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PubMed1989

Neurofilament phosphorylation in neuronal perikarya following axotomy: a study of rat spinal cord with ventral and dorsal root transection.

Rat spinal cord was stained by indirect immunofluorescence with 11 neurofilament monoclonal antibodies that recognize phosphorylated epitopes. All monoclonals were axon-specific in this location. The large motoneurons containing bundles of neurofilaments did not stain and the pattern remained unchanged after transection of the sciatic nerve in the thigh. With nine monoclonals, stained motoneurons were observed in the ventral horns 3 days, 5 days, 1 week, and 2 weeks after transection of the ventral roots close to the spinal cord. The abnormal motoneurons were typically scattered among normal (i.e., nonstained) cells. Even in animals showing the most severe reaction, the whole motoneuron population at the site of rhizotomy was not affected, stained and nonstained perikarya often coexisting side by side. Stained motoneurons were no longer observed 3 weeks after ventral root transection. Changes in neuronal immunoreactivity were also observed after dorsal root transection. However, a different population was affected, i.e., middle-sized neurons in dorsal horns and at the base of ventral horns. With two monoclonals (A9 and D21), cell bodies remained negative following all operations. It is concluded that axotomy in proximity of the cell body may induce certain neurofilament phosphorylation events in motor neuron perikarya, whereas other phosphorylation events remain confined to the axons under these experimental conditions. The absence of changes after transection of the sciatic nerve in the thigh suggests that neurofilament phosphorylation is a reaction to cell injury rather than a cellular event related to nerve regeneration.

Animals↗
PubMed1992

Fine structure of rat septohippocampal neurons: II. A time course analysis following axotomy.

Previous light microscopic immunocytochemical studies with antibodies against transmitter-synthesizing enzymes have suggested that septohippocampal neurons undergo retrograde degeneration following transection of their axons by cutting the fimbria-fornix. However, a fine-structural analysis of the degeneration process in these cells is lacking so far. Here we have identified septohippocampal neurons by retrograde tracing with Fluoro-Gold. Thereafter, the fimbria-fornix was transected bilaterally. Fine-structural changes in prelabeled septohippocampal neurons were then studied after varying survival times up to 10 weeks. Examination under the fluorescence microscope of Vibratome sections through the septal region revealed numerous retrogradely labeled cells after all survival times following axotomy. These neurons were then intracellularly injected with the fluorescent dye Lucifer Yellow in order to stain their dendritic arbor. Many cells were found after each survival time that displayed characteristics of septohippocampal neurons in control rats (see Naumann et al., J Comp Neurol 325:207-218, 1992). In addition, increasing with survival time, there were many shrunken neurons with a reduced dendritic arbor. Representative examples of both normal appearing and shrunken neurons were photoconverted for subsequent electron microscopic analysis. Relatively few signs of neuronal degeneration were found at each survival time analyzed. The majority of cells, including the heavily shrunken ones, displayed fine-structural characteristics of normal neurons. However, a few degenerating neurons and reactive glial cells were present in all survival stages. We conclude that axotomized septohippocampal projection neurons cease the expression of transmitter-synthesizing enzymes and shrink, but many more cells survive for extended periods of time without target-derived neurotrophic factor than was assumed in previous light microscopic studies.

Animals↗
PubMed1993

A motor neuron-specific epitope and the low-affinity nerve growth factor receptor display reciprocal patterns of expression during development, axotomy, and regeneration.

Somatic motor neurons begin to express the transmitter synthesizing enzyme, choline acetyltransferase (ChAT) and the low-affinity nerve growth factor receptor (NGFR) during embryonic development. However, as motor neurons mature in postnatal life, they lose immunoreactivity for NGFR and acquire a motor neuron-specific epitope that is recognized by the monoclonal antibody, MO-1. The present study was undertaken to examine the effect of nerve injury in adult rats on these three developmentally regulated markers in two populations of somatic motor neurons. Unilateral transection, ligation, or crushing of the sciatic nerve resulted in a loss of MO-1 binding and a concomitant rise in immunoreactivity for NGFR within axotomized motor neurons in lumbar levels of the spinal cord. These changes, detectable within 5 days following nerve injury, are reversed with reinnervation, but persist if reinnervation is prevented by chronic axotomy. Thus, regulation of the expression of NGFR and the MO-1 epitope appears to be critically dependent upon interactions between motor neurons and target muscles. These observations are also consistent with the idea that during regeneration, neurons may revert to a developmentally immature state; in motor neurons, this state is characterized by the presence of NGFRs and the absence of the MO-1 epitope. Transection of the hypoglossal nerve, a purely motor nerve, resulted in a similar loss of MO-1 binding and a selective rise in NGFR immunoreactivity in neurons within the ipsilateral hypoglossal motor nucleus. In addition, immunoreactivity for ChAT was also lost in axotomized hypoglossal motor neurons. In contrast, injury to the sciatic nerve, which bears both sensory and motor axons, did not result in any detectable change in ChAT immunoreactivity in spinal motor neurons.

Animals↗
PubMed1994

Motor neurons in Onuf's nucleus and its rat homologues express the p75 nerve growth factor receptor: sexual dimorphism and regulation by axotomy.

The present study establishes that populations of neurons in the lumbosacral cord, which innervate pelvic striated muscles, express p75NGFR throughout their life spans. These neuronal groups comprise the Onuf's nucleus in humans and its principal rat homologues, dorsolateral (DL) and dorsomedial (DM) nuclei, as well as the cremasteric (CRE) nucleus. The p75NGFR in these neurons is localized in the rough endoplasmic reticulum, Golgi complex, and lysosomes. Almost all neurons that project to striated perineal muscles in the male rat express p75NGFR; very low levels of p75NGFR are detected in neurons that innervate perineal sphincters of the female. In the female rat, p75NGFR expression is masculinized with perinatal androgen treatment. In addition, the expression of p75NGFR in DM and DL neurons in the adult is up-regulated by injury (i.e., pudendal axotomy) but is not influenced by gonadectomy. The results of this study establish that neurons of Onuf's nucleus and its rat homologues differ from general somatic motor neurons in that they express p75NGFR from early postnatal life (i.e., when all motor neurons express p75NGFR) into the adult (when the former, but not the latter, express the receptor). In view of growing evidence for the role of neurotrophins in the physiology of motor neurons, the above differentiating feature between general somatic and sexually dimorphic motor neurons suggests that p75NGFR may be involved in motor neuron plasticity and may participate in mechanisms by which neurons can protect themselves from degenerative insults.

Androgens↗
PubMed1994

Evidence for survival of the central arbors of trigeminal primary afferents after peripheral neonatal axotomy: experiments with galanin immunocytochemistry and Di-I labelling.

Studies employing axoplasmic transport techniques have suggested that the central arbors of vibrissae-related primary afferents are rapidly and permanently lost from the trigeminal (V) brainstem complex after transection of the intraorbital nerve (ION). The present study reexamined this issue using immunocytochemistry for galanin (GAL) and anterograde labelling with Di-I to evaluate V brainstem organization in rats that sustained damage to the ION or individual vibrissae follicles in infancy or adulthood. After adult nerve damage, GAL-positive fibers are increased in layers I and II of V subnucleus caudalis (SpC). This was apparent by 3 days after the lesion. In rats that sustained nerve damage at birth (P0), GAL immunoreactivity (IR) appeared throughout the V brainstem complex and had a patchy distribution similar to that of vibrissae-related V primary afferents in normal rats. Increased GAL-IR in rostral portions of the V brainstem complex was observed in rats that sustained ION damage as late as P14. Additional experiments in which nerve damage was followed by destruction of the V ganglion demonstrated that this GAL-IR was contained in primary afferents. Damage to single vibrissa follicles or to a row of follicles produced a single patch or row of GAL-IR terminals in the somatotopically appropriate portion of the ipsilateral V brainstem complex. Di-I labelling in neonatally nerve-damaged rats demonstrated that primary afferent axons filled the central territory normally innervated by this nerve and that their terminal distribution was patchy. These results suggest that the V ganglion cells that survive neonatal axotomy may retain somatotopically organized projections to the V brainstem complex for at least a limited postnatal period.

Afferent Pathways↗
PubMed1995

Birth dates and survival after axotomy of neurochemically defined subsets of trigeminal ganglion cells.

Trigeminal (V) ganglion cells with different neurochemical phenotypes or different birth dates are affected differently by neonatal axonal transection. The aim of the present study was to determine if V ganglion cell birth date and neurochemical phenotype were correlated and if these two variables could be related to responses to neonatal axonal transection. Immunocytochemistry, histochemistry, and [3H]thymidine labelling were used to determine the birth dates of V ganglion cells recognized by antibodies directed against neurofilament protein (NF), calcitonin gene-related peptide (CGRP), and substance P (SP) and those that bound the lectin Bandierea simplicifolia-I (BS-I). All V ganglion cells were born between embryonic days (E-) 9.5 and 14.5. All ganglion cells were born between E-9.5 and E-14.5. In a normalized population (percentages normalized to equal 100%), over 90% of NF-positive V ganglion cells were born between E-10.5 and E-12.5. The majority of CGRP-positive and SP-positive ganglion cells (> 90%) were generated from E-13.5 to E-14.5 and E-12.5 through E-14.5, respectively. Almost 85% of BS-I-positive ganglion cells were generated on E-12.5 through E-14.5. Previous results and additional data from this study indicated that NF- and BS-I-positive ganglion cells are proportionally more likely to be lost after neonatal axotomy and that SP-positive cells are more likely to remain. The percentage of CGRP-positive cells in the V ganglion was not significantly altered by neonatal infraorbital nerve transection. Overall, these findings do not indicate a strong relationship between cell birth date and the probability of survival after neonatal axonal damage for all V ganglion cell phenotypes.

Animals↗
PubMed1995

Metamorphosis of spinal-projecting neurons in the brain of the sea lamprey during transformation of the larva to adult: normal anatomy and response to axotomy.

The spinal projecting system of the sea lamprey (Petromyzon marinus) has been used extensively in studies of axonal regeneration in both larvae and adults. However, little is known about the changes that are undergone by this system during metamorphosis. In order to determine the developmental changes in the size of the descending spinal projection and in the morphology of its neurons, larval, transforming, and adult lamprey brains were labeled by retrograde transport of horseradish peroxidase (HRP) injected into the spinal cord at 25% of body length. Examination of brain wholemount preparations revealed that the total number of labeled neurons doubled during metamorphosis. Most of this increase could be explained by elongation of reticulospinal axons from the rostralmost segments of the spinal cord to locations caudal to the injection site. There were no additions or deletions of either identified reticulospinal neurons or of reticulospinal nuclear groups between the larval and the adult stages. The proportions of Müller and Mauthner cells that were labeled reached a maximum of 93% during the early stages of metamorphosis. Axons of these neurons are known to project almost the entire length of the cord, even in larvae. Therefore, the efficiency of retrograde transport appears to be greater during metamorphosis than during larval or adult stages. While changes in efficiency of retrograde transport could account for some of the apparent increase in reticulospinal neuron numbers between larvae and animals undergoing metamorphosis, this could not contribute to the further increase in the apparent size of the reticulospinal system in the adult, since efficiency of retrograde labeling in these animals was lower than that at earlier stages. With retrograde labeling, a significant increase was seen in the profusion of dendritic arborization of some Müller and Mauthner cells during the early stages of metamorphosis. This correlated with an increase in the incidence of extreme axonal die-back, as indicated by the presence of retraction bulbs within the brainstem. However, intracellular injection of Neurobiotin in untransected animals showed similar degrees of dendritic arborization at all examined stages of development. Therefore, the dendritic profusion did not reflect developmental changes in neuronal morphology but rather reflected an increased sensitivity to axotomy during metamorphosis. We conclude that, during the transformation of the lamprey from the large larval to the adult form, there is little change in either the size or the dendritic morphology of the identified giant reticulospinal neurons. With respect to the smaller reticulospinal neurons, the distance of projection of many of their axons increases during metamorphosis, but there is very little increase in the number of reticulospinal neurons.

Animals↗
PubMed1992

5'-Nucleotidase immunoreactivity of perineuronal microglia responding to rat facial nerve axotomy.

The ecto-enzyme 5'-nucleotidase was localized immunocytochemically in the axotomized rat facial nucleus. As revealed by the monoclonal antibody 5N4-2,5'-nucleotidase immunoreactivity markedly increased on perineuronal microglia during the first week following axotomy, and gradually disappeared from these cells by the end of the third post-operative week. Interestingly, parenchymal microglia were not or only weakly stained. These findings indicate that 5'-nucleotidase 5N4-2-immunoreactivity may serve as a marker for perineuronal microglia, a population of satellite glial cells that appear to be actively engaged in lesion-induced synaptic changes during regeneration.

5'-Nucleotidase↗
PubMed1988

Axotomy of the rat facial nerve leads to increased CR3 complement receptor expression by activated microglial cells.

Axotomy of the rat facial nerve leads to mitotic divisions of microglial cells without developing into phagocytes. In order to study the functional characteristics of those activated, i.e., proliferating but nonphagocytic, microglia we investigated the expression of monocyte/macrophage antigens by these cells. Our results show that activated microglia lack monocyte/macrophage antigens recognized by the monoclonal antibodies Ox-41, ED1, ED2, and Ki-M2R but express high levels of CR3 complement receptors in situ.

Animals↗
PubMed1994

Neurite outgrowth and GAP-43 mRNA expression in cultured adult rat dorsal root ganglion neurons: effects of NGF or prior peripheral axotomy.

Adult dorsal root ganglion (DRG) cells are capable of neurite outgrowth in vivo and in vitro after axotomy. We have investigated, in cultured adult rat DRG cells, the relative influence of nerve growth factor (NGF) or a prior peripheral nerve lesion on the capacity of these neurons to produce neurites. Since there is evidence suggesting that the growth-associated protein GAP-43 may play a crucial role in axon elongation during development and regeneration, we have also compared the effect of these treatments on GAP-43 mRNA expression. NGF increased the early neurite outgrowth in a subpopulation of DRG cells. This effect was substantially less, however, than that resulting from preaxotomy, which initiated an early and profuse neurite outgrowth in almost all cells. No difference in the expression of GAP-43 mRNA was found between neurons grown in the presence or absence of NGF over 1 week of culture, in spite of the increased growth produced by NGF. In contrast, cultures of neurons that had been preaxotomized showed substantial increases in GAP-43 mRNA and NGF had, as expected, a significant effect on substance P mRNA levels. Two forms of growth may be present in adult DRG neurons: an NGF-independent, peripheral nerve injury-provoked growth associated with substantial GAP-43 upregulation, and an NGF-dependent growth that may underlie branching or sprouting of NGF-sensitive neurons, but which is not associated with increased levels of GAP-43 mRNA.

Animals↗
PubMed1985

Sprouting and functional regeneration of an identified serotonergic neuron following axotomy.

An identified serotonergic neuron (C1) in the cerebral ganglion of Helisoma trivolvis sprouts following axotomy and rapidly (seven to eight days) regenerates to recover its regulation of feeding motor output from neurons of the buccal ganglia. The morphologies of normal and regenerated neurons C1 were compared. Intracellular injection of the fluorescent dye, Lucifer Yellow, into neuron C1 was compared with serotonin immunofluorescent staining of the cerebral and buccal ganglia. The two techniques revealed different and complimentary representations of the morphology of neuron C1. Lucifer Yellow provided optimal staining of the soma, major axon branches, and dendritic arborization. Immunocytochemical staining revealed terminal axon branches on distant targets and showed an extensive plexus of fine fibers in the sheaths of ganglia and nerve trunks. In addition to C1, serotonin-like immunoreactivity was localized in approximately 30 other neurons in each of the paired cerebral ganglia. Only cerebral neurons C1 had axons projecting to the buccal ganglia. No neuronal somata in the buccal ganglia displayed serotonin-like immunoreactivity. Observations of regenerating neurons C1 demonstrated: Actively growing neurites, both in situ and in cell culture, displayed serotonin-like immunoreactivity; severed distal axons of C1 retained serotonin-like immunoreactivity for up to 28 days; axotomized neurons C1 regenerated to restore functional control over the feeding motor program.

Animals↗
PubMed1994

Intravitreal transplantation of a segment of peripheral nerve enhances axonal regeneration of retinal ganglion cells following distal axotomy.

Neurons of the central nervous system are able to regenerate their axons into a peripheral nerve (PN) graft when they are axotomized close to the cell bodies. Very few, if any, damaged axons can regrow into the PN graft when the axonal injury is made distant to the cell bodies. We show here that a segment of viable PN transplanted intravitreally enhances the regenerative response of distally axotomized retinal ganglion cells. We hypothesize that trophic substances released from the intravitreal PN segment may enable retinal ganglion cells to regenerate their damaged axons into the PN graft even after a distal axotomy. This suggests that the regenerative behavior of an axotomized neuron is influenced by both the local environment at the damaged tip of the axon and the local environment surrounding the cell body. This finding provides evidence that the PN grafting technique may be useful for repairing long tract pathways in the central nervous system even when the damage is inflicted far away from the cell bodies.

Animals↗
PubMed1995

Corticospinal motor neurons in the adult rat: degeneration after intracortical axotomy and protection by ciliary neurotrophic factor (CNTF).

Little is known about the neurotrophic factors that may regulate maintenance, growth, and/or repair of corticospinal motor neurons (CSMN) in the developing or the adult mammal. We have developed an adult rat in vivo model of CSMN injury involving (i) bilateral prelabeling of CSMN with a cervical spinal cord injection of cholera toxin B subunit (CTB), (ii) unilateral axotomy close to the cell bodies by an intracortical lesion between cell layer V and the corpus callosum, and (iii) implantation of a continuous infusion device in the cortical parenchyma near the lesion. Two weeks later, coronal sections of the cortex are immunostained for CTB, and CTB-stained neurons are counted over defined section areas and compared to those on the contralateral (nonlesioned, noninfused) side. CTB-stainable neurons were 30-40% of the control side when the lesion was about 200 microns from the deeper face of the cell layer, and survival increased with increasing lesion depths. The model can be used to assess protective effects of potential CSMN trophic factors. The low survival achieved with the more superficial lesions (200 and 300 microns) was markedly improved by continuous infusion of ciliary neurotrophic factor at 0.1 to 1.0 microgram/day.

Animals↗
PubMed1995

Selective loss of slow and enhancement of fast Na+ currents in cutaneous afferent dorsal root ganglion neurones following axotomy.

Voltage-dependent Na+ currents were recorded via patch-clamp from identified adult rat lumbar cutaneous dorsal root ganglion (DRG) neurones using whole-cell and bleb-patch-clamp configurations. Na+ currents in DRG neurones studied 18 days after sciatic nerve ligation were compared with those in control neurones. Control neurones tended to have a singular kinetically slow Na+ current or net Na+ current suggestive of two kinetic varieties of channel in a single neurone. Three changes occurred following axotomy: (1) the peak Na+ current increased significantly, (2) kinetically slow TTX-resistant Na+ current, which predominated in controls, was significantly attenuated or lacking altogether, and (3) a singular, TTX-sensitive kinetically fast form of Na+ current predominated. These findings suggest that as part of the response to axonal injury, DRG neurones increase Na+ channel biosynthesis and/or modify preexisting channels such that their kinetics are accelerated. The results are consistent with the idea that axotomized DRG neurones become hyperexcitable due to the emergence of a high density of kinetically fast, pharmacologically distinguishable, Na+ channels in the membrane.

Animals↗
PubMed1996

An ultrastructural study of the ciliary ganglia of the cat and monkey (Macaca fascicularis) following preganglionic axotomy.

The present study describes ultrastructural changes in the ciliary ganglia of the cat and monkey following preganglionic axotomy. At 3, 5 and 7 days after operation, the nucleus of some neurons was irregular, with prominent indentations, and displaced to the periphery of the neuron. The surface of most neurons was irregular. Neurofilaments and glycogen-like granules were much increased in some neurons. At 21 and 28 days after operation, neurons again appeared normal. Dendritic profiles, packed with many mitochondria and glycogen-like granules, could often be observed from 3 days after operation. In longitudinal section such profiles represented expanded trunks of dendrites; dilated mitochondria and dense bodies were sometimes encountered within them. At later stages after operation, some of these profiles were synaptically contacted by, or closely associated with, axon terminals. In myelinated axons, mitochondria and glycogen-like granules were also increased in number and dilated profiles and dense bodies were found within the axoplasm. In unmyelinated axons, dilated profiles and myelin-like figures were present, as were vesiculo-tubular structures and dense bodies. Electron-dense and -lucent changes could both be observed in myelinated and unmyelinated axons. Almost all the axon terminals were affected 3 days after operation. Within such degenerating axon terminals, the synaptic vesicles had accumulated to form one or several clumps; sometimes the degenerating axon terminals had undergone filamentous hyperplasia. At 45 days after operation, hardly any axon terminals were encountered. Non-neuronal cells, including satellite cells, macrophages and Schwann cells, were actively involved in removing degenerating axons and other cell debris.

Animals↗
PubMed1980

Ultrastructural alterations in the initial segments and in the recurrent collateral terminals of Purkinje cells following axotomy.

Transection of Purkinje cell axons in adult male rats made 1.5 mm or further from the cell body does not lead to the death of the neuron and results in compensatory structural alterations of the surviving axonal portions of the nerve cell. Near to, and at the emergence of recurrent collaterals of Purkinje cell axons, huge varicosities filled with filaments, granular material, lysosomes and mitochondria develop. Terminals of recurrent axon collaterals also exhibit different degrees of structural changes. Most striking of the morphological alterations is the regular presence of nematosomes in the hypertrophic axonal branches, especially in synaptic terminals. Since nematosomes were shown to contain RNA in other types of neurons, their presence in recurrent collaterals may indicate an enhanced synthetic activity in Purkinje axonal processes and endings after axotomy.

Animals↗
PubMed1976

Fulminant Purkinje cell death following axotomy and its use for analysis of the dendritic arborization.

Young and adult cats were operated upon and a number of the vermal cerebellar folia were either transected with a vertical incision or isolated by a horizontal cut. In the proximity of the lesion, Purkinje cell bodies and their dendritic trees became stainable with the Fink-Heimer method. Electron microscopy of the silver stained sections show that the argyrophilic Purkinje neurons undergo an electron dense type of degeneration. Stellate cell dendrites adjacent to the degenerating Purkinje trees are normal, suggesting that the cause of cell death is axotomy close to the perikaryon rather than direct injury. The retrograde Purkinje cell degeneration is fulminant since it is evident 6 hours after the lesion. In Fink-Heimer stained sections the entire dendritic tree is impregnated 1-3 days after the lesion. 4-10 days post-operatively, the flattened dendritic tree becomes fragmented and is partially phagocytized. The silver stained arborizations are approximately 280 mu in width and have an uneven thickness (8-16 mu). In longitudinal and horizontal silver stained sections of lesioned cerebellar folia, uninterrupted fields of degenerating Purkinje cell arborizations can be seen, suggesting that the arborizations overlap. The overlap was demonstrated in electron micrographs of single degenerating arborizations surrounded by normal dendritic trees. The degree of overlap varies with the thickness of the arborization and is in the order of 1-2 mu. This approach indicates that each Purkinje tree occupies an exclusive sheet of molecular layer 8 mu thick and may overlap for as much as 2 mu on each side with neighboring trees. The average thickness of the Purkinje tree is approximately 12 mu.

Animals↗
PubMed1986

Vasoactive intestinal polypeptide increases in areas of the dorsal horn of the spinal cord from which other neuropeptides are depleted following peripheral axotomy.

Peripheral nerve section or local capsaicin application produces depletion of substance P and an enzymatic marker, fluoride-resistant acid phosphatase (FRAP), from circumscribed regions of the terminal areas in the spinal cord. We have made use of this phenomenon to map the extent of central termination of subpopulations of primary afferent neurons containing substance P (SP), somatostatin (SOM), cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP) and FRAP in the rat lumbar spinal cord following sciatic nerve section at midthigh level under ether anaesthesia. Between 2 days and 1 year postoperatively, the animals were perfused transcardially and SP, CCK, VIP and SOM were localised in frozen transverse sections of spinal cord segments L1 to S2 and their corresponding ganglia using unlabelled antibody immunohistochemistry. FRAP was localised using a modified Gomori method. SP, SOM, CCK and FRAP were maximally depleted from identical restricted areas of the dorsal horn of the third, fourth and fifth lumbar segments fifteen days after nerve section and remained so for a year. In contrast, VIP staining increased dramatically in the areas from which the other markers were depleted and showed the same time course. Moreover, a large number of neurons in the corresponding ganglia showed positive VIP immunoreactivity after axotomy but were absent from the unoperated side.

Acid Phosphatase↗