, immunoreactivity in this site was negative when the cells were preincubated in the presence of protein synthesis inhibitors. Release from taxol results in the reappearance of Tyr immunoreactivity at the distal end of the axon. Taken collectively, the present results indicate 1) that in cerebellar macroneurons axonal differentiation is accompanied by a temporal and spatial differentiation of microtubules and 2) that there is an active site of tyrosinated tubulin assembly at the tip of axonal processes, and they suggest that the highly tyrosinated domain in this region is a consequence of rapid microtubule turnover and tubulin tyrosine ligase activity.

Alkaloids↗
PubMed1999

Embryonic lens repels retinal ganglion cell axons.

During development of the vertebrate visual system, retinal ganglion cell (RGC) axons follow a precise path toward their midbrain targets. Although much is known about the cues that direct RGC axons once they have left the optic disc, less is known about the guidance of axons at earlier stages, when RGCs first send out their axons to navigate within the developing retina. Using collagen gel coculture experiments, we find that the embryonic lens produces a powerful diffusible repulsive activity for RGC axons. We also find that this activity is localized to the lens epithelium and not the lens fiber layer, while the pigmented epithelium and vitreous humour are devoid of activity. The further observation that the lens also chemorepels primary sensory axons, but does not repel olfactory bulb axons, shows that this activity is specific for subsets of axons. Our experiments have excluded two candidate repellents for RGC axons (collapsin-1/sema III and chondroitin sulfate proteoglycans). These results implicate the lens in the earliest stages of RGC axon guidance. One function of the lens repellent may be to prevent aberrant targeting toward the lens, and it may also be involved in the directional guidance of RGC axons toward the optic disc.

Animals↗
PubMed2002

Innervation of the uvea by galanin and somatostatin immunoreactive axons in macaques and baboons.

The neuropeptide galanin has not been localized previously in the primate uvea, and the neuropeptide somatostatin has not been localized in the uvea of any mammal. Here, the distribution of galanin-like and somatostatin-like immunoreactive axons in the iris, ciliary body and choroid of macaques and baboons using double and triple immunofluorescence labeling techniques and confocal microscopy was reported. In the ciliary body, galanin-like immunoreactive axons innervated blood vessels and the ciliary processes, particularly at their bases. In the iris, the majority of these axons was associated with the loose connective tissue in the stroma. Somatostatin-like immunoreactive axons were found in many of the same areas of the uvea supplied by cholinergic nerves. In the ciliary body, there were labelled axons within the ciliary processes and ciliary muscle. They were also found alongside blood vessels in the ciliary stroma. In the iris, somatostatin-like immunoreactive axons were abundant in the sphincter muscle and less so in the dilator muscle. A unilateral sympathectomy had no effect on the distribution of somatostatin-like or galanin-like immunoreactive axons, and these axons did not contain the sympathetic marker tyrosine hydroxylase. They did not contain the parasympathetic marker choline acetyltransferase, either. The galanin-like immunoreactive axons contained other neuropeptides found in sensory nerves, including calcitonin gene-related peptide, substance P and cholecystokinin. Somatostatin-like immunoreactive axons did not contain any of these sensory neuropeptides or galanin-like immunoreactivity, and they were neither labelled with an antibody to 200kDa neurofilament protein, nor did they bind isolectin-IB(4). Nevertheless, they are likely to be of sensory origin because somatostatin-like immunoreactive perikarya have previously been localized in the trigeminal ganglion of primates. Taken together, these findings indicate galanin and somatostatin are present in two different subsets of sensory axons in primate uvea.

Animals↗
PubMed1995

Sprouts from cut corticospinal axons persist in the presence of astrocytic scarring in long-term lesions of the adult rat spinal cord.

Small, circumscribed electrolytic lesions were made in the corticospinal tract at the upper cervical level of the adult rat spinal cord. At increasing survival times, immunohistochemistry of glial fibrillary acidic protein and electron microscopy showed that the predominantly longitudinal astrocytic processes underwent a progressive hypertrophy, which spread from the lesion, increasing in intensity from 1 week and reaching a maximum at between 9.5 and 13 weeks, by which time the lesion was completely surrounded by a dense astrocytic scar. A previous study with orthograde transport of axonal tracers showed that from 2 weeks after the lesion the main axonal stems of both cut and adjacent uncut corticospinal axons had large varicosities. The swollen ends of the cut axons, and also the adjacent uncut axons, emitted extensive arborizations of sprouts directed into the central, macrophage-filled area of the lesion. The present experiments indicated that the axon sprouts persisted apparently undiminished over the period (from 9.5 to 13 weeks) when the astrocytic scarring process was reaching its maximum. Surrounding the center of the lesion was an area in which the axons had become demyelinated. By 3 weeks a few axons were remyelinated with peripheral myelin formed by Schwann cells which had migrated into the lesions. By 4 months the scar region was densely colonized by Schwann cells, which now had remyelinated a wide swath of both cut and uncut axons. The cut axons were myelinated by Schwann cells as far as their large terminal expansions, which were sheathed, but not myelinated, by satellitic Schwann cells. Thus, at survivals long enough for the formation of a dense, astrocytic scar, cut corticospinal axons retain extensive terminal and collateral arborizations even in the macrophage-filled central lesion area and are myelinated or ensheathed by endogenous Schwann cells.

Animals↗
PubMed1998

Sympathetic and sensory axons invade the brains of nerve growth factor transgenic mice in the absence of p75NTR expression.

Collateral sprouting, a nerve growth factor (NGF)-mediated growth response of undamaged peripheral axons, can be divided into reparative and aberrant axonal growth. We have previously shown that aberrant growth occurs in transgenic mice overexpressing NGF centrally under the control of the glial fibrillary acidic protein promoter. Both sympathetic and sensory fibers, stained immunohistochemically for tyrosine hydroxylase and calcitonin gene-related peptide, respectively, invade the cerebellum of postnatal transgenic mice, whereas no such axons are seen in age-matched wild-type cerebellum. Recent examination of mice possessing a null mutation for p75NTR has suggested that axon growth may be influenced by the functional expression of this receptor. To address the potential role of p75NTR in axon growth, we have generated a new line of hybrid mice overexpressing NGF but lacking functional p75NTR expression. Postnatal (day 14) hybrid cerebellum possessed fewer aberrant sensory and sympathetic fibers compared to their age-matched transgenic counterparts. By adulthood, however, hybrid cerebellum displayed a robust plexus of axons stained immunohistochemically for calcitonin gene-related peptide and tyrosine hydroxylase. No neuronal or nonneuronal localization of p75NTR-immunoreactive elements was observed in postnatal and adult hybrid cerebellum. Interestingly, sympathetic axons within the hybrid cerebellum displayed a markedly reduced axon density and staining intensity for NGF, suggesting a possible alteration in axonal sequestration of NGF. These results show that p75NTR is not vital for new growth of NGF-sensitive sympathetic and sensory axons and that immunohistochemical detection of NGF at sympathetic axons requires the functional expression of p75NTR.

Animals↗
PubMed1993

An analysis of HRP-filled basket cell axons in the cat's cerebellum. I. Morphometry and configuration.

Basket cell axons terminate directly on the Purkinje cell body in the mammalian cerebellum and thus are in a position to have a direct influence on this neuron. In the present study, individual basket cells were intracellularly filled with horseradish peroxidase and the morphological characteristics and distribution of their axons were analyzed and quantified. The horizontally directed axon of basket cells preferentially distributes toward one side of the cell body, and is usually directed toward the base of the folium. In their course, the axons give rise to three types of axonal specializations including descending collaterals that form the complex endings around the axon hillocks and somata of Purkinje cells (i.e. the pinceau), beaded tendrils that arise from the descending collaterals and distribute to the Purkinje cell and upper granule cell layer, and beaded tendrils that arise directly from the horizontal axon to enter the molecular layer. In some respects, basket cells comprise a heterogeneous population of neurons on the basis of the length of their axon, as well as the number, distribution, and morphological characteristics of the axonal collaterals. The major finding of this study is that a single basket cell does not form a pinceau around the axon hillock of every Purkinje cell located along the course of its horizontal axon. Further, the pinceaux that are formed vary in their complexity. These findings suggest that the classic concept of off-beam inhibition mediated by basket cells is more complex than previously described.

Animals↗
PubMed1981

Regeneration of motor axons in crayfish limbs: distal stump activation followed by synaptic reformation.

Severed distal stumps of limb motor axons in the crayfish Procambarus clarkii remain ultrastructurally intact for at least 2-3 ms after being severed from their cell body. Initial regeneration of a motor axon is associated with the appearance of up to 200 small profiles (satellite axons) having no glial sheath adjacent to the large surviving stump for about 1 cm distal to the lesion at 4-5 wks postoperatively. These satellite axons are seen 2-4 cm distally at the target muscles 3-4 ms postoperatively. By 14-15 ms postoperative, the motor sheaths from the lesion site to the target muscles contain small axonal processes having thick glial sheaths. Behavioral tests show that some axons that are reconnected to the CNS at 4-5 wks may not be connected at 14-15 ms, whereas other axons not connected by 3-4 ms may be connected at 14-15 ms when the original distal stumps have degenerated. We suggest that all these data can best be explained by the view that motor axons in crayfish limbs initially regenerate via activation of the surviving distal stump by satellite axons which grow out from proximal stump. In most cases, these satellite axons continue to activate the surviving distal stump as they slowly grow to the target muscle. Eventually the satellite axons reform synapses on the target muscle and the original distal stump degenerates.

Animals↗
PubMed1984

Development of the axon cap neuropil of the Mauthner cell in the goldfish.

Development of the axon cap neuropil of the Mauthner neuron in post-hatching larval goldfish brains was observed electron-microscopically. The axonal initial segment of newly hatched (day-4) larvae is completely covered with synaptic terminals containing clear spherical synaptic vesicles. Profiles of thin terminal axons, the spiral fibers, containing similar synaptic vesicles, rapidly increase in number around the initial segment and form glomerular neuropil similar to the central core of the adult axon cap by day 7. Three types of synapses are formed in the core neuropil. Bouton-type synapses contacting the initial segment are most abundant in day-4 to -14 larvae; they decrease thereafter and are rare on the distal half of the initial segment of day-40 larvae. Asymmetric axo-axonic synapses are commonly observed between spiral fibers in the core neuropil of day-7 to -19 larvae, but become fewer by day 40. Unique symmetrical axo-axonic synapses showing accumulation of synaptic vesicles on either side of apposed membrane thickenings first appear in day-14 core neuropil, gradually increase in number, and become the predominant type in day-40 core neuropil. Thick myelinated axons, which lose their myelin sheaths in the glial cap cell layer, start to penetrate into the axon cap on day 10. They gradually increase in number and form the peripheral part of the axon cap together with the cap dendrites, which finally grow into the axon cap from the axon hillock region of the Mauthner cell by day 40.

Age Factors↗
PubMed1981

Ultrastructural organization of actin filaments in neurosecretory axons of the rat.

The ultrastructural organization of actin filaments was studied in the neurohypophysial system of the rat after heavy meromyosin (HMM) labeling. This structural pattern is characterized by (1) a straight arrangement of the filaments parallel to the axonal axis in the proximal nondilated parts of axons, (2) a central location within axonal dilatations, and (3) a higher concentration within axonal endings where the filaments form a complex three-dimensional network. The relationships of the filaments to other axonal structures and organelles was further studied by use of electron microscopic stereoscopy. The actin filaments frequently appear anchored to the axolemma with either polar arrangements of the arrowhead decoration (i) at structurally undifferentiated sites, and (ii) more particularly within perivascular endings, at sites with electron-dense thickenings. In all axonal divisions actin filaments are also found to bind to filamentous material surrounding the microtubules and to various organelles. Within the terminal portions of the axons actin filaments exhibit close relationships to neurosecretory granules and to the numerous smooth microvesicles found in this region. Such preferential relationships are particularly observed both in axon ;terminals and in pituicytes, with coated vesicles frequently binding actin filaments. In water-deprived rats, the concentration of actin filaments is conspicuously increased along the axons and more clearly in the axonal swellings and endings, where they form a more complex and interconnected network. These data are discussed in the light of a possible involvement of contractile proteins in the mechanisms of axonal transport and terminal release of neurosecretory products.

Actins↗
PubMed1975

Fine structure of labelled axons in the cerebellar cortex and nuclei of rodents and primates after intraventricular infusions with tritiated serotonin.

The cerebellar cortex and deep cerebellar nuclei in rats and rhesus monkey were studied after treatment with monoamine oxidase inhibitor and continuous intraventricular infusion with 10(-5) M serotonin-3H. Autoradiographs were prepared for light and electron microscopy. The cerebellum contained no labelled cells. Labelled unmyelinated axons arrive from the brain stem via the periventricular zones of the aqueduct and fourth ventricle. In the parafloccular cortex about 1 per cent of the mossy fibers are labelled, together with a small number of fine varicose axons in the molecular layer that run parallel to the folial axes (less than 0.1%). In the paravermal and vermal cortex there are few labelled fibers in the granular layer and a five-fold greater number of labelled axons in the molecular layer (about 0.5%). Apparently three systems of serotonin-containing axons are present in the cortex: mossy fibers, parallel fiber-like, and a diffuse system in granular and molecular layers. The fastigial (medial), interpositus, and dentate (lateral) nuclei, lateral vestibular and other vestibular nuclei all have numerous labelled axons. The dentate and interpositus nuclei receive labelled fibers which arrive through the superior cerebellar peduncle as well as from the periventricular area. Six morphologically different classes of labelled axon terminals have been differentiated. Class 1a, the mossy fiber rosettes, and class 1b, the CAT2 axons, have small, round, clear synaptic vesicles and large granular vesicles (lgv); class 2 axons have a distinctive collection of round granular vesicles; class 3 boutons have numerous tubular profiles, a few containing dense dots, packed in a dark axoplasmic matrix; class 4 axons have tiny 250 A granular vesicles, clear tubular profiles and occasional LGV; class 5 terminals have numerous LGV, both round and elongated, with clear round and tubular profiles; class 6 terminals have LGV, clear and granular synaptic vesicles and clear tubular profiles. All these axons have LGV 900 A in diameter with 500-600 A variably dense centers that do not fill the vesicle, and Gray's type 1 axodendritic or axasomatic synapses on postsynaptic locations in the cortex and nuclei. Labelled axons in the cortex end as mossy fibers upon granule cell dendrites in glomeruli (Class 1a) or upon dendrites of cortical interneurons, e.g. Golgi cells, basket and stellate cells, and not on Purkinje cells. ...

Animals↗
PubMed1986

Traumatically induced axonal damage without concomitant change in focally related neuronal somata and dendrites.

Traumatic head injury has long been associated with the genesis of reactive axonal change, which many believe to be a major factor in influencing neurological outcome. Although much significance has been attached to such a traumatically induced axonal change, little information exists as to whether such a reactive change occurs as an isolated event or rather as an event associated with concomitant focal tissue damage, possibly involving related neuronal somal and dendritic elements. This issue was critically assessed in mechanically brain-injured cats in which the anterograde axonal transport of horseradish peroxidase was employed to detect reactive axonal change. Following such traumatically induced reactive axonal change over a 21-day post-traumatic period, altered axons were consistently observed within the red, vestibular and reticular nuclei and any evidence for concomitant change within the related neuronal somal and dendritic elements was assessed using light and electron microscopy. Typically, such axonal change occurred without any evidence of focally related somatic or dendritic alteration. Isolated examples of reactive axons approximating neurons undergoing chromatolysis were observed. However, such neuronal chromatolytic change appeared not to be a primary response to trauma, but rather a response secondary to severence of these neurons' axonal projections. The results of this study demonstrate that, in mild to moderate head injury, reactive axonal change does occur in isolation from other forms of focal parenchymal abnormality. This finding, therefore, emphasizes the concept that the number of axons damaged is most likely related to the magnitude of any ensuing neurological abnormality.

Animals↗