Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Axotomy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed1979

The effects of post-ganglionic axotomy on selective synaptic connexions in the superior cervical ganglion of the guinea-pig.

Stimulation of preganglionic axons arising from different levels of the thoracic spinal cord causes different effects on end-organs supplied by the superior cervical ganglion (Langley, 1892; Nja & Purves, 1977a; Lichtman, Purves & Yip, 1979). For example, stimulation of the first thoracic ventral root (T1) causes pupillary dilatation and widening of the palpebral fissure; stimulation of T4, on the other hand, has little effect on the eye, even though axons arising from this level innervate about as many superior cervical ganglion cells as those from T1. Thus ganglion cell innervation is selective. (1) Three months after crushing the major post-ganglionic branches of the superior cervical ganglion this differential effectiveness is lost: T1 and T4 stimulation have approximately equal effects on the end-organs of the eye. (2) In normal animals, the cellular counterpart of selective end-organ effects is the innervation of each ganglion cell by a contiguous subset of the spinal segments that innervate the ganglion as a whole. One of these segments is usually dominant, the strength of innervation from adjacent segments falling off as a function of distance from the dominant one (Nja & Purves, 1977a). Intracellular recordings from ganglion cells 3 months after post-ganglionic axotomy showed that this selective pattern is re-established. (3) Since the innervation of ganglion cells appears normal, the abnormal end-organ responses after post-ganglionic axotomy suggest that ganglion cell axons are not limited to their original targets during peripheral re-innervation. This suggestion is supported by the finding that ganglion cells sending axons to different peripheral destinations via the second and third cervical spinal nerves were no longer distinguishable on the basis of their segmented inputs 3 months after post-ganglionic axotomy. (4) Similar results were obtained when the preganglionic cervical trunk was cut at the same time as the post-ganglionic axons were crushed; the pattern of end-organ responses was abnormal, whereas individual ganglion cells were re-innervated according to the rules of contiguity and segmental dominance. (5) These results indicate that ganglion cells do not undergo a compensatory change in the segmental innervation they receive when their axons regenerate to targets different from, or in addition to those they originally innervated, even when an entirely new set of ganglionic connexions is formed. This suggests that ganglion cells, or some aspect of their immediate environment, possess a permanent label that determines the segmental innervation they receive.

Animals↗
PubMed1980

Long-term effects of axotomy on neural activity during cat locomotion.

1. Neural activity was recorded from cats during locomotion on a treadmill using electrodes in Silastic cuffs placed around the sciatic nerve and the lateral gastrocnemius-soleus, medial gastrocnemius, common peroneal and tibial nerve branches. Each branch gave characteristic patterns of activity which were studied before and after it was cut distal to the recording cuffs. Sensory and motor components were separated and measured using cross-correlation techniques. The amplitude of the cross-correlation peaks was compared with the amplitude of compound action potentials evoked by electrical stimulation and recorded from the same sites in the anaesthetized animal. 2. Sensory activity declined rapidly following axotomy and did not recover unless reinnervation occurred. Sensory activity even 5 months after nerve section and resuture had recovered to only a fraction of the control values. This reduction is attributed to a decline in the evoked compound potentials and to many fibres being unsuccessful in regenerating to appropriate sensory organs. 3. Motor activity declined more than could be accounted for by a decline in evoked potentials over the first month after axotomy. The extra reduction represents a decline in the number of impulses generated by alpha-motoneurones after axotomy. If regeneration was permitted, motor activity recovered to higher levels than did the evoked potentials for the whole nerve. Even if regeneration was prevented by nerve ligation, motoneurones continued to generate activity at a stable level over a period of months during which whole nerve compound potentials continued to decline. 4. The modulation of motor activity in ligated nerves during the step cycle was still appropriate to the required movement. Thus, activity recorded from severed nerves in human amputees may be useful in controlling powered artificial limbs. The persistence of motor activity may be responsible for the lesser degree of atrophy found in motor fibres than in sensory fibres following ligation (Hoffer, Stein & Gordon, 1979b).

Action Potentials↗
PubMed1984

Effects of axotomy on the distribution of passive electrical properties of cat motoneurones.

Previously obtained experimental results concerning the effect of axotomy on motoneurone passive electrical properties have been re-analysed. As shown earlier, axotomy causes an average increase of motoneurone input resistance, membrane time constant and after-hyperpolarization duration. The present analysis suggests that the increased input resistance is related to a higher specific membrane resistivity, a decreased cell size and an altered dendritic geometry. The results also suggest that the change takes place only in neurones projecting to fast-twitch muscle units and produces in them passive electrical properties normally exhibited only by motoneurones projecting to slow-twitch units. Based on the notion that axotomy causes a 'dedifferentiation' of motoneurone properties, the present results might be taken to indicate that undifferentiated motoneurones are slow in character. A possible scheme in which a post-natal differentiation of motoneurone properties may lead to muscle differentiation is discussed.

Animals↗
PubMed1986

Outgoing synapses of small granule-containing cells in the rat superior cervical ganglion after post-ganglionic axotomy.

Small granule-containing cells are intrinsic and interneurone-like in the rat superior cervical ganglion, being innervated by preganglionic axons and giving outgoing synapses of asymmetrical type to the principal neurones. A quantitative ultrastructural investigation has been made of the effect on these outgoing synapses of axotomy of the major post-ganglionic nerve trunks 18.5 h-390 days previously. Cutting, or cutting and ligating, the internal and external carotid nerves 2-3 mm from the ganglion in rats aged 1.5-5.5 months resulted in a statistically significant mean loss of up to 85% of the asymmetrical synapses given by small granule-containing cells in the injured ganglion. The reduction of synapses was maximal 5-9 days post-operatively, and thereafter the incidence of synapses showed significant signs of progressive recovery. The time course and magnitude of the change in incidence of these synapses resembled those found earlier (Matthews & Nelson, 1975) for the loss of preganglionic synapses to principal neurones in the same ganglia, and after an identical post-ganglionic lesion. Control experiments showed that there was no loss of outgoing synapses from the small granule-containing cells as a result of surgical stress or of simple ageing. Older rats (5.5 and 13 months) showed a small but significant increase in the incidence of these synapses. Unilateral post-ganglionic axotomy produced the same reaction in the injured ganglia as did bilateral lesions. Uninjured ganglia contralateral to unilateral axotomies, however, also showed some deficit of outgoing synapses from small granule-containing cells, but this was slight, amounting to 9.9% over-all in comparison to normal values in young rats, and this difference did not reach statistical significance. Cutting the cervical sympathetic trunk to produce preganglionic denervation 2 days before surgical removal of ganglia for analysis did not alter the incidence of outgoing synapses of the small granule-containing cells, either in ganglia post-ganglionically axotomized 5-128 days earlier or in contralateral ganglia, indicating that at no stage was any significant proportion of these synapses given to preganglionic axons. These findings suggest that most of the outgoing synapses from the intra-ganglionic small granule-containing cells are directed to principal neurones whose axons leave with the injured branches, the internal and external carotid nerves.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Effects of axotomy or target atrophy on membrane properties of rat sympathetic ganglion cells.

1. The electrical properties of rat superior cervical ganglion cells were examined in vitro with intracellular microelectrodes after axotomy or atrophy of the submandibular salivary gland. 2. Membrane time constant, input resistance and excitatory synaptic potentials (EPSPs) were decreased to about 50% of their control values 7-10 days after axotomy. 3. Axotomized ganglion cells also showed reduced action potentials and after-hyperpolarizations (AHPs). The AHP duration was reduced to 40% of the control value. 4. In 25% of the axotomized cells, the action potential was followed by an after-depolarization (ADP) instead of the AHP that was always present in control cells. In eleven out of seventeen axotomized cells with ADP, preganglionic stimulation failed to evoke an EPSP, whereas the failure of the synaptic response was never observed in control cells and occurred only in two of fifty-three axotomized cells with AHP. 5. In some axotomized cells with AHP, a depolarizing potential developed after a train of action potentials. This was never observed in control cells. 6. Sympathetic neurones innervating the submandibular gland in control animals had membrane properties similar to those observed in other ganglion cells. 7. The properties of neurones innervating the submandibular gland remained unaltered after the experimentally induced atrophy of the gland. 8. It is concluded that the marked effects of short-term axotomy on membrane properties of sympathetic ganglion cells are not reproduced by long-term atrophy of the target tissue.

Action Potentials↗
PubMed1986

Altered excitability of goldfish Mauthner cell following axotomy. II. Localization and ionic basis.

The ionic basis and spatial localizations of spike generation were examined in normal and axotomized goldfish Mauthner (M-) cells using intra- and extracellular recordings and pharmacological manipulation of ionic conductances, including localized iontophoretic drug applications. Tetrodotoxin (TTX) abolished both the initial segment (IS) spike in normal cells and the larger, two-component action potential in axotomized cells, whereas calcium (Ca2+) blockers did not. Thus, sodium (Na+) appears to be the major inward current carrier in both cases. A shoulder or plateau following the fast-rising Na+-dependent action potential was unmasked in both normal and axotomized M-cells by intracellular injections of tetraethylammonium (TEA), either alone or in conjunction with 4-aminopyridine (4-AP) or cesium (Cs+). This plateau potential was abolished by superfusing with saline containing the Ca2 antagonists, Co2+, Mn2+, or Cd2+. However, barium (Ba2+), which normally substitutes for Ca2+ and also blocks K+ conductances, did not produce a plateau spike, and no action potentials could be evoked in the presence of TTX. Simultaneous extra- and intracellular recordings from the soma and lateral dendrite revealed that both the full-sized axotomized spike and its individual labile components were always maximal at the soma. These data support the earlier suggestion that the axotomy-induced electrogenicity is primarily localized to that region. Iontophoretic application of TTX inside the axon cap, a distinctive neuropil surrounding the initial segment and the axon hillock and circumscribed by a glial border, and at various positions along the lateral dendrite confirmed the Na+-dependency of the action potentials recorded in normal and axotomized cells and further demonstrated that the soma generates the additional spike component in the latter. The results suggest that axotomy causes a persistent change in voltage-gated Na+ channel distribution in the M-cell, with Na+ channels appearing or becoming more numerous in the soma while becoming less concentrated in the initial segment-axon hillock. Possible related shifts in other voltage-dependent conductances are also discussed. Finally, these are the first detailed studies of the ionic basis of axotomy-induced electrogenicity in a vertebrate neuron, central or peripheral, and the similarity to the results obtained with invertebrate neurons suggests common mechanisms underlying the axon reaction.

Action Potentials↗
PubMed1996

Exogenous heat shock cognate protein Hsc 70 prevents axotomy-induced death of spinal sensory neurons.

Elevation of intracellular heat shock protein (Hsp)70 increases resistance of cells to many physical and metabolic insults. We tested the hypothesis that treatment with Hsc70 can also produce that effect, using the model of axotomy-induced neuronal death in the neonatal mouse. The sciatic nerve was sectioned and in some animals purified bovine brain Hsc70 was applied to the proximal end of the nerve immediately thereafter and again 3 days later. Seven days postaxotomy, the surviving sensory neurons of the lumbar dorsal root ganglion (DRG) and motoneurons of the lumbar ventral spinal cord were counted to assess cell death. Axotomy induced the death of approximately 33% of DRG neurons and 50% of motoneurons, when examined 7 days postinjury. Application of exogenous Hsc70 prevented axotomy-induced death of virtually all sensory neurons, but did not significantly alter motoneuron death. Thus, Hsc70 may prove to be useful in the repair of peripheral sensory nerve damage.

Animals↗
PubMed1998

Influence of FK506, Cyclosporin A, Testosterone and Nimodipine on Motoneuron Survival Following Axotomy.

Injury to immature motoneurons results in extensive nerve cell death. Avulsion injury in adult animals has a similar effect. Rescuing injured neurons from degeneration and death is a prerequisite for succesful functional recovery. Here, we have explored the possible survival promoting effect of the immunosuppressant agents FK506 and cyclosporin A, the calcium channel blocker nimodipine as well testosterone on axotomized neonatal facial motoneurons. In addition, we examined the effect of cyclosporin A and Nimodipine, a calcium channel blocker, on survival of adult motoneurons following hypoglossal nerve avulsion. FK506 and cyclosporin A were administered intraperitoneally, testosterone intramuscularly and Nimodipine via the food. After the appropriate postoperative survival periods, the number of surviving facial or hypoglossal motoneurons respectively was calculated. FK506 and Cyclosporin A were found to enhance facial motoneuron survival following neonatal axotomy. Cyclosporin A and Nimodipine were found to promote motoneuron survival in adult rats after hypoglossal nerve avulsion. Nimodipine possibly also reduced motoneuron death in neonatal rats twenty-one days after facial nerve transsection, but failed to rescue motoneurons in neonatal rats during the first seven days after nerve injury. Treatment with testosterone was ineffective in preventing neonatal facial motoneurons from axotomy-induced death at seven days postaxotomy. The restults indicate that motoneuron degeneration can be counteracted to a large extent by immunosuppressant agents as well as by calcium channel blockers. Taken together with findings form previous studies, we conclude that motoneuron survival following axotomy can be promoted by a variety of endogenous and exogenous molecules acting on different cellular mechanisms.

Journal Article↗
PubMed1991

Effects of axotomy on the cholinesterase and carbonic anhydrase activities of axons in the proximal and distal stumps of rabbit sciatic nerves: a temporal study.

The temporal changes in transected sciatic nerves of rabbits were studied using recently developed histochemical techniques for discriminating between sensory and motor axons. A segment of the nerve was removed to inhibit spontaneous regeneration across the gap. Staining characteristics of the proximal and distal nerve stumps were studied at 1, 2, 3, 4, 9, and 35 days following axotomy and compared with control sciatic nerves. In the control and test nerves, subpopulations of myelinated sensory axons were identified histochemically by carbonic anhydrase (CA) staining, and a subset of alpha motor axons were visualized by cholinesterase (CE) staining. Axon staining patterns were reciprocal; i.e., sensory axons were CA-positive and CE-negative, whereas motor axons were CE-positive and CA-negative. Histochemical activities persisted at day 35 after axotomy in the proximal stump and until day 9 after axotomy in the distal stump. This implies that these techniques may aid in both immediate and delayed primary nerve repair. With time, there is buildup of scar tissue adding to the proximal and distal stumps. Therefore, sections for demonstrating sensory and motor axons must be taken progressively further back from the nerve stump ends. Histochemical axon typing indicated that sensory axons regenerated earlier and to a greater degree than motor axons in the developing neuroma. Use of both the carbonic anhydrase and cholinesterase staining methods is more accurate than either technique alone as an adjunct for examining normal and injured peripheral nerves.

Animals↗
PubMed1991

Axotomy-induced changes in rabbit hindlimb nerves and the effects of chronic electrical stimulation.

Chronic electrical stimulation and extracellular recording combined with morphological examination of nerves in this study provided a detailed description of the time course and extent of fiber atrophy when the trophic influence of the target was removed by ligation of axotomized nerves and neural activity was replaced by chronic stimulation. The major findings are that decline in amplitude of compound action potentials (CAPs) and fiber diameters is rapid after axotomy and is not reversed or prevented by chronic electrical stimulation, as would be predicted if neural activity played an essential role in maintaining normal fiber caliber. Chronic stimulation had a small short-term sparing effect in the first month after axotomy but was counterproductive over long periods. Comparison of the time course of the decline in CAP amplitude and reduction of fiber diameters with described alterations in mRNA expression of neurofilament protein indicates that the early atrophy is too rapid to be accounted for by reduced synthesis and transport of neurofilaments. It is more likely to result from modification of axonal proteins after axotomy. Replacement of neural activity with stimulation may reduce the initial atrophy but, over longer periods, exacerbates the atrophy, possibly by affecting the synthesis and transport of cytoskeletal proteins. These studies show that the trophic control of nerve fiber size is mediated primarily by functional contacts with peripheral targets and that neural activity plays a relatively small role. Without functional contacts, nerve fibers decline in diameter to stable but lower values. The atrophy was exacerbated by imposing neural activity on the relatively quiescent axotomized neurons.

Action Potentials↗
PubMed1990

Axotomy, axocompression, axocontusion: effects of mechanical injuries on the catecholamine content of unmyelinated syC fibers.

Authors studied the effects of transection (axotomy) and crush of the rat sciatic nerve, by means of De La Torrés glyoxalic acid fluorescence histochemical technique. It was shown that a simple nerve crush (axocompression) did not induce any major change in the number and fluorescence intensity of unmyelinated axons in the distal stump of the sciatic nerve, even though myelinated axons underwent Wallerian degeneration. By contrast, axotomy resulted in a complete cessation of catecholamine-induced fluorescence; similar effect was exerted by an intense, controlled crush (axocontusion). Supposing that not only postganglionic (syC) but also sensory (drC) unmyelinated axons undergo similar alterations after various mechanical injuries, the apparently controversial results regarding the effects of axotomy and nerve crush, in producing transganglionally mediated depletion of marker substances in the upper dorsal horn, can easily be reconciled.

Animals↗
PubMed1995

Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis.

PURPOSE: To investigate whether retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis. METHODS: Chronic elevated eye pressure was produced in 20 monkey eyes, and the optic nerve was transected unilaterally in the orbit of 10 monkeys and 14 rabbits. Sixteen monkey and 14 rabbit eyes were studied as normal controls. Analytic methods included light and electron microscopy, histochemistry for DNA fragmentation (TUNEL method), and DNA electrophoresis in agarose gels. RESULTS: Dying ganglion cells in the experimental retinas exhibited morphologic features of apoptosis, including chromatin condensation and formation of apoptotic bodies. Cells with a positive reaction for DNA fragmentation were observed in eyes subjected to axotomy and experimental glaucoma but were only rarely encountered in control eyes. No evidence of internucleosomal fragmentation was detected electrophoretically, possibly because of the small proportion of cells that were dying at any given time. CONCLUSION: Some retinal ganglion cells injured by glaucoma and by axotomy die by apoptosis.

Animals↗
PubMed1996

Pattern of degeneration of the rat inferior olivary complex after the early postnatal axotomy of the olivocerebellar projection.

Neuronal death of inferior olivary neurons after early axotomy of the olivocerebellar tract was studied in newborn (P1) hemicerebellectomized rats during the first six days after lesion. The degeneration of the inferior olive showed a topographic pattern from one (P2) to six days after axotomy (P7), after which this complex had almost completely disappeared. The first degenerative changes were observed in the principal olive (P2), while the medial accessory olive was the later-degenerated area (P5). The analysis of these degenerative changes provides a reference for future experimental studies. Furthermore, the topographic study of the degenerative process demonstrated that: i) the most vulnerable neurons were dorsolaterally located, whereas the most resistant ones occupied the medial aspect of the inferior olivary complex, ii) the comparison between the topographical arrangement of the inferior olivary neurons according to their birth dates, and the rate of degenerative changes observed after hemicerebellectomy, open the possibility that the neuronal generation date and the response to the axotomy of the inferior olivary neurons could be related.

Animals↗
PubMed1996

Changes in neuropeptide phenotype after axotomy of adult peripheral neurons and the role of leukemia inhibitory factor.

Adult peripheral neurons undergo dramatic shifts in gene expression following axotomy that are collectively referred to as the cell body reaction. Changes in neuropeptide expression are a prominent feature of these axotomized neurons. For example, while sympathetic, sensory, and motor neurons do not normally express the neuropeptides galanin and vasoactive intestinal peptide, they begin to do so within days after axotomy. In contrast, the expression of other peptides, which these neurons normally express, such as neuropeptide Y in sympathetic neurons and substance P in sensory neurons, is decreased. Recent studies in sympathetic neurons have demonstrated that leukemia inhibitory factor plays an important role in triggering these changes in neuropeptide phenotype in adult neurons. Future studies will be directed at determining to what extent LIF triggers the many other changes in gene expression after sympathetic axotomy and whether this cytokine plays a similar role in sensory and motor neurons.

Animals↗
PubMed1998

Expansion of the dendritic tree of motoneurons innervating neck muscles of the adult cat after permanent axotomy.

The morphologic characteristics of neck motoneurons with intact axons were compared with those of neck motoneurons that had been permanently axotomized for 11 to 17 weeks. Motoneurons were identified antidromically, intracellularly stained with horseradish peroxidase (HRP) and examined after reconstructions of their entire dendritic tree. Axotomized motoneurons differed qualitatively and quantitatively from motoneurons with intact axons. The distal branches of axotomized motoneurons exhibited two novel features: some gave rise to tangled appendages that exhibited growth cone-like specializations resembling lamellipodia and filopodia; others followed a meandering path and had unusually large diameters. These branches showed a discontinuous pattern of staining that was similar to the appearance of myelinated axons stained intra-axonally with HRP. A quantitative analysis of the dendritic trees of 13 completely reconstructed dendritic trees (five axotomized motoneurons and eight motoneurons with intact axons) showed that total dendritic surface area, total dendritic length, and total number of branches increased 38, 34, and 215%, respectively, after axotomy. These measurements were confirmed by comparing the sizes of a larger number of motoneurons (16 axotomized and 21 intact), calculated on the basis of correlations between dendritic tree size and proximal dendritic diameter. We conclude, therefore, that neck motoneurons, in contrast to other types of motoneurons, expand their dendritic trees after axotomy. It is suggested that this expansion is a consequence of two mechanisms: one involves dendritic growth, possibly leading to new synaptic connections; the other causes a conversion of some dendrites into axons.

Animals↗
PubMed2001

Nicotinic acetylcholine receptor subunit proteins alpha7 and beta4 decrease in the superior cervical ganglion after axotomy.

Synaptic transmission in the superior cervical ganglion (SCG) is mediated by nicotinic acetylcholine receptors (nAChR). After transection of the postganglionic nerves of the SCG in the adult rat, the transcript levels of four of the five nAChR subunits present in the ganglion, alpha3, alpha5, alpha7, and beta4, decrease dramatically. In the present study, the effect of axotomy on nAChR subunit expression was examined at the protein level, focusing on the alpha7 and beta4 subunits. Immunohistochemistry with monoclonal antibody mAb306 (for the alpha7 subunit) and polyclonal antibody 4886 (for the beta4 subunit) showed that immunoreactivities for both alpha7 and beta4 subunits were concentrated in neurons in the intact ganglion. Results from double staining with antibodies to these subunits and to tyrosine hydroxylase, the enzyme that catalyzes the rate-limiting step in the biosynthesis of the sympathetic neurotransmitter norepinephrine, demonstrated that most neurons in the SCG express both the alpha7 and beta4 subunits. Three days after axotomy, the number of immunolabeled neurons and the intensity of the immunostaining per labeled neuron were decreased for both subunits. Decreases in subunit levels were also observed by Western blot analysis. Observing changes in these subunits over time after surgery revealed that, while the protein level of the alpha7 subunit recovered substantially within 2 weeks after the lesion, that of the beta4 subunit stayed low. These data demonstrate that decreases in nicotinic receptor subunits are among the changes in proteins that occur in axotomized sympathetic neurons, and suggest that these decreases may contribute to the depression in ganglionic synaptic transmission observed in axotomized ganglia.

Animals↗
PubMed2006

On-line confocal imaging of the events leading to structural dedifferentiation of an axonal segment into a growth cone after axotomy.

The transformation of a transected axonal tip into a growth cone (GC) after axotomy is a critical step in the cascade of events leading to regeneration. However, the mechanisms underlying it are largely unknown. In earlier studies we reported that axotomy of cultured Aplysia neurons leads to a transient and local increase in the free intracellular Ca2+ concentration, calpain activation, and localized proteolysis of the submembranal spectrin. In a recent ultrastructural study, we reported that calpain activation is critical for the restructuring of the microtubules and neurofilaments at the cut axonal end to form a compartment in which vesicles accumulate. By using on-line confocal imaging of microtubules (MTs), actin, and vesicles in cultured Aplysia neurons, we studied the kinetics of the transformation and examined some of the mechanisms that orchestrate it. We report that perturbation of the MTs' polymerization by nocodazole inhibits the formation of an MT-based compartment in which the vesicles accumulate, yet actin repolymerization proceeds normally to form a nascent GC's lamellipodium. Nevertheless, under these conditions, the lamellipodium fails to expand and form neurites. When actin filament polymerization is inhibited by cytochalasin D or jasplakinolide, the MT-based compartment is formed and vesicles accumulate at the cut axonal end. However, a GC's lamellipodium is not formed, and the cut axonal end fails to regenerate. A growth-competent GC is formed only when MT restructuring, the accumulation of vesicles, and actin polymerization properly converge in time and space.

Actins↗
PubMed2006

Axotomy induces contrasting changes in calcium and calcium-binding proteins in oculomotor and hypoglossal nuclei of Balb/c mice.

Motor neurons with different susceptibility to degeneration have been identified in amyotrophic lateral sclerosis (ALS). Increase of intracellular calcium has been proposed as a mediator, amplifying the damage through a positive feedback of the known pathological processes. Accordingly, the potential of motor neurons to limit calcium increases during injury might be proportional to their viability. A basic mechanism of reducing calcium amplitudes depends on the calcium-buffering capacity, determined by the calcium-binding protein content. In this study, oculomotor and hypoglossal neurons, prototypes of resistant and vulnerable motor neurons in ALS were examined in axotomy experiments. Total calcium-, parvalbumin-, and calbindin-D28k levels of motor neurons of adult mice were characterized by electron microscopic histochemistry and light microscopic immunostaining. In hypoglossal neurons, compared with oculomotor neurons, larger and more enduring increases of calcium were detected. The perikarya of hypoglossal neurons remained immunonegative for both parvalbumin and calbindin-D28k. Qualitatively, no major cell loss was noted after axotomy, but a decreased neuronal marker staining at days 1-14 suggested a reversible injury of hypoglossal neurons. Oculomotor neurons were not stained for calbindin-D28k but stained for parvalbumin in control conditions, staining which increased at postoperative days 7-14 before returning to baseline. Neuronal marker staining did not change in these cells during the observed period. The higher level of parvalbumin in resistant motor neurons and their ability to up-regulate parvalbumin after injury, paralleled by a smaller increase of intracellular calcium suggest that parvalbumin may have a protective effect in these cells.

Animals↗