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PubMed1991

Growth cones and axon trajectories of a sensory pathway in the amphibian spinal cord.

Central axons of sensory ganglion (SG) neurons of the Xenopus tail enter the spinal cord via the ventral roots and travel dorsally and rostrally following a diagonal course within the lateral marginal zone (LMZ) to reach the dorsolateral fasciculus (DLF) (Nordlander et al.: Brain Res., 440:391-395, 1988). Axons are dispersed as they cross the cord. At the DLF they turn and travel together rostrally, sharing the fascicle with axons of primary sensory neurons (Rohon-Beard cells) already present in the tract. In this paper we analyze the growth patterns of the central projections of SG axons in the tail by using HRP applied to proximal branches of tail spinal nerves. Growth cones of the diagonal route are variable in configuration, often bearing processes that spread within the LMZ. Once the DLF, growth cones change shape, becoming distinctly linear. While growth cones navigating the diagonal part of the route never contact or fasciculate with other diagonal SG axons, SG growth cones and axons of the DLF are more closely associated with their fellows. Measurements of the slopes of SG axons in the diagonal route indicated a limited range with a mean of 23 degrees with respect to the cord axis. On the basis of these observations, we conclude that 1) navigational patterns for growth cones of this pathway differ for the diagonal versus the DLF part of its course, and 2) fasciculation is not a mechanism used by SG axons to reach the DLF, but that instead, each axon is able to find its way independently.

Afferent Pathways↗
PubMed1991

Transient retinal axon collaterals to visual and somatosensory thalamus in neonatal hamsters.

We have studied the postnatal development of individual axons in the optic tract and thalamus of the Syrian hamster, concentrating attention on retinal ganglion cell axons that make a transient projection to the main somatosensory nucleus, the ventrobasal complex. We bulk-filled axons with horseradish peroxidase in hemithalami maintained en bloc, in vitro. After processing and reaction with diaminobenzidine, we reconstructed individual axons from serial sections. In hamsters and other rodents, the optic tract is composed of superficial and internal components, either or both being possible sources of the retino-ventrobasal projection. Both project to the midbrain, but in normal adults only the superficial optic tract maintains collaterals in the thalamus. We found that the axons of the internal component bear numerous transient thalamic collaterals on postnatal days 0, 1, and 2, and some of these extend into the ventrobasal complex. Axons in the superficial optic tract also bear collaterals on days 0 to 2, but these are confined to the superficial half of the dorsal lateral geniculate nucleus. Thus the transient retino-ventrobasal projection comprises solely transient collaterals originating from axon trunks in the internal optic tract. On days 1 and 2, some collaterals from the superficial optic tract appear to have begun to arborize in the lateral geniculate nucleus. In contrast, collaterals from internal optic tract axons to the ventrobasal complex branch little if at all as they traverse the lateral geniculate nucleus, and at no time prior to their elimination do they develop an appreciable terminal arbor. These long collaterals often terminate in growth cones that include lamellopodia. Our HRP-impregnation method also revealed some transient non-retinofugal axons that pass medially from the ventral lateral geniculate nucleus to the ventrobasal complex but then return without terminating or branching. By day 4, they are absent, as are collaterals from the internal optic tract to the ventrobasal complex.

3,3'-Diaminobenzidine↗
PubMed1991

Evidence for new growth and regeneration of cut axons in developmental plasticity of the rubrospinal tract in the North American opossum.

We have shown previously that rubral axons can grow around a lesion of their spinal pathway in the developing opossum and that a critical period exists for that plasticity (Martin and Xu, Dev Brain Res 39:303, 1988). Since most rubrospinal neurons degenerate after axotomy during the critical period, we have proposed that plasticity results primarily from growth of late arriving axons around the lesion rather than regeneration of cut axons (Xu and Martin, J Comp Neurol 279:368, 1989). In the present study, we used a double-labeling paradigm to test that hypothesis. Four groups of pouch young opossums received bilateral or unilateral injections of Fast Blue (FB) into the caudal thoracic or rostral lumbar cord (T12-L2) at different ages in order to label rubrospinal neurons. Three or 4 days later, the rubrospinal tract was transected unilaterally, four to five segments rostral to the injection(s). If the injection was unilateral, the lesion was made ipsilateral to it. The animals were maintained for about 1 month before a second marker, Diamidino Yellow (DY), was injected, usually bilaterally, between the FB injection(s) and the lesion. The animals were maintained for about 5 days before sacrifice and sections through the red nucleus and spinal cord were examined with a fluorescence microscope. During the critical period for plasticity, only a few rubral neurons contralateral to the lesion were labeled by FB alone, supporting our previous contention that most axotomized neurons degenerate. In contrast, many neurons were labeled by DY alone, indicating that their axons were not present in the caudal cord at the time of the FB injection and that they grew around the lesion during the 1 month survival to incorporate DY. A few double-labeled neurons were also found. One interpretation of such neurons is that they survived axotomy, as evidenced by the presence of FB, and supported axons which grew around the lesion to take up DY. Another interpretation is that they supported late growing axons which incorporated residual FB as well as DY. In order to choose between these alternatives, a similar double-labeling paradigm was carried out, but with removal of FB at the time of the lesion. Since a few neurons were still double labeled, we conclude that regeneration of cut axons also contributed to rubrospinal plasticity. Our results support our previous suggestion that developmental plasticity of the rubrospinal tract results primarily from growth of late arriving axons around the lesion, but they also suggest that regeneration of cut axons occurs.

Amidines↗
PubMed1991

Preferential regeneration of spinal axons through the scar in hemisected lamprey spinal cord.

Axons of lamprey spinal cord can regenerate across a complete spinal transection. Thus, unlike the scar of injured mammalian spinal cords, the scar in the lamprey is not an absolute impediment to regeneration. However, it is still not known whether the scar is a relative impediment or whether it provides a favorable environment for regeneration compared to the spinal cord parenchyma. In order to answer this question, the cords of 12 large larval sea lampreys (4-5 years old) were hemisected at the level of the third gill and the animals allowed to recover for 10 weeks. The large reticulospinal neurons (Müller and Mauthner cells) or their giant axons were injected intracellularly with HRP and their regenerating neurites visualized in central nervous system (CNS) wholemounts. Forty-five of seventy-one regenerating neurites (64%) grew beyond the level of the hemisection. Of these, 36 (82%) regenerated through the scar and remained on the same side of the cord as their parent axons, while only 8 (18%) crossed the midline and grew around the scar. Thus, regenerating neurites of giant reticulospinal axons tended to grow through the hemisection scar rather than around it. Once they passed the level of injury, they continued to elongate in their appropriate paths. It is possible that this tendency for axons to regenerate through the scar reflects the greater amount of empty spaces on the hemisected side. In order to rule this out, 13 animals received contralateral simultaneous hemisections at the level of the 3rd and 7th gills. This procedure created large numbers of degenerating axons and potential empty spaces both rostral and caudal to the scars within both hemicords; 92 of 158 neurites (58%) regenerated beyond the level of their respective hemisections. All of these grew through the scar and none crossed to the contralateral side. Distal to either hemisection, neurites remained on their correct side regardless of whether the contralateral cord contained normal CNS parenchyma or axonal debris and empty spaces produced by Wallerian degeneration. Moreover, in hemisected and double hemisected animals, as well as in completely transected control animals, neurites regenerating in their correct direction grew further than those that were misrouted. Because lamprey spinal axons grow preferentially through a scar rather than around it, the scar may play a positive role in supporting axonal regeneration.

Animals↗
PubMed1993

Electron microscopic immunocytochemical study of the distribution of parvalbumin-containing neurons and axon terminals in the primate dentate gyrus and Ammon's horn.

Five green monkeys were examined with light and electron microscopic preparations to explore the regional differences in the distribution of parvalbumin (PV)-positive neurons and axon terminals in the primate hippocampus. PV-positive neurons were mainly found in the hilus of the dentate gyrus and the strata oriens and pyramidale of Ammon's horn. In electron microscopic preparations, the PV-positive cells displayed nuclear infoldings, intranuclear rods, a large rim of perikaryal cytoplasm with numerous organelles and both asymmetric and symmetric axosomatic synapses. One prominent PV-positive cell type in CA1 was a large multipolar neuron that resembled the large basket cells of the neocortex. Although most PV-positive dendrites were aspiny and postsynaptic to numerous axon terminals, some PV-positive dendrites in the molecular layer of the dentate gyrus displayed filipodia-like appendages with no synapses or spines that were postsynaptic to multiple axon terminals. The PV-positive dendrites in the hilus and stratum oriens were apposed at specialized junctions that resembled gap junctions. PV-positive axons were concentrated in the principal cell layers, and formed axosomatic, axodendritic, and axon initial segment synapses. In cases where these axons were observed to appose the surface of granule cells for a long length, only one axosomatic symmetric synapse per cell was found. In the hilus, PV-positive axon terminals formed synapses onto thorny excrescences of spiny cells. Both semithin sections and electron microscopic preparations indicated that more PV-positive axon terminals formed symmetric axosomatic synapses with pyramidal cells in CA2 than in CA1 and CA3. Also, CA2 displayed a unique plexus of PV-positive axon terminals in stratum lacunosum moleculare. These results indicate that the PV-positive hippocampal cells form a subset of GABAergic local circuit neurons, including the basket and chandelier cells. The ubiquitous finding of PV-positive dendrites linked by gap junctions throughout the dentate gyrus and Ammon's horn adds further data to indicate that this subset of GABAergic neurons is linked electrotonically. The synaptic organization of PV-positive neurons in the hippocampus suggests their participation in both feedback and feedforward inhibition. The PV-positive neurons in the hippocampus are only a proportion of the basket and chandelier cells, whereas virtually all of these cells in neocortex are PV-positive.

Animals↗
PubMed1993

Chiasmatic course of temporal retinal axons in the developing ferret.

Recent studies on the distribution of optic axons in the mature visual pathways, as well as on the genesis of their ganglion cells of origin, suggest that the time of axonal arrival at the optic chiasm determines the side of the brain to which a temporal retinal axon will project. The present study has examined this issue directly in fetal ferrets, by determining the projection of the temporal retina at different developmental stages. Fetuses of known gestational age were fixed with paraformaldehyde and subsequently implanted with crystals of the carbocyanine dye, DiI, into either the temporal retina, or into one optic tract. The lipophilic diffusion of the dye within the plasma membrane of the axons revealed the course of temporal retinal fibers through the fetal chiasm, as well as the distribution of ganglion cells across the two retinae projecting to one optic tract. During early fetal stages, the temporal retina extends axons preferentially into the ipsilateral optic tract: the early retinal projection shows a classical partial decussation pattern. During later fetal stages, temporal retinal axons can be traced into both optic tracts, and the distribution of cells with crossed and uncrossed optic axons in the temporal retina is overlapping. These results indicate that the mature decussation patterns of retinal ganglion cell classes are not primarily the consequence of regressive phenomena such as cell death; rather, they are formed as axons navigate the chiasmatic region during development. The differences in decussation pattern between cell classes arise from the fact that the mechanisms producing the segregation of nasal and temporal retinal axons at the chiasm must change as development proceeds.

Animals↗
PubMed1995

Axonal regeneration into Schwann cell-seeded guidance channels grafted into transected adult rat spinal cord.

Schwann cells (SC) have been shown to promote regeneration in both the peripheral and central nervous systems. In this study we tested the ability of SC to enhance axonal regeneration in adult rat spinal cord by grafting SC-seeded guidance channels into transected cords. SC were purified in culture from adult inbred rat sciatic nerves, suspended in Matrigel, and seeded into semipermeable PAN/PVC channels (2.6 mm I.D. x 10 mm long) at a final density of 120 x 10(6) cells/ml. Channels filled with Matrigel alone served as controls. Adult isologous rat spinal cords were transected at the T8 level, and segments T9-T11 were removed. The rostral stump was inserted 1 mm into channels with capped distal ends. One month after grafting, a vascularized tissue cable was present within the channel in all animals. In SC-seeded channels (n = 14), a mean of 501 myelinated axons was found in the cable, and many axons extended 9-10 mm. Electron microscopy revealed typical SC ensheathment and myelination of axons with four times more unmyelinated than myelinated axons. Control channels (n = 8) contained fewer myelinated axons (mean = 71). When SC were prelabeled in culture with a nuclear dye, labeled nuclei were observed at 30 days, confirming SC survival. Astrocytes identified by glial fibrillary acidic protein staining did not migrate far into the cable, and prelabeled SC did not enter the cord. Lack of immunostaining for serotonin and dopamine beta-hydroxylase indicated that supraspinal axons did not regenerate into the cable. Fast Blue injections into the middle of the cable (n = 3) marked spinal cord interneurons (mean = 306) as far as nine segments rostral (25 mm, C7) extending axons into the graft; fewer dorsal root ganglion neurons were retrogradely labeled. In conclusion, purified populations of SC transplanted within channels promote both propriospinal and sensory axonal regeneration in the adult rat thoracic spinal cord.

Animals↗
PubMed1995

Precocious invasion of the optic stalk by transient retinopetal axons.

This study demonstrates that the fetal optic nerve contains a conspicuous population of transient retinopetal axons. Implants of the carbocyanine dye, DiI, were made into the retina or diencephalon of fetal ferrets to label the retinopetal axons retrogradely or anterogradely, respectively, and sections were immunostained for beta-tubulin to label the early differentiating axons in the optic nerve. Dye implants into the optic nerve head, but not the retinal periphery, retrogradely labeled somata in the ventrolateral diencephalon, provided the implants were made before embryonic day (E) 30. When dye implants were made into the ventrolateral diencephalon, these same retinopetal axons were anterogradely labeled, coursing through the optic nerve but never invading the retina. The axons course as 2-5 fascicles from their cells of origin and turn laterally to enter the optic nerve where it joins the future hypothalamus. The retinopetal cells can be retrogradely labeled as early as E20, before optic axons have left the retina. The optic nerve and fiber layer are immunoreactive for beta-tubulin on E24 and thereafter, whereas on E20 and E22, they are immunonegative. Yet at these early embryonic ages, immunopositive fascicles of axons course from the diencephalon into the optic stalk, confirming the precocious nature of the retinopetal projection. Implants of dye made into the future optic nerve head at these very early stages also retrogradely label retinopetal cells in the future chiasmatic region. These cells are distributed primarily on the side ipsilateral to the midline, but a few can be found contralateral to it. Both these, as well as the retinopetal axons arising from the ventrolateral diencephalon, may serve a transient guidance function for later developing optic axons.

Afferent Pathways↗
PubMed2005

Neuropilin-1a is involved in trunk motor axon outgrowth in embryonic zebrafish.

Neuropilin-1, a receptor for axon-repellent semaphorins and vascular endothelial growth factor (VEGF), functions both in angiogenesis and axon growth. Here, we show strong expression of neuropilin-1a in primary motor neurons in the trunk of embryonic zebrafish. Reducing the expression of neuropilin-1a using antisense morpholino oligonucleotides induced aberrant branching of motor nerves, additional exit points of motor nerves from the spinal cord, and migration of neurons out of the spinal cord along the motor axon pathway in a dose-dependent manner. These phenotypes could be partially rescued by co-injecting neuropilin-1a mRNA. Other axons in the spinal cord and head appeared unaffected by the morpholino treatment. In addition, neuropilin-1a morpholino treatment disturbed normal formation of blood vessels in the trunk of 24 hours postfertilization embryos, as shown by microangiography. Morpholinos to VEGF also disturbed formation of blood vessels but did not affect motor axons, indicating that correct formation of blood vessels is not needed for the growth of primary motor axons. Morpholinos to the semaphorin 3A homologs semaphorin 3A1 and semaphorin 3A2 also had no effect on motor axon growth. However, combined injections of neuropilin-1a morpholino, at a concentration that did not elicit axonal aberrations when injected alone, with VEGF, semaphorin 3A1, or semaphorin 3A2 morpholinos synergistically increased the proportion of embryos showing aberrant motor axon growth. Thus, neuropilin-1a in primary motor neurons may integrate signals from several ligands and is needed for proper segmental growth of primary motor nerves in zebrafish.

Animals↗
PubMed1994

Microglial response to degeneration of serotonergic axon terminals.

The neurotoxic drug p-chloramphetamine (PCA) causes widespread degeneration of fine, unmyelinated serotonergic (5-HT) axons in the forebrain. PCA toxicity is selective for 5-HT axon terminals; preterminal axons and cell bodies are spared. Degeneration is followed by slowly progressive axonal sprouting and partial reinnervation. PCA is injected subcutaneously; this route of administration avoids mechanical disruption of the blood brain barrier. The present study analyzed the response of microglia and astrocytes in rat brain to selective ablation of 5-HT axons by PCA. Several microglial markers were analyzed with immunocytochemical methods. An increase in the number of microglial processes and in immunoreactive staining was observed with antibodies directed against CR-3, MHC-I, CD4, and rat LCA. The microglial response was maximal 3 weeks after PCA treatment, became less evident 6 weeks after treatment, and by 9 weeks no difference was observed between treated and control rats. No change was detected in MHC-II or the macrophage marker ED1, nor in expression of GFAP by astrocytes. Thus, degeneration of 5-HT axon terminals affects only a subset of the microglial markers examined; in comparison, retrograde reaction to facial nerve transection causes a robust increase in all of these markers and in GFAP. The microglial response to PCA-induced axon loss is slow in onset and small in magnitude. These findings indicate that CNS microglia are activated by degeneration of fine, unmyelinated 5-HT axon terminals; furthermore, sensitive microglial markers can detect a subtle axonal lesion that provokes no detectable increase in GFAP expression by astrocytes.

Animals↗
PubMed1988

Synaptic organization of primary axons in trigeminal nucleus oralis.

This report examines the morphology and synaptic connections of small-diameter primary trigeminal axons that terminate in the border zone (BZ) and ventrolateral (VL) subdivisions of rat trigeminal nucleus oralis (Vo). Primary axons were made visible for light and electron microscopic analysis by utilizing the method of anterograde transport of horseradish peroxidase. BZ receives the terminal arborizations of two different populations of small-diameter primary axons. One of these arises from unmyelinated parent fibers and terminates in the dorsal one-half of BZ, while the other has small myelinated parent branches that arborize throughout the subdivision. Terminating within VL are the arbors of a second population of small myelinated primary axons. The endings of all three populations of primary axons lie in synaptic glomeruli. Endings in both subdivisions derived from small myelinated parent fibers lie centrally in glomeruli. Those in VL form axodendritic synapses on numerous dendritic shafts and spines, while endings in BZ glomeruli make at least one axodendritic synapse on one or two dendritic shafts. Endings of unmyelinated primary axons in BZ lie at the periphery of glomeruli where each forms a single axodendritic synapse on a central dendrite. It is at these asymmetrical axodendritic synapses that these three populations of primary axons are thought to transfer their inputs directly to the dendritic arbors of second-order BZ and VL neurons. Common to all three glomeruli is one or more small axonal endings filled with flattened synaptic vesicles that establish axoaxonic synapses on the primary ending as well as axodendritic synapses on the dendritic element(s) receiving primary input. In view of their symmetrical to intermediate synaptic contacts, these endings are thought to belong to axons derived from at least one source that can inhibit or diminish the firing rate of second-order BZ and VL neurons in response to primary input.

Animals↗
PubMed2001

Distribution and origin of corticotropin-releasing factor-immunoreactive axons in the female rat lumbosacral spinal cord.

Corticotropin-releasing factor (CRF) is a neuropeptide traditionally known for its hormonal role in the hypothalamic/pituitary/adrenal stress axis. However, CRF has been reported in axons in sites that may be considered outside of the direct stress axis, e.g., in axons in the lumbosacral spinal cord associated with the micturition response. Whether any of these CRF-immunoreactive axons interacts with uterine-related preganglionic autonomic neurons or projection neurons in the lumbosacral spinal cord is unknown. Thus, immunohistochemistry and retrograde tracing were employed to determine the presence, distribution, and origin of CRF-immunoreactive axons in the L6/S1 spinal cord of the female rat and to ascertain whether these axons are associated with uterine-related neurons. CRF-immunoreactive axons were present in the dorsal horn, medial and lateral collateral pathways, dorsal intermediate gray, laminae VlI and X, and sacral parasympathetic nucleus of the spinal cord. Nitric oxide-synthesizing, i.e., NADPH-d-positive neurons and pseudorabies virus labeled uterine-related neurons were in the sacral parasympathetic nucleus and were closely apposed by CRF-immunoreactive axons. Injection of retrograde tracers (fluorogold or fast blue) into the L6/S1 spinal cord labeled neurons in the hypothalamic paraventricular nucleus and pontine Barrington's nucleus, and some of these neurons were immunoreactive for CRF. This study demonstrates that CRF-immunoreactive axons are present in the L6/S1 spinal cord of the female rat in areas associated with sensory and autonomic processing. Some of these axons originate from the paraventricular nucleus and Barrington's nucleus and are adjacent to uterine-related neurons. These results indicate that CRF may influence neural activity related to the female reproductive system.

Animals↗
PubMed2003

Limited growth of severed CNS axons after treatment of adult rat brain with hyaluronidase.

Many chondroitin sulfate proteoglycans (CSPGs) have been shown to influence CNS axon growth in vitro and in vivo. These interactions can be mediated through the core protein or through the chondroitin sulfate (CS) glycosaminoglycan (GAG) side chains. We have shown previously that degrading CS GAG side chains using chondroitinase ABC enhances dopaminergic nigrostriatal axon regeneration in vivo. We test the hypothesis that interfering with complete CSPGs also limit axon growth in vivo. Neurocan, versican, aggrecan, and brevican CSPGs may be anchored within extracellular matrix through binding to hyaluronan glycosaminoglycan. We examine whether degradation of hyaluronan using hyaluronidase might release these inhibitory CSPGs from the extracellular matrix and thereby enhance regeneration of cut nigrostriatal axons. Anesthetized adult rats were given knife cut lesions of the right hemisphere nigrostriatal tract and cannulae were secured transcranially thereby allowing repeated perilesional infusion of saline or saline containing hyaluronidase once daily for 10 days post-axotomy. Eleven days post-transection brains from animals under terminal anesthesia were recovered for histological evaluation. Effective delivery of substance was inferred from the observed reduction in perilesional immunoreactivity for neurocan and versican after treatment with hyaluronidase (relative to saline). Immunolabeling using antibodies against tyrosine hydroxylase was used to examine the response of cut dopaminergic nigral neurons. After transection and treatment with saline, dopaminergic nigral neurons sprouted in a region lacking astrocytes, neurocan and versican. Axons did not regenerate into the lesion surround that contained astrocytes and abundant neurocan and versican. After transection and treatment with hyaluronidase, there was a significant increase in the number of cut dopaminergic nigral axons growing up to 800 microm anterior to the site of transection. However, cut dopaminergic nigral axons still did not regenerate into the lesion surround that contained reduced (albeit residual) neurocan and versican immunoreactivity. Thus, partial degradation of hyaluronan and chondroitin sulfate and depletion of hyaluronan-binding CSPGs enhances local sprouting of cut CNS axons, but long-distance regeneration fails in regions containing residual hyaluronan-binding CSPGs. Hyaluronan, chondroitin sulfate and hyaluronan-binding CSPGs therefore likely contribute toward the failure of spontaneous axon regeneration in the injured adult mammalian brain and spinal cord.

Animals↗
PubMed2001

Hypothalamic paraventricular axons projecting to the female rat lumbosacral spinal cord contain oxytocin immunoreactivity.

Oxytocin-containing axons project from the hypothalamic paraventricular nucleus to the neurohypophysis and thoracic spinal cord to ultimately influence uterine contractions and autonomic activity, respectively. Whether or not oxytocin-immunoreactive axons project to the female rat lumbosacral spinal cord to influence autonomic outflow to pelvic organs has not been investigated. Thus, the present study was designed to investigate the presence, distribution, and origin of oxytocin-immunoreactive axons in the female rat lumbosacral spinal cord. Immunohistochemistry, spinal cord transections, and axonal tracing with Fluorogold, True Blue, and pseudorabies virus were used. Oxytocin-immunoreactive nerve fibers were present in the L6/S1 segments of the spinal cord. Prominent varicose axons were evident throughout the dorsal horn, along the lateral and medial collateral pathways, in the dorsal intermediate gray area, around the central canal in lamina X, and throughout the sacral parasympathetic nucleus. Injection of retrograde tracer into the L6/S1 spinal cord labeled neurons in the hypothalamic paraventricular nucleus. Transection of the thoracic spinal cord eliminated oxytocin-immunoreactive nerve axons in the L6/S1 spinal cord. In addition, transection of the thoracic spinal cord eliminated transport of retrograde axonal tracer from the L6/S1 spinal cord to the paraventricular nucleus. Pseudorabies virus, a transneuronal retrograde tracer, injected into the uterus and cervix marked uterine-related preganglionic neuronal cell bodies in the sacral parasympathetic nucleus and uterine-related neurons in the hypothalamic paraventricular nucleus. Double immuno-labeling of viral-infected spinal cord sections showed oxytocin-immunoreactive axons closely associated with viral labeled uterine-related preganglionic cell bodies of the sacral parasympathetic nucleus. The results of this study revealed that oxytocin-immunoreactive neurons of the hypothalamic paraventricular nucleus project axons to the lumbosacral spinal cord to areas involved in sensory processing and parasympathetic outflow to the uterus.

Animals↗
PubMed1985

Growing tips of embryonic cerebellar axons in vivo.

Few studies have focused on the transformation of growth cones to mature synaptic arbors. To study these events in developing axons in vivo, we have labeled growing cerebellar axons with horseradish peroxidase (HRP) in postnatal stages [Mason and Gregory, 1984]. This report will provide the first data on embryonic cerebellar axons, and will ask whether growth cones differ in tracts and in target tissue and what features characterize axons that enter the cerebellum in fetal periods. During the earliest embryonic (E) periods examined (E16-19), axons in tracts have enlarged growth cones with lamellopodia and short filopodia that contain small and large vesicles. In contrast, axons within the cerebellar anlage from E16-postnatal day (P) 5 have fine calibers with a minimum of branching, and have small tapered growing tips. If synaptic contacts are made by such growing tips, there is little concomitant change in their shape. As target cells from layers and as their dendrites extend (P5-P7), growing tips and synaptic boutons differentiate according to the type of synaptic arrangement in which they engage. Enlarged, irregular expansions of growing tips correspond to synaptic contacts with multiple dendritic partners and are filled with large and small clear vesicles. Filopodia arising from such swellings, like the small undifferentiated growing tips of the type seen on embryonic axons, contain a mixture of vesicle types but make simple synapses with single profiles. Many axons make both kinds of synaptic structures, especially during the period when maturing axons give rise to long filopodia. Thus, growing tips have immature forms long after synaptogenesis begins, and use filopodial structures to elaborate synaptic arrangements. This analysis should elucidate the changes in growth cone form and cytology that reflect cell-cell interactions during synaptogenesis.

Animals↗
PubMed2004

Target tissue influences the peripheral trajectory of mouse primary sensory olfactory axons.

Primary olfactory neurons situated in the nasal septum project axons within fascicles along a highly stereotypical trajectory en route to the olfactory bulb. The ventral fascicles make a distinct dorsovental turn at the rear of the septum so as to reach the olfactory bulb. In the present study we have used a brain and nasal septum coculture system to examine the role of target tissue on the peripheral trajectory of olfactory sensory axons. In cultures of isolated embryonic nasal septa, olfactory axons form numerous parallel fascicles that project caudally in the submucosa, as they do in vivo. The ventral axon fascicles in the septum, however, often fail to turn, and do not project dorsally towards the roof of the nasal cavity. The presence of olfactory bulb, cortical, or tectal tissue apposed to the caudal end of the septum rescued this phenotype, causing the ventral fascicles to follow a normal in vivo-like trajectory. Ectopic placements of the explants revealed that brain tissue is not tropic for olfactory axons but appears to maintain the peripheral trajectory of growing axons in the nasal septum. Although primary olfactory axons are able to penetrate into olfactory bulb in vitro, they only superficially enter cortical tissue, whereas they do not grow into tectal explants. The ability of axons to differentially grow into different brain regions was shown to be unrelated to the migratory behavior of olfactory ensheathing cells, indicating that olfactory axons are directly responsive to guidance cues in the brain.

Animals↗
PubMed1984

Axonal transport of [3H] GABA and [3H] glutamate in excitatory and inhibitory neurons innervating lobster exoskeletal musculature.

This paper describes the results of intracellular injections of radiolabelled neurotransmitters and transmitter precursor substances, including glutamate, GABA, aspartate, octopamine, tyramine, tryptophan, and choline, into cell bodies of identified excitatory and inhibitory neurons innervating lobster extensor musculature. The distributions and identities of radioactive substances appearing in axons were examined at various times following injection and in vitro incubation. Injected GABA and glutamate were found in appreciable quantities in both excitatory and inhibitory axons and migrated down axons at an estimated rate of between 16 and 22 mm/day at 12 degrees C, whereas the other substances tested were present in substantially smaller quantities and migrated at an estimated rate of less than 7.5 mm/day at 12 degrees C. Injected GABA, D-glutamate and L-glutamate accumulated proximal to ligatures tied around nerves, whereas neither octopamine nor aspartate accumulated proximal to ligatures. Since GABA is the transmitter substance released by inhibitory neurons and L-glutamate is thought to be released from excitatory nerve terminals, these results are consistent with the suggestion that amino acids serving as neurotransmitters are axonally transported. The specificity of axonal transport does not appear to be restricted to the cognate neurotransmitter, as indicated by the movement of L-glutamate in inhibitory axons and GABA in excitatory axons and of D-glutamate in both excitatory and inhibitory axons, but rather may be relaxed to include substances closely related to the neurotransmitter. Some restrictions, however, are apparently placed on axonal transport of small charged molecules in these neurons in that other substances tested migrated down nerves at a considerably slower rate.

Animals↗
PubMed1989

Mosaic Drosophila wings reveal regional heterogeneity in the guidance of ectopic axons.

In most studies of axon guidance in the peripheral tissues of insects, the ability of experimentally perturbed axons to pathfind was examined only along their normal pathways. This means that regions normally devoid of axons have not been sampled for their ability to influence axonal trajectories. To examine this question, we have induced the formation of single sensory neurons in a variety of abnormal locations in the developing wing of Drosophila and have examined the course taken by their axons. The axons of such ectopic neurons have a regionally varying tendency to grow in the normal, proximal direction. This proximal bias approaches 100% for neurons located in the distal part of vein L2 and 70% in distal vein L4 but falls to chance (50%) along vein L5. Thus, neurons forming in ectopic regions of the wing, especially those found near the normal axon pathways (veins L1 and L3), have a high probability of growing axons in the correct direction. We conclude that information relevant to axon outgrowth is not restricted to the normal pathways. Whether this information is intrinsic or extrinsic to the neurons, and why its strength shows such conspicuous regional variation, awaits further study.

Animals↗