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PubMed1997

Axotomy increases the expression of glucose-regulated protein 78 kDa in rat facial nucleus.

Nerve injuries lead to metabolic and morphological changes in the cell bodies of the neurons of origin. Increases in glucose turnover in axotomized facial and hypoglossal motor nuclei have been described. Glucose-regulated protein 78 kDa (GRP78) is implicated in cellular protein folding and subunit assembly and responds to glucose deficiency. We performed Western blot and immunohistochemistry to determine the effect of axotomy on the expression and regulation of GRP78 in the facial nucleus (FN). Facial nerve axotomy caused a larger and longer increase of GRP78 in the ipsilateral FN than in the contralateral FN. In right ipsilateral FN, axotomy resulted in elevation of GRP78 protein levels, first detected at 12 h and which reached significant, maximal induction at 24 h (75 +/- 27% increase). GRP78 protein levels decreased at later time points, but remained elevated over sham-operated controls. In contrast, no significant increase in GRP78 concentrations was found in contralateral left FN. Immunocytochemically, positive GRP78 staining was found mainly in the cytoplasm of motoneurons; there was no nuclear staining. Prominent GRP78-immunostaining appeared in axotomized motoneurons at 24 h postaxotomy as compared with the contralateral, unoperated controls. This augmentation was also observed at 4 and 7 days postaxotomy. The possibility that glucose metabolism and GRP78 levels are two parallel events in the injured facial nucleus is discussed.

Animals↗
PubMed1997

c-Jun expression in adult rat dorsal root ganglion neurons: differential response after central or peripheral axotomy.

The response of the mature central nervous system (CNS) to injury differs significantly from the response of the peripheral nervous system (PNS). Axotomized PNS neurons generally regenerate following injury, while CNS neurons do not. The mechanisms that are responsible for these differences are not completely known, but both intrinsic neuronal and extrinsic environmental influences are likely to contribute to regenerative success or failure. One intrinsic factor that may contribute to successful axonal regeneration is the induction of specific genes in the injured neurons. In the present study, we have evaluated the hypothesis that expression of the immediate early gene c-jun is involved in a successful regenerative response. We have compared c-Jun expression in dorsal root ganglion (DRG) neurons following central or peripheral axotomy. We prepared animals that received either a sciatic nerve (peripheral) lesion or a dorsal rhizotomy in combination with spinal cord hemisection (central lesion). In a third group of animals, several dorsal roots were placed into the hemisection site along with a fetal spinal cord transplant. This intervention has been demonstrated to promote regrowth of severed axons and provides a model to examine DRG neurons during regenerative growth after central lesion. Our results indicated that c-Jun was upregulated substantially in DRG neurons following a peripheral axotomy, but following a central axotomy, only 18% of the neurons expressed c-Jun. Following dorsal rhizotomy and transplantation, however, c-Jun expression was upregulated dramatically; under those experimental conditions, 63% of the DRG neurons were c-Jun-positive. These data indicate that c-Jun expression may be related to successful regenerative growth following both PNS and CNS lesions.

Animals↗
PubMed1996

NGF but not NT-3 or BDNF prevents the A fiber sprouting into lamina II of the spinal cord that occurs following axotomy.

There is a stereotypical pattern of primary afferent terminations within the mature spinal cord; however, this pattern is not immutable. Peripheral axotomy causes A fibers to sprout into lamina II, a region from which they are normally excluded. We have investigated the role of neurotrophins in this response. Rats which had undergone sciatic axotomy were treated intrathecally with NGF, BDNF, or NT-3. A fibers were visualized using transganglionic labeling with cholera toxin B subunit; small fibers were visualized using CGRP immunostaining. NGF (12 microg/day for 2 weeks), but not NT-3 or BDNF, prevented both the axotomy-induced reduction in CGRP staining within lamina II and the sprouting of A fibers into this region. It is likely that the prevention of A fiber sprouting is a secondary consequence of NGF rescuing small fibers. This effect of NGF on dorsal horn sprouting has implications both for our understanding of the maintenance of CNS connectivity and for the treatment of neuropathic pain states.

Animals↗
PubMed1993

Expression of neuropeptides and neuropeptide mRNAs in spinal cord after axotomy in the rat, with special reference to motoneurons and galanin.

The extent to which the plasticity in peptide expression observed in developing spinal motoneurons occurs following proximal peripheral axotomy in the adult rat was examined using in situ hybridization and immunohistochemical techniques to visualize the changes. Transient upregulation of galanin, vasoactive intestinal polypeptide (VIP) and substance P messenger ribonucleic acids (mRNAs) was observed within subpopulations of motoneurons ipsilateral to lesion for periods lasting 2-3 weeks after injury. In contrast, the axotomy-induced heterogenous increases in somatostatin and neuropeptide tyrosine mRNA expression in ipsilateral motoneurons remained elevated, or, in the case of somatostatin, continued to increase for the time period studied (1 month). Immunohistochemical analysis agreed with the in situ hybridization results, showing some motoneurons within the injured ventral horn to contain galanin-, VIP- or somatostatin-like immunoreactivity. In some instances, galanin-immunoreactive motoneurons colocalized with calcitonin gene-related peptide immunoreactivity. Most of the neurons expressing the injury-induced peptides appeared large, presumably alpha-motoneurons but there were also many small neurons expressing galanin in the ventral horn ipsilateral to lesion. This may represent evidence for peptide synthesis in gamma-motoneurons. The only peptide mRNA studied to be down-regulated in response to axotomy was enkephalin. The results show that peptide expression in injured motoneurons is dramatically altered, the significance of which remains to be determined.

Animals↗
PubMed1994

Increased expression of phosphotyrosine after axotomy in the dorsal motor nucleus of the vagus nerve and the hypoglossal nucleus.

To investigate the role of tyrosine kinase underlying glial cell proliferation after axotomy, the localization of phosphotyrosine was studied immunohistochemically in the dorsal motor nucleus of the vagus nerve and the hypoglossal nucleus after nerve transection in adult rats. An anti-phosphotyrosine antibody weakly stained the cytoplasm of the neurons and some glial cells on the control side of both nuclei, while preferentially staining the plasma membrane of perineuronal microglial cells and neurons weakly on the severed side 2 days after axotomy and intensely between 3 and 7 days. Some of the microglial cells reacted positively with both anti-bromodeoxyuridine and anti-phosphotyrosine antibodies, suggesting that tyrosine kinase is involved in microglial cell proliferation. Proliferation of numerous microglial cells was observed in the severed nuclei between 2 and 4 days after axotomy, while only a few were detected on days 5 and 7. These findings suggest that tyrosine kinase is involved in not only the proliferation of perineuronal microglial cells but also in some retrograde neuronal reactions such as differentiation and regeneration.

Animals↗
PubMed1991

Basal cells in the mouse olfactory epithelium after axotomy: immunohistochemical and electron-microscopic studies.

The olfactory epithelium of mice after axotomy was investigated to clarify the stem cells of olfactory cells by double immunostaining using antikeratin (MA903) and anti-bromodeoxyuridine (BrdU) antibodies and by conventional electron microscopy. When a single dose of BrdU was given to mice 9 days after axotomy, immunostaining for BrdU was found in the globose basal cells which were negative for MA903, but not in the basal cells proper which were positive for MA903. The BrdU-immunoreactive cells increased 3- to 6-fold over the number of these cells in the controls, indicating active cell proliferation. At other postoperative days (4 and 14 days), fewer BrdU-immunoreactive cells were found. Furthermore, three pulses of BrdU resulted in numerous BrdU-immunolabelings in the globose basal cells and a few in the basal cells proper. There was no detectable difference in the number of labeled basal cells proper in operated and unoperated mice. In the electron micrographs 9 days after axotomy, the basal cells proper, flat-shaped in unoperated mice, appeared cylindrical or pyramidal in shape and the globose basal cells often lay between the basal cells proper. In unoperated controls, the globose basal cells were located above the flat-shaped basal cells proper. The results suggest that the stem cells of the olfactory cells are globose basal cells and not basal cells proper, and that the shape of basal cells proper changes in relation to the active proliferation of stem cells.

Animals↗
PubMed1986

Effects of "partial axotomy" upon synaptic function.

A lesion limited to the dorsal columns, at the level of L3-L4, was carried out in chronic cats. This operation produced a "partial axotomy" type of lesion on the ascending branches of Ia hind limb afferents. Two to six months after this operation, intracellular studies on L7-S1 motoneurons were carried out. Similar studies were done in normal animals. The peak amplitude and the rate of rise (dV/dt) of heteronymous EPSP's were studied during control conditions (sampling at 1 Hz) and during the post-tetanic potentiation produced by a 500 Hz tetanus (for 3 s). The analysis of these synaptic potentials makes us conclude that: The amplitude of the enlarged EPSP's, observed during PTP, seems to be linearly dependent on their amplitude during control (i.e., pre-tetanus) conditions. Judging by their amplitude, there is no difference between potentiated EPSP's of operated and normal animals. There is also a linear relationship between the rate of rise of EPSP's and their peak amplitude. The slope of this relationship becomes steeper after "partial axotomy", i.e., for a given EPSP amplitude, the dV/dt of its rising part is steeper in operated cats. This steeper slope is also present in EPSP's studied during PTP. The sharper rate of rise of EPSP's, induced by the "partial axotomy" of Ia fibers, would be the mechanism behind the larger monosynaptic reflex previously observed in these operated cats.

Afferent Pathways↗
PubMed1987

Differential effects of axotomy on immature and mature hamster facial neurons: a tritiated-uridine autoradiographic study.

In this study, tritiated-uridine incorporation was autoradiographically examined following axotomy of hamster facial motor neurons (HFMN) at the critical development age of 15 days postnatal and in the adult. The postoperative times selected were 0.5, 1, 2, and 4 days. In the 15-day operative series, no changes in incorporation were observed at any of the postoperative times, except at 4 days postoperative, when there was a decrease in tritiated-uridine incorporation in the axotomized neurons relative to the controls. In the adult operative series there were no changes in incorporation at 0.5 or 1 day postoperative, relative to the controls. At 2 days postoperative in the adult, there was a transient increase in tritiated-uridine incorporation that returned to control levels by 4 days postoperative. When axotomized and control cytoplasmic/nuclear grain densities were compared, no changes were found in either operative series. These results of the time course of axotomy-induced changes in RNA synthesis in HFMN corroborate our previous findings of an age-dependent reactive sequence in HFMN and lend support to the hypothesis that the young neurons are synthesizing at peak capacity related to final growth and cannot be stimulated further by axotomy. As discussed, the transient increase in RNA levels in the adult, the lack of any changes in the rate of transfer of RNA from the nucleus to the cytoplasm, and the decrease in RNA levels in the 15-day neurons may be related to the presence of an unusual intranucleolar body within the nucleolus of HFMN that contains ribosomal precursors.

Aging↗
PubMed1991

Vimentin mRNA expression increases after corticospinal axotomy in the adult hamster.

We examined changes in vimentin gene expression during Wallerian degeneration after corticospinal axotomy in the adult hamster. Vimentin, which is the product of a type III intermediate filament (IF) gene, is expressed in various cells of mesenchymal origin, including microvascular endothelial cells, microglia and developing astrocytes. While increases in vimentin protein have been observed after various types of central nervous system (CNS) injury, it is not known whether this increase is due to increased vimentin mRNA expression. There is also conflicting evidence as to which cells are expressing increased levels of vimentin. In the present study we used in situ hybridization and double-label immunofluorescence techniques to address these issues. A 35S-labeled vimentin cDNA probe was used for in situ hybridizations of brain stem sections obtained 2, 7 and 14 days after unilateral transection of the corticospinal tract in the caudal medulla of adult hamsters. Autoradiography showed that an increase in vimentin mRNA associated with the degenerating corticospinal tract occurred by 2 days after axotomy and that the levels remained elevated for at least 14 days. Immunoblotting and immunocytochemical studies indicated that vimentin protein levels were increased in the degenerating corticospinal tract. Double-label immunofluorescence revealed many vimentin-positive cells and processes that were also labeled with GFAP antibody. In addition, cells and processes that were vimentin-negative but GFAP-positive were also found in the degenerating tract. We suggest that the reactive cells which possessed both vimentin and GFAP were reactive astrocytes of astroblastic origin while those that expressed only GFAP were derived from mature astrocytes. Other vimentin-positive cells/processes did not label with anti-GFAP and thus were either microglial, endothelial or inflammatory cells. These results demonstrate that an increase in vimentin mRNA occurs during Wallerian degeneration after corticospinal axotomy and that this increase is likely to be due to contributions from more than one cell type.

Animals↗
PubMed1996

Acetylcholinesterase inhibitor treatment delays recovery from axotomy in cultured dorsal root ganglion neurons.

We have previously reported that dorsal root ganglion neurons cultured in the presence of the highly specific, reversible acetylcholinesterase inhibitor 1,5-bis-(4-allyldimethylammoniumphenyl) pentan-3-one dibromide (BW284c51), showed significantly reduced neurite outgrowth and contained massive perikaryal inclusions of neurofilaments. In the present report we have more closely examined these changes in a time course study over a 21-day culture period using a combined morphological, immunocytochemical and enzymatic approach and additionally, describe, the effects of acetylcholinesterase inhibitor treatment on the state of neurofilament phosphorylation. Finally, we have examined the effects of co-administration of N6,2'-0-dibutyryladenosine 3':5'-cyclic monophosphate (dbcAMP) with BW284c51. At 1 day in culture, both control and treated cells displayed eccentrically located nuclei, numerous polysomes and perikaryal accumulations of neurofilaments which were immunoreactive with both phosphorylation- and nonphosphorylation-dependent neurofilament antibodies. These cytological changes, which are common features of the chromatolytic reaction following axotomy in vivo, rapidly resolved in the control neurons, where by 7 days in culture, the neurofilament accumulations had completely disappeared and neurite outgrowth was robust. In contrast, inhibitor-treated neurons retained the post-axotomy features up to 21 days and had significantly reduced neurite outgrowth. In addition, we have investigated a possible role of cyclic adenosine monophosphate (cAMP) in the recovery process since it has been shown to enhance neuritic outgrowth in cultured neurons. Our results demonstrate that the addition of dbcAMP, a membrane permeable analog of cAMP, significantly enhanced neuritic outgrowth and accelerated the recovery of BW284c51-treated dorsal root ganglion cells, as gauged by the disappearance of the axotomy-related cytological changes. Treatment with dbcAMP also increased acetylcholinesterase activity which has been positively correlated with neurite outgrowth both in vivo and in vitro. Together, these observations suggest that acetylcholinesterase has a non-cholinolytic, neurotrophic role in neuronal regeneration and development.

Acetylcholinesterase↗
PubMedDate not supplied

Neuropeptide messenger plasticity in the CNS neurons following axotomy.

Neuronal peptides exert neurohormonal and neurotransmitter (neuromodulator) functions in the central nervous system (CNS). Besides these functions, a group of neuropeptides may have a capacity to create cell proliferation, growth, and survival. Axotomy induces transient (1-21 d) upregulation of synthesis and gene expression of neuropeptides, such as galanin, corticotropin releasing factor, dynorphin, calcitonin gene-related peptide, vasoactive intestinal polypeptide, cholecystokinin, angiotensin II, and neuropeptide Y. These neuropeptides are colocalized with "classic" neurotransmitters (acetylcholine, aspartate, glutamate) or neurohormones (vasopressin, oxytocin) that are downregulated by axotomy in the same neuronal cells. It is more likely that neuronal cells, in response to axotomy, increase expression of neuropeptides that promote their survival and regeneration, and may downregulate substances related to their transmitter or secretory activities.

Adrenocorticotropic Hormone↗
PubMed1975

The effects of axotomy on the development of the rat superior cervical ganglion.

The effects of division of the postganglionic axons of the adrenergic neurones in the superior cervical ganglion of the rat were examined with regard to the total ganglionic protein content and tyrosine hydroxylase and DOPA decarboxylase activities. Axotomy before the twelfth postnatal day results in a marked atrophy of the ganglion and a reduction in the total enzyme content of the ganglion. Axotomy after postnatal day 21 results in the normal adult ganglion response with a large increase in the total protein content of the ganglion and only minor changes in the total enzyme content of the ganglion. Axotomy between the postnatal days 12 and 21 results in an intermediate response. Thus it can be concluded there is a critical period during the development of the ganglion during which the adrenergic neurones undergo a maturation governed by their contact with the peripheral target cell via axons. These results suggest a trophic role of the end organ on the adrenergic neurone.

Age Factors↗
PubMed1975

The response of adrenergic neurones to axotomy and nerve growth factor.

Division of the axons of adrenergic neurones by crushing the postganglionic nerve trunks of rat superior cervical ganglia (SCG) at 6 days of age resulted in a permanent atrophy of the SCG reflected by a persistent decrease in the total protein content and in the activities of the enzymes tyrosine hydroxylase and DOPA decarboxylase. Administration of nerve growth factor (NGF) to rats with unilateral axotomy at a dose of 10 mug/g/day for the period 7-21 days of age resulted in hypertrophy of both normal and axotomised SCG. There was a progressive rise in the total protein content and in the activities of the two enzymes till the end of the treatment period in both SCG. After treatment ceased there was a progressive fall in the total protein content and activities of the two enzymes reaching a stable level after 4 weeks. The level reached for treated unoperated SCG remained elevated when compared to untreated control SCG. Axotomised treated SCG had approximately the same biochemical parameters as untreated control SCG and very much elevated over untreated axotomised SCG. These final levels persisted for at least 56 days after treatment had ceased. Animals showed a persistent ptosis after axotomy at 6 days of age but treatment with NGF resulted in a functional recovery by 11 weeks of age. It is suggested that there is normally a retrograde transfer of a factor durind development from the target cell to the perikarya of the neurone permitting survival if the appropriate connections are made. Failure to make such a contact results in cedd death. The cell death occurring normally, and the cell death resulting from axotomy, can both be prevented by NGF treatment leading to an hypertrophy of both SCG. This consistent with the hypothesis than NGF is the retrograde trophic agent for the sympathetic nervous system in the developing animal.

Age Factors↗
PubMed1979

Retinal ganglion cell response to axotomy and nerve growth factor in the regenerating visual system of the newt (Notophthalmus viridescens): an ultrastructural morphometric analysis.

Nerve growth factor (NGF) treatment, given as a single 200 BU intraocular injection at the time of optic nerve transection, was found to significantly accelerate the retinal ganglion cell response to axotomy in the newt (Notophthalmus viridescens). In the control series the per cent of neurons in the retinal ganglion layer demonstrating nuclear reactivity (i.e. chromatin changes) reaches a peak by 14 days post axotomy (14 DPA), plateaus through 21 DPA and falls thereafter, returning to control levels by 90 DPA. NGF treatment is shown to significantly accelerate the entrance of responding retinal ganglion cells into the reactive nuclear phase between 1 and 7 DPA, and by 7 DPA nuclear reactivity has reached a peak, in contrast to 14 DPA for control values. Consequently, NGF treatment causes retinal ganglion cells to be in the nuclear reactive state a week longer than controls but reactivity diminishes after 21 DPA as in controls. Electron microscopic morphometric analysis further substantiates these observations by demonstrating that NGF treatment can elicit certain cellular organelle changes a week earlier (i.e. at 7 DPA) than they would normally occur (i.e. at 14 DPA) in response to axotomy. In addition to eliciting cellular hypertrophy at 7 DPA, NGF treatment significantly increases Golgi field densities in the neuronal perikaryal cytoplasm as well as a doubling of the number of nucleoli per nucleus and stimulating a significant increase in nucleolar cross-sectional areas. A dose-response relationship exists between the per cent of retinal ganglion cells demonstrating nuclear reactivity at 7 DPA and various NGF concentrations which compares favorably with the dose response study involving the number of regenerating axons per nerve cross-section at 14 DPA. Studies to determine if the NGF mediated responses were a specific effect elicited by this protein molecule or whether they are also produced by other peptides which share some properties in common with NGF demonstrate that only NGF is capable of eliciting these responses.

Animals↗
PubMed1982

Neurogenesis in the vomeronasal epithelium of adult garter snakes. 1. Degeneration of bipolar neurons and proliferation of undifferentiated cells following experimental vomeronasal axotomy.

Postnatal cell proliferation, presumably for the purpose of neuronal replacement, was demonstrated in the vomeronasal epithelium of adult garter snakes using experimental vomeronasal axotomy. The luminal supporting cell layer of the epithelium did not undergo mitosis, nor necrosis, but exhibited some morphological modifications following axotomy. The bipolar layer underwent progressive irreversible degeneration following denervation. Degeneration of neurons progressed initially from alteration of cellular ultrastructure, to gross distortion of neuronal shapes followed by disintegration and disappearance of necrotic neurons. Maximal depletion of neurons occurred two weeks following surgery. The columnar epithelium at that time was characterized by the presence of a cell-depleted zone located between the luminal supporting cell layer and the basal, undifferentiated (Ud) cell layer. This cell-depleted zone occupied 70-80% of each degenerated cell column. Regeneration of axotomized neurons did not occur. The basally located, Ud cells exhibited no changes indicative of necrotic processes, but underwent active cell proliferation following axotomy. Changes in proliferative properties in the Ud cell layer were temporally related to the degeneration of the neuronal cell layer following nerve lesion. The Ud cell proliferation rate was slower than the rate of Bp cell degeneration. Proliferating Ud cells in the denervated epithelium may serve as the source of reconstituted vomeronasal bipolar neurons.

Afferent Pathways↗
PubMed1985

Peripheral axotomy induces neurofilament decrease, atrophy, demyelination and degeneration of root and fasciculus gracilis fibers.

We have recently shown that peripheral axotomy by hindlimb amputation in adult cats sequentially results in neurofilament and microtubule decrease and axonal atrophy, myelin wrinkling, myelin remodeling (de- and remyelination), more atrophy and axonal degeneration in proximal sciatic and L7 segmental nerve fibers. The neuropathologic, morphometric and teased fiber alterations in the myelinated fibers (MF) of roots and sampled levels of fasciculus gracilis in groups of adult cats 24 months after hindlimb amputation have now been studied. We found: a severe decrease of neurofilaments, axonal atrophy, myelin wrinkling, de- and remyelination and axonal loss in posterior root axons; that these morphologic abnormalities extended up the fasciculus gracilis in the appropriate territories established from degenerative studies; that the retrograde effect was less severe in ventral root fibers, although atrophy and sprouting were demonstrated here, and that the cellular sequence of retrograde atrophic degeneration of ascending axons was similar to that observed in proximal stump axons. These findings confirm that primary afferent neurons are more vulnerable to axotomy than lower motor neurons and may provide an additional explanation for the poorer functional restoration of sensory than of motor deficit after root compression and in delayed nerve reconnection. Our observations also have important implications for interpretation of neuropathologic alterations in roots and fasciculus gracilis, since the observed features may be secondary to axotomy of peripheral nerve fibers induced by disease and not evidence of a primary derangement.

Amputation, Surgical↗
PubMed1986

Differences in horseradish peroxidase labeling of sensory, motor and sympathetic neurons following chronic axotomy of the rat sural nerve.

In an attempt to clarify the ultimate fate of permanently axotomized adult primary neurons, horseradish peroxidase (HRP) was used as a cell marker to label the motor, sensory and postganglionic sympathetic neurons of rat sural nerves which had been sectioned at the ankle and prevented from regenerating for periods of up to 80 weeks. Axotomy did not affect sympathetic neurons, but resulted 4 weeks later in a sudden reduction in the number of labeled sensory and motor cells which persisted to the end of the study. The missing neuronal population amounted to 44.4% and 45.9% respectively of the normal sensory and motor contingent and included most of the large afferent and efferent neurons. However, examination of sural nerves at the thigh, 30 mm proximal to the neuroma, revealed marked axonal atrophy but no change in the number of myelinated and unmyelinated fibers up to 52 weeks after axotomy. Such prolonged survival of the peripheral processes is indirect evidence that axotomized neurons can endure long-term detachment from their end organs and suggests that the lack of HRP labeling in certain sensory and motor neurons does not imply their degeneration, but expresses one of many retrograde dysfunctions triggered by axotomy.

Animals↗
PubMed1990

Axotomy affects density but not properties of potassium leak channels, in the leech AP neurons.

Leech AP neurons react to axotomy by increasing excitability and resting potential of the cell body membrane. In a previous report we described single potassium channels contributing to the leak conductance in the soma membrane of AP cells. Here we compare both properties and density of single potassium leak channels in cell-free patches from normal and axotomized AP neurons. We show that properties such as single channel conductance, outward rectification, time constants of open and shut interval distributions and absence of inactivation do not significantly differ between normal and axotomized cells. On the other hand, we find that the number of channels per patch progressively increases with time after axotomy. We conclude that changes in density rather than alterations in properties of single channels can account for the increase in the resting potential, observed after axotomy.

Animals↗