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PubMed1993

Rapid and transient alterations in transglutaminase activity in rat superior cervical ganglia following denervation or axotomy.

The activity of transglutaminase (TG), a Ca(2+)-dependent enzyme contributing to cross-linkage formation of intracellular polypeptide chains decreased rapidly to ca. 25% of control level in superior cervical ganglia (SCG) within 0.5 h following denervation. The reduced level was maintained for at least 24 h. By contrast, following axotomy, ganglionic TG activity increased by ca. 50% within 1 h, maintained the increase to 4 h, and returned to control level by 24 h. When SCG were transferred to aerobic in vitro incubation conditions 3 h following denervation, the addition of the protein kinase C (PKC) inhibitor, trifluoperazine (TFP, 10 micrograms/ml), to the medium partially reversed the denervation-induced reduction in ganglionic TG activity. Addition of a PKC activator, 12-O-tetradecanoylphorbol 13-acetate (TPA, 1 microM), had no effect on the TG activity. These findings suggest that the pathway resulting in the rapid, denervation-induced inhibition of TG activity may involve the transsynaptic activation of PKC. When SCG were placed in vitro 3 h following axotomy, addition of nerve growth factor (NGF, 0.25 micrograms/ml) to the medium reversed approximately one-half of the axotomy-induced increase in TG activity. Thus, following axotomy, the reduction in delivery to the SCG of NGF, which can be transported retrogradely within the axon and is indispensable for morphological and functional survival of sympathetic neurons, may trigger the transient, axotomy-induced TG activation in the SCG.

Animals↗
PubMed1996

Peripheral axotomy induces increased expression of neurotensin in large neurons in rat lumbar dorsal root ganglia.

In normal rat lumbar 4 and 5 dorsal root ganglia (DRGs) a few large neurons expressed neurotensin-like immunoreactivity (LI). Twenty hours after crushing the lumbar 4 and 5 dorsal roots or the sciatic nerve, accumulations of neurotensin-LI were seen in many nerve fibers on the ganglionic side of both crushes, indicating a significant centrifugal transport of neurotensin under normal circumstances. A distinct increase in expression of neurotensin (peptide and mRNA) was observed in many large neuron profiles in the ipsilateral lumbar 4 and 5 DRGs two days after unilateral sciatic nerve transection. Two weeks after axotomy the number of neurotensin-positive neuron profiles was reduced and had almost reached normal levels. In the superficial dorsal horn of the lesion side the number of neurotensin immunoreactive fibers in laminae I-II was markedly reduced 7 days after peripheral axotomy. There was no detectable increase in neurotensin-L1 in laminae III-IV of spinal dorsal horn, in the dorsal column nuclei or in the peripheral neuroma (2-28 days after axotomy), suggesting that the amounts of neurotensin transported centrifugally from DRG neurons after axotomy are low. Neurotensin-LI only sometimes colocalized with neuropeptide Y-LI, another peptide known to be upregulated in large DRG neurons. These two peptides may therefore partly be localized in different populations of large DRG neurons. The present results show that, in contrast to the nerve injury-induced general downregulation of neurotensin systems in the superficial dorsal horn and of neurotensin receptor mRNA expression in DRGs as shown in previous studies, axotomy causes upregulation of expression of neurotensin peptide in some large DRG neurons.

Animals↗
PubMedDate not supplied

Active electrophysiological properties of spinal motoneurons in aged cats following axotomy.

The present study was designed to examine the effects of the aging process on the response of motoneurons to axotomy. Accordingly, in aged cats using intracellular recording techniques, the electrophysiological properties of axotomized lumbar spinal cord motoneurons were compared with those of control (nonaxotomized) motoneurons. In motoneurons that were subjected to axotomy, there was a reduction in axonal conduction velocity compared to that exhibited by control motoneurons. In addition, there were a number of changes in the configuration of the action potential following axotomy. The amplitude of the spike and the overshoot increased as did the slope of the soma-dendritic spike, whereas the delay between the initial segment and the soma-dendritic spikes decreased. The duration of the action potential's afterhyperpolarization increased; its amplitude remained unaffected although the calculated afterhyperpolarization current decreased. Following the spike, most of the axotomized motoneurons exhibited hyperpolarization undershoots and delayed depolarizations. Axotomized motoneurons exhibited a small decrease in the membrane potential and a reduction in the rheobasic current compared to control cells. The changes in the frequency distribution of axonal conduction velocity, afterhyperpolarization duration, afterhyperpolarization current and rheobase measurements suggest that aged motoneurons dedifferentiated following axotomy. These results indicate that axotomy, in aged motoneurons, results in the disruption of a variety of electrophysiological parameters and that the specific patterns of the responses that occur in axotomized motoneurons of adult cats also emerge in axotomized motoneurons of aged animals.

Action Potentials↗
PubMed1990

Axotomy-induced alterations in the electrophysiological characteristics of neurons.

The electrophysiological alterations provoked by axotomy have now been studied for almost half a century, in a number of different cell types. Consequently, it is now possible to detail some common mechanisms underlying these changes and to sort out certain trends in the data. The major phenomena reviewed in this section and some possible future directions are summarized below. (1) It is now possible to advance a unified hypothesis for the effects of axotomy on the conduction velocity of myelinated fibers. The key is that axon diameter, which is directly correlated with conduction velocity, is regulated, at least in part, by neurofilament protein gene expression and transport into the axon. Thus, the largest myelinated axons, with the fastest conduction velocities, have the highest neurofilament contents, and in turn, experience greater or faster declines in neurofilament content, axon caliber, and conduction speed following nerve injury. This regulation of neurofilament gene expression also appears to be target- and/or accessory cell-dependent. In fact, Hoffman and colleagues (1988) have hypothesized that neuron interactions with specific targets (via as yet unknown target-induced signals) may either specify or permit specification of the level of neurofilament gene expression in neurons. Imposed on this primary size determinant is an influence of activity, which also underlies the differential atrophy and decrement in conduction velocity exhibited by motor and sensory fibers of comparable diameters in the same lesioned nerve. Unmyelinated axons, whose structures are not dominated by neurofilament content and metabolism, react very differently to axotomy. The structural and metabolic basis of their reaction is not known. (2) Passive membrane properties, in particular neuronal input resistance, remain relatively stable in the majority of neurons after axotomy. The major exceptions, vertebrate spinal motoneurons, lamprey dorsal interneurons, and mammalian vagal motoneurons, all show an increase in input resistance after axotomy. This change in input resistance appears to be correlated with structural or geometric simplification of dendritic trees and real or apparent changes in specific membrane resistance in one case and with a reduction in cell body size in the other two; however, changes in specific membrane resistance cannot be excluded even in the latter two cases. In the spinal motoneurons, input resistance changes may be more pronounced in those neurons with the most extensive or complex dendritic geometries (i.e. F-type motoneurons). More combined electrophysiological (ideally under voltage or patch clamp conditions) and morphological investigations of single neurons need be done to resolve these questions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Ultrastructural studies on peptides in the dorsal horn of the rat spinal cord--III. Effects of peripheral axotomy with special reference to galanin.

In this study co-localization of galanin- with calcitonin gene-related peptide (CGRP)-like immunoreactivity was examined in dorsal root ganglion neurons 14 days after sciatic nerve cut using a laser scanning confocal microscope. CGRP- and galanin-like immunoreactivities were also analysed in the dorsal horn of the spinal cord of these animals with immunofluorescence microscopy. The ultrastructural changes in galanin-immunoreactive, presumably primary afferent terminals in the superficial dorsal horn, were studied as well as the relationship between galanin-, substance P- and CGRP-like immunoreactivities in primary afferent terminals. Local galanin-positive neurons in lamina II were also analysed after peripheral axotomy. Under the confocal microscope, CGRP-like immunoreactivity was located in the perinuclear region, probably the Golgi complex, and in dot-like structures, probably representing large dense-core vesicles, in normal dorsal root ganglion neurons. However, after peripheral axotomy CGRP was mainly detected in dot-like structures. Only a slight decrease in percentage of CGRP neurons in dorsal root ganglion was seen after axotomy, and about 84% of the galanin-positive neurons contained CGRP. The field of galanin-positive nerve fibres in the superficial lumbar (L)4 and L5 dorsal horn expanded and the intensity of staining for CGRP was reduced in these regions 14 days after sciatic nerve cut. Using pre-embedding immunoelectron microscopy, several morphological changes were observed in galanin-positive terminals in laminae I and II ipsilateral to the lesion. Most importantly, the most frequently occurring type of galanin-positive terminals (type 1) showed distinct changes with a granular matrix, many immunoreactive, peripherally located large dense-core vesicles, empty large vesicles and synaptic vesicles which were displaced from the presynaptic zone. Other galanin-positive terminals underwent even more pronounced morphological changes, including extensive vesiculolysis, also of large dense-core vesicles, filamentous degeneration or formation of axonal labyrinths. An increased number of galanin-positive nerve terminals was observed in lamina III of the ipsilateral dorsal horn after axotomy. They did not form glomeruli and contained few large dense-core vesicles. Post-embedding immunocytochemistry combined with quantitative analysis revealed that significant changes occurred in a proportion of terminals also with regard to peptide content in large dense-core vesicles after axotomy. Thus, the percentage of galanin-positive large dense-core vesicles increased in several cases and that of substance P- and CGRP-immunoreactive ones decreased.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1994

Plasticity of tyrosine hydroxylase and vasoactive intestinal peptide messenger RNAs in visceral afferent neurons of the nodose ganglion upon axotomy-induced deafferentation.

The nodose ganglion contains placode-derived visceral sensory neurons of the vagus nerve. Previous study showed that axotomy-induced deafferentation reduced the number of tyrosine hydroxylase-immunoreactive and increased the number of vasoactive intestinal peptide-immunoreactive neurons in the ganglion. The present study was conducted to determine whether the changes in neuropeptide/neurotransmitter enzyme content are associated with changes in the expression of tyrosine hydroxylase and vasoactive intestinal peptide messenger RNAs in the nodose ganglion. We used in situ hybridization histochemistry with 35S-labeled oligonucleotide probes for tyrosine hydroxylase and vasoactive intestinal peptide precursor messenger RNAs. Peripheral axotomy of visceral afferent inputs reduced tyrosine hydroxylase messenger RNA and increased vasoactive intestinal peptide messenger RNA expression in neurons of the nodose ganglion of the rat. The number of tyrosine hydroxylase messenger RNA-containing neurons was significantly reduced at three, seven and 14 days after axotomy-induced deafferentation compared with intact and sham-operated controls. Labeling density of tyrosine hydroxylase messenger RNA-containing neurons was significantly reduced at three and seven days. Conversely, the number of vasoactive intestinal peptide messenger RNA-containing neurons increased significantly at three, seven and 14 days, while the labeling density of vasoactive intestinal peptide messenger RNA-containing neurons also increased at one, three, seven and 14 days. The results of the present study indicate that the axotomy-induced down-regulation of tyrosine hydroxylase and up-regulation of vasoactive intestinal peptide in the neurons of the nodose ganglion are associated with changes in their messenger RNAs in response to axotomy-induced deafferentation.

Animals↗
PubMed1993

Axotomy-induced neurofilament phosphorylation is inhibited in situ by microinjection of PKA and PKC inhibitors into identified lamprey neurons.

Close axotomy of identified lamprey neurons induces phosphorylation of somatodendritic neurofilaments (NFs), followed by ectopic regeneration of neurofilamentous sprouts from the dendrites. We used in situ intracellular microinjection to study the mechanism of axotomy-induced NF phosphorylation. We found that inhibitors of protein kinase C (PKC) and protein kinase A (PKA) block somatodendritic NF phosphorylation for up to 15 days when injected at the time of axotomy. Injection of PKA catalytic subunit, diacylglycerol, or okadaic acid induces somatodendritic NF phosphorylation in intact neurons with the same time course as close axotomy. These results suggest that transient activation of PKC, PKA, and/or serine phosphatase inhibition by axotomy triggers persistent intracellular changes that may be related to polarity loss in these neurons.

Animals↗
PubMed1992

Expression of nerve growth factor in vivo from a defective herpes simplex virus 1 vector prevents effects of axotomy on sympathetic ganglia.

Sympathetic neurons in the superior cervical ganglion (SCG) of adult rats depend on target-derived nerve growth factor (NGF) for maintenance of tyrosine hydroxylase (TH) levels and the noradrenergic neurotransmitter system. Axotomy of a SCG results in NGF deprivation, causing a decline in TH activity; continuous local application of NGF can prevent this decline in TH activity. We now report that injection of a defective herpes simplex virus 1 vector that expresses NGF (pHSVngf) into a SCG can prevent the decline in TH activity that follows axotomy. SCG of adult rats were injected with either pHSVngf virus or pNFlac virus, which expresses Escherichia coli beta-galactosidase. Analysis of RNA from pHSVngf-infected SCG indicated that the NGF gene was efficiently transcribed and processed. Furthermore, 4 days after pHSVngf injection animals underwent axotomy of the virus-injected SCG. After another 10 days, animals were sacrificed and both the injected-axotomized and contralateral control ganglia were assayed for TH activity. Axotomy of SCG injected with pNFlac virus produced a 50% decline in TH activity relative to control ganglia (P = 0.02). In contrast, SCG injected with pHSVngf virus did not show a decline in TH activity following axotomy; instead, these ganglia manifested an 18% increase in TH levels relative to control ganglia. These data demonstrate that herpes simplex virus 1 vectors can be used to modify neuronal physiology in vivo; specifically, expression of a critical gene product by neural cells that do not normally produce it has potential applications for gene therapy.

Base Sequence↗
PubMed1996

Proximal sciatic axotomy does not inhibit the induction of neurofilamentous inclusions following intracisternal aluminum chloride exposure.

We have previously demonstrated an acute, dose-dependent suppression of low molecular weight neurofilaments (NFL) and intermediate molecular weight neurofilaments (NFM) steady state mRNA levels while sparing those of high molecular weight (NFH) mRNA 48 hours (h) following the intracisternal inoculation of AlCl3 in young adult New Zealand white rabbits. To determine whether this alteration in NF steady state mRNA stoichiometry is a necessary prerequisite to the induction of neurofilamentous inclusions, we examined the response of spinal motor neurons to aluminum exposure in vivo following axotomy. Forty-eight h following a complete transection of the proximal sciatic nerve, rabbits were inoculated intracisternally with either 1000 microg AlCl3 in 100 microl 0.9% NaCl or 0.9% NaCl alone. Rabbits were killed at either 48 or 120 h post-inoculation, and the extent of neurofilamentous inclusion formation quantified in both the cervical and the lumbosacral cord. Following the axotomy, rabbits developed an ipsilateral hind-limb paralysis. In spinal motor neurons ipsilateral to the axotomy, chromatolytic changes were observed and both NFH and NFM mRNA levels were significantly reduced (p<0.001). At 48 h post-AlCl3 inoculation, 29% of motor neurons contralateral to the axotomy demonstrated inclusions, whereas 43% of ipsilateral motor neurons demonstrated inclusions (Fisher's test, two tailed, p = 0.0196). At 120 h post-axotomy 75% and 83%, respectively, of neurons were involved (p = 0.0212). Neurofilamentous inclusions did not form in NaCl-inoculated rabbits. These observations indicate that an altered stoichiometry of NF mRNA steady levels, with a relative overexpression of NFH mRNA, is not critical to the induction of neurofilamentous inclusions following AlCl3 exposure.

Aluminum Chloride↗
PubMed1993

GAP-43, aFGF, CCK and alpha- and beta-CGRP in rat spinal motoneurons subjected to axotomy and/or dorsal root severance.

The mRNA levels for growth-associated protein 43 (GAP-43), acidic fibroblast growth factor (aFGF), alpha- and beta-calcitonin gene-related peptide (CGRP), cholecystokinin (CCK) and choline acetyltransferase (ChAT) in rat lumbar spinal motoneurons were studied by in situ hybridization 1, 5 and 21 days and 20 weeks following unilateral peripheral nerve sectioning, ventral rhizotomy or dorsal rhizotomy. Furthermore, CGRP- and aFGF-like immunoreactivities in the ventral horn were studied using immunohistochemistry. One to 21 days after axotomy, GAP-43 and alpha-CGRP mRNAs increased in lesioned motoneurons, while the aFGF mRNA levels were marginally higher in motoneurons on the lesion side as compared to the control side. beta-CGRP, CCK and ChAT mRNA levels, on the other hand, decreased during the short-term response (1-21 days) to axotomy. After ventral rhizotomy, but not peripheral axotomy, there was complete disappearance of aFGF-like immunoreactivity in the ventral root proximal to the lesion. In animals subjected to long-term survival (20 weeks) after peripheral axotomy, the expression of all studied substances had returned to normal levels. Unilateral dorsal rhizotomy did not induce any substantial short- or long-term shifts in the cellular expression of the GAP-43, aFGF, CGRP and CCK peptides or their mRNAs in motoneurons of lesioned segments. These results indicate that peptides/proteins in motoneurons are expressed differentially after axotomy. Whereas alpha-CGRP and GAP-43 are up-regulated, CCK and beta-CGRP become down-regulated and aFGF is largely unaffected.

Animals↗
PubMed1993

Interleukin-6 and transforming growth factor-beta 1 mRNAs are induced in rat facial nucleus following motoneuron axotomy.

Transection of the rat facial nerve leads to a rapid activation of both astrocytes and microglia around axotomized motoneurons. The factors involved in glial activation in vivo are poorly defined but cytokines have been implicated as major regulators of glial activity in vitro. In the present study we have investigated the expression of cytokine mRNAs in the axotomized facial nucleus that might be involved in glial activation. Eight hours after axotomy unilateral transection of the facial nerve had already induced a rapid accumulation of interleukin (IL)-6-mRNA, with a peak at 24 hours. No IL-6 mRNA was detected on the unoperated control side. Transforming growth factor (TGF)-beta 1 mRNA was detected at low levels in the normal facial nucleus, increasing to three times the normal level 2 days after axotomy. After day 7 TGF-beta 1 mRNA levels gradually declined, with a second minor peak 21 days after axotomy. In situ hybridization experiments, 4 and 21 days after axotomy, localized TGF-beta 1 mRNA to activated microglial cells around regenerating motoneurons, as well as probably some astrocytes. Motoneurons did not express TGF-beta 1 mRNA. TGF-beta 3 was found to be normally expressed in the facial nucleus but was not regulated by axotomy. No mRNA for IL-1, tumour necrosis factor-alpha or interferon-gamma was found in the regenerating facial nucleus at any point in time.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Beta APP gene expression is increased in the rat brain after motor neuron axotomy.

The response of the beta APP gene to neuronal injury was studied in the facial and hypoglossal nerve nuclei of the rat after corresponding nerve axotomy. Increased levels of beta APP 695, 714, 751 and 770 mRNAs were observed after either facial or hypoglossal nerve axotomy in the parent ipsilateral motor neurons. The increase was gradual, with maximal values 7 days after axotomy. beta APP mRNA expression returned to normal values 60 days after the lesion. Increased beta APP immunostaining was also detected in ipsilateral chromatolytic motor neurons. No change in beta APP immunoreactivity was observed in oligodendrocytes, another cell type expressing beta APP under normal conditions. A rapid increase in the expression of the GFAP gene was observed in reactive astrocytes surrounding chromatolytic neurons in the ipsilateral facial or hypoglossal nuclei. Thus, in contrast with other models of neuronal injury, where only the Kunitz protease inhibitor-containing beta APP mRNA isoforms are increased, all beta APP mRNAs are increased in the axotomy model. Furthermore, although beta APP expression has been shown to be increased in reactive astrocytes following neuronal injury, in the present study the increase was essentially found in the motor neurons reacting to axotomy.

Amyloid beta-Protein Precursor↗
PubMed1996

Increased expression of BDNF and trkB mRNA in rat facial motoneurons after axotomy.

Motoneurons of the adult survive after axotomy even though they are deprived of putative target derived trophic factors. Alternative sources of trophic support may substitute. In this study we test the hypothesis that the immediate environment of the motoneuronal cell body or the cell body itself increases the production of trophic factors after axonal injury. Using in situ hybridization (ISH) and reverse transcription-polymerase chain reaction (RT-PCR), we report that after axotomy, rat facial motoneurons increase the expression of mRNA for brain-derived neurotrophic factor (BDNF) and its receptor trkB. After transection of the facial nerve, we measured a 2- to 4-fold increase in BDNF mRNA expression which had its onset between 3 and 8 h after injury. The BDNF mRNA levels peaked at approximately 1-2 days and gradually declined thereafter to return to contralateral levels within 7 days of injury. Western blotting revealed a several-fold increase in BDNF as early as 24 h, which subsequently reached a maximum in approximately 5-7 days and was still sustained at 2 weeks post-axotomy. Using exon-specific primers, we determined that the increase in BDNF mRNA is largely due to an increased expression from the promoters of exons IV and III, and to a lesser extent from exons I and II. Analysing the mRNA expression for the BDNF receptor, trkB, we found a 2- to 3-fold increase in full-length trkB mRNA expression starting 2 days after axotomy which lasted 2-3 weeks. These findings suggest that BDNF might act locally on axotomized motoneurons in an autocrine fashion, providing support for axotomized motoneurons during the first weeks after axotomy.

Animals↗
PubMed1996

Axotomy as an experimental model of neuronal injury and cell death.

Axonal transection provides very useful paradigms to study cellular responses to injury, mechanisms of regeneration and plasticity, and processes that lead to nerve cell degeneration. Moreover, models of axotomy are valuable for testing experimental therapeutic approaches. Lesions can be made with great precision, and, depending on the neural system, location of the lesion, and age of the animal, these models allow the opportunity to examine a range of neuronal responses. Many parameters influence the character, evolution, and outcomes of axotomy-related processes. The most severe outcome of axotomy is cell death, very common in lesions of neurons of the central nervous system (CNS), although neurons of the peripheral nervous system (PNS) may also die if the transection is sufficiently close to the neuronal cell body or if lesions are performed in young animals. Studies of axotomy models have provided clues into the cellular/molecular events associated with neuronal death and the ways in which interventions can delay or prevent processes that lead to cell death. In this review, we select examples, primarily from our own work, to illustrate how axotomy models have enhanced our understanding of neuronal responses to injury, clarified mechanisms of both regeneration/plasticity and degeneration/ cell death, and allowed assessments of the utility of therapeutic approaches.

Aging↗
PubMed1986

Incoming synapses and size of small granule-containing cells in a rat sympathetic ganglion after post-ganglionic axotomy.

A quantitative ultrastructural study has been made of the reaction of the incoming synapses of small granule-containing cells after axotomy of the major post-ganglionic branches of the superior cervical ganglion of the young adult rat. These cells are intrinsic and interneurone-like in this ganglion, receiving a preganglionic input and giving outgoing synapses to principal post-ganglionic neurones. Unlike their outgoing synapses, which are lost after post-ganglionic axotomy (Case & Matthews, 1986), the incoming synapses of the small granule-containing cells in axotomized ganglia increased in incidence post-operatively. The increase first became clearly evident 5-7 days post-operatively and was greater, being both more sustained and progressive, after bilateral than after unilateral axotomy. After bilateral axotomy the incidence of incoming synapses rose to more than four times that of normal ganglia and was still elevated at 128 days post-operatively, but was within normal limits at 390 days. After a unilateral lesion, increases of similar extent and time course to those in the axotomized ganglia were seen in the incoming synapses of small granule-containing cells in the uninjured contralateral ganglia. The incoming synapses of the small granule-containing cells are multifocal, i.e. show several points or active foci of synaptic specialization. The increase in synapses expressed itself both through an increased incidence of these synaptic active foci per nerve terminal and through an increase in the number of presynaptic nerve terminal profiles associated with the cells. Control observations indicated that the increase in synapses was not due to surgical stress, nor was it attributable solely to post-operative ageing. The nerve terminals which were presynaptic to the small granule-containing cells post-operatively were all of preganglionic origin: no incoming synapses or presynaptic nerve terminals remained at 2 days after a preganglionic denervation of axotomized or contralateral ganglia, at whatever stage this was performed throughout the range of survival intervals. There was some evidence that the synapses had increased by sprouting, including terminal sprouting, of the preganglionic nerve fibres. In the shorter term there was an increase in the proportion of small nerve terminal profiles. In the longer term the mean size of the terminal profiles increased, and very large terminals of unusual form were seen. After post-ganglionic axotomy, and in particular after a bilateral lesion, the small granule-containing cells became hypertrophied.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

The effects of axotomy on bullfrog sympathetic neurones.

1. The effects of axotomy on the electrical properties of B cells in paravertebral sympathetic ganglia were studied using standard intracellular recording techniques. The effects were apparent after 1 week and persisted throughout the 47 days of study. 2. Action potential duration (spike width) and amplitude (spike height) were significantly increased in axotomized neurones. 3. The duration of the after-hyperpolarization which followed the action potential showed considerable scatter in control neurones (mean +/- S.E. of mean, 159.0 +/- 5.8 ms for 100 cells). Following axotomy, the duration was significantly reduced (50.9 +/- 2.3 ms for 97 cells). The amplitude of the after-hyperpolarization was also significantly smaller in axotomized neurones. 4. Changes in the characteristics of the action potential and the after-hyperpolarization in axotomized neurones were not due to alteration in resting membrane potential or input resistance which were unchanged after axotomy. Rheobase current was significantly increased. 5. There was neither a significant depression of the rate of rise or the amplitude of orthodromically evoked nicotinic e.p.s.p.s nor any obvious ultrastructural alteration following axotomy. 6. Despite the decrease in the duration of the after-hyperpolarization, the rate of discharge in response to constant current injection was little changed in axotomized neurones. 7. Although axotomy produces significant changes in several measurable electrophysiological parameters in bullfrog sympathetic ganglion cells, the present results imply that mature neurones are able to maintain relatively normal electrical activity despite injury.

Action Potentials↗
PubMed1986

The effect of axotomy on posttetanic potentiation of group Ia synapses in the cat.

Posttetanic potentiation (PTP) of composite Ia excitatory postsynaptic potentials (EPSPs) has been studied in normal cat alpha-motoneurons and in motoneurons axotomized 2-3 wk earlier by ventral root section. The maximal amount of PTP of EPSP amplitude (expressed relative to unpotentiated amplitude) was considerably less in the axotomized population compared with the normal population. The decrease in PTP provoked by axotomy occurs in association with a postaxotomy increase of input resistance, the net effect being that PTP in axotomized cells was much the same as that observed by others in normal motoneurons possessing similarly high input resistance. In agreement with previous results, EPSP peak amplitudes were decreased after axotomy. This decrease seemed to be largely related to an absence of the largest EPSPs, since otherwise the EPSP distributions of normal and axotomized motoneurons showed considerable overlap. It is suggested that the observed decrease in PTP after axotomy is related to a change in synaptic release properties and not secondary to changes in the electrical properties of motoneurons. A previous analysis has suggested that axotomy causes an alteration of the distribution of passive electrical properties among motoneurons such that axotomized cells resemble normal high-resistance motoneurons. The present results suggest that axotomy may affect the distribution of Ia synaptic release properties in a similar manner, since PTP in axotomized motoneurons resembles that observed in normal high-resistance motoneurons.

Animals↗
PubMed1988

Electrophysiological characteristics of hamster dorsal root ganglion cells and their response to axotomy.

1. The active and passive membrane properties of neurons in the lower lumbar (L6, L7) or sacral (S1) dorsal root ganglia from golden hamsters were examined in vitro by means of conventional intracellular recording techniques. Data were collected from neurons exhibiting action potentials (AP) of 70 mV or more in amplitude. 2. Cells with axonal conduction velocities (CV) greater than 20 m/s were termed fast-A-cells, those with CVs between 2.5 and 20 m/s were termed A-delta-cells, and those with CVs less than 1 m/s were termed C-cells. 3. Fast-A-cells usually exhibited short-duration APs (2.51 +/- 0.41 ms, n = 19) followed by short (less than 50 ms) afterhyperpolarizations (AHPs). C-cells usually exhibited long-duration APs (10.5 +/- 0.69 ms, n = 18) followed by long-duration AHPs (much greater than 50 ms). The characteristics of APs in A-delta-cells (AP mean duration 3.34 +/- 0.42 ms, n = 32) were intermediate between those of fast-A- and C-cells. Long AHPs (duration much greater than 50 ms) were manifest in 43.8% of A-delta-cells. 4. A time-dependent sag in hyperpolarizing electrotonic potentials (rectification) was found in 68.8% of fast-A-cells, 45.5% of A-delta-cells, and 62.5% of C-cells. 5. To examine neuronal properties 1-6 wk after transection of the sciatic nerve (axotomy), cells were reclassified as SAP (short action potential) cells and LAP (long action potential) cells. Cells in the SAP category had AP durations less than 5 ms and included all fast-A-cells and the majority of A-delta-cells. The LAP category included cells with AP durations greater than 8 ms contained only C-cells. 6. Axotomy failed to decrease the CV of LAP cells or A-delta-cells in the SAP group. The CV of LAP cells may have increased (P less than 0.05), whereas that of SAP cells was unchanged. 7. The duration of the AP and AHP of SAP cells were slightly increased (0.1 greater than P greater than 0.05), whereas AP and AHP duration of LAP cells were unchanged after axotomy. AHP amplitudes of all cell types tended to be smaller (0.1 greater than P greater than 0.05). Axotomy did not alter the resting membrane potential or reduce the incidence of rectification in any cell type. 8. Invasion of the soma by axonally evoked APs was impeded in all cell types after axotomy even though a decrease (P less than 0.05) in rheobase of SAP cells occurred.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗