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 271 records · Page 15Linked to original sources
PubMed2000

Modulation of taurine uptake in the goldfish retina and axonal transport to the tectum. Effect of crushing the optic nerve or axotomy.

Although there are a great number of studies concerning the uptake of taurine in several tissues, the regulation of taurine transport has not been studied in the retina after lesioning the optic nerve. In the present study, isolated retinal cells of the goldfish retina were used either immediatly after cell suspension or in culture. The high-affinity transport system of [3H]taurine in these cells was sodium-, temperature- and energy-dependent, and was inhibited by hypotaurine and beta-alanine, but not by gamma-aminobutyric acid. There was a decrease in the maximal velocity (Vmax) without modifications in the substrate affinity (Km) after optic axotomy. These changes were mantained for up to 15 days after the lesion. The results might be the summation of mechanisms for providing extracellular taurine to be taken up by other retinal cells or eye structures, or regulation by the substrate taurine, which increases after lesioning the optic nerve. The in vivo accumulation of [3H]taurine in the retina after intraocular injection of [3H]taurine was affected by crushing the optic nerve or by axotomy. A progressive retinal decrease in taurine transport was observed after crushing the optic nerve, starting at 7 hours after surgery on the nerve. The uptake of [3H]taurine by the tectum was compensated in the animals that were subjected to crushing of the optic nerve, since the concentration of [3H]taurine was only different from the control value 24 hours after the lesion, indicating an efficient transport by the remaining axons. On the contrary, the low levels of [3H]taurine in the tectum after axotomy might be an index of the non-axonal origin of taurine in the tectum. Axonal transport was illustrated by the differential presence of [3H]taurine in the intact or crushed optic nerve. The uptake of [3H]taurine into retinal cells in culture in the absence or in the presence of taurine might indicate the existence of an adaptive regulation of taurine transport in this tissue, however taurine transport probably differentially occurs in specific populations of retinal cells. The use of a purified preparation of cells might be useful for future studies on the modulation of taurine transport by taurine in the retina and its role during regeneration.

Animals↗
PubMed2004

Cytochrome c release and caspase-3 activation in retinal ganglion cells following different distance of axotomy of the optic nerve in adult hamsters.

This study examined the relationship between the distance of axotomy and the death of injured retinal ganglion cells (RGCs) in adult hamsters and the relationship of cytochrome c and caspase-3 on the death pathway of RGCs. The left optic nerve (ON) of adult hamsters was transected either at 1 or 3 mm away from the optic disc, and retrogradely labeled with Flurogold on the ON stump. After a predetermined period of postoperative time, the surviving RGCs were counted by retina flat-mount, and the activation of cytochrome c and caspase-3 were investigated by immunohistochemistry. Cell loss was found to be much faster (P < 0.01), more cells with cytochrome c were observed (P < 0.05) and the activation of caspase-3 was earlier when ON was transected 1 mm away from the optic disc than when was transected 3 mm away from the optic disc. Distance of axotomy affects the axotomized cell death rate where more RGCs died when the ON transection was applied closer to the eye. The timing of activation of caspase-3 in the RGCs may be linked to the distance of axotomy.

Animals↗
PubMed2006

Bax and Bcl-2 expression and TUNEL labeling in lumbar enlargement of neonatal rats after sciatic axotomy and melatonin treatment.

Peripheral axotomy in neonatal rats induces neuronal death. We studied the anti-apoptotic protein Bcl-2 and cell death promoter Bax in spinal cord of neonatal rats after sciatic transection and treatment with melatonin, a neuroprotective substance. Pups were unilaterally axotomized at P2 and received melatonin (1 mg/kg; sc) or vehicle 1 h prior to lesion, immediately after, at 1 h, 2 h and then once daily. Rats were sacrificed at 3 h, 6 h, 24 h, 72 h and 5 days postaxotomy. Intact animals were used as controls. Lumbar enlargement was processed for Nissl staining, immunohistochemistry and RT-PCR for Bax or Bcl-2 and TUNEL reaction. Motoneurons (MN) of lesioned (L) and normal (N) sides were counted, and MN survival ratio (MSR=L/N) was calculated. Bax and Bcl-2 showed cytoplasmic immunoreactivity (IR). Bax IR was noticeable in small cells but less evident in MN. In unlesioned pups, some Bax-positive small cells (B+) and TUNEL-positive nuclei (T+) were mainly seen in the dorsal horn. In lesioned animals given vehicle, Bax mRNA levels and numbers of B+ and T+ were increased in comparison with intact controls at 24 h postaxotomy. The basal IR for Bax in MN was not changed by axotomy. Bcl-2 IR was noted in all cells and, like Bcl-2 mRNA, was unaltered after lesion. Melatonin reduced MN loss at 24 h, 72 h and 5 days and T+ at 24 h after lesion but did not interfere with Bax or Bcl-2 expression. These results suggest that (1) sciatic transection at P2 increases Bax mRNA and the amount of B+ and T+ in the lumbar enlargement, (2) Bax IR in immature MN is not altered by axotomy and (3) melatonin protects MN and dorsal horn cells through a mechanism independent of Bax and Bcl-2.

Analysis of Variance↗
PubMed2005

Partial resistance of ataxin-2-containing olivary and pontine neurons to axotomy-induced degeneration.

Spinocerebellar ataxia type 2 (SCA2) is caused by the expansion of a polyglutamine tract in ataxin-2, the SCA2 gene product. In spite of the identification of the genetic defect and the coded protein, the function of wild-type ataxin-2 has not been clarified. In order to identify the possible resistance of ataxin-2-containing neurons to degeneration, we investigated in this study the distribution and the characteristics of cell reaction to axotomy in ataxin-2-positive olivary and pontine neurons in a model of cerebellar damage represented by hemicerebellectomy. We also performed double immunofluorescence studies of ataxin-2 and purinergic receptors to characterize ataxin-2-positive surviving neurons. The present data demonstrated that after axotomy olivary and pontine ataxin-2-expressing neurons survived longer than the ataxin-2-negative cell population. Cell counting performed in the different olivary subdivisions failed to reveal any topographical prevalence in the distribution of ataxin-2-positive neurons. Therefore, the relative resistance to axotomy appears to be an intrinsic property of the ataxin-2 cell population. In addition, the capacity to modify the pattern of purinergic receptor expression in response to damage was present in only one subset of ataxin-2-positive surviving neurons. These data suggest that ataxin-2 is involved in resistance to degeneration phenomena which may be lost after mutation.

Animals↗
PubMed2005

Cell death and axon regeneration of Purkinje cells after axotomy: challenges of classical hypotheses of axon regeneration.

Although adult mammalian neurons are able to regenerate their axons in the peripheral nervous system under certain conditions, they are not able to do it in the central nervous system. The environment surrounding the severed axons appears to be a key factor for axon regeneration. Many studies aiming to enhance axon regeneration in the CNS of adult mammals have successfully manipulated this environment by adding growth permissive molecules and/or neutralizing growth inhibitory molecules. In both cases, the number of axons able to regenerate was low and the different neuronal populations were not equal in their regenerative response, suggesting that manipulation of the environment is not always sufficient. This is particularly well illustrated in the cerebellar system, in which axotomized inferior olivary neurons regenerate when confronted with a permissive environment, whereas mature Purkinje cells do not. The intrinsic ability of a neuron to regenerate its axon is generally correlated with the intensity of its reaction to axotomy (expression of molecules, probability to die). Furthermore, molecules such as GAP-43 (growth-associated molecule) and c-Jun are involved in both axon regeneration and cell death suggesting that these two processes are linked. Surprisingly, Purkinje cells lose their capacity to regenerate their axon (even in the absence of myelin) during development before losing their capacity to react to an axotomy by cell death. These results emphasize the different reactions to axotomy between neuron types and underline that in Purkinje cells, the two cell decisions (axon regeneration and cell death) are differently regulated and therefore not part of the same signaling pathway.

Animals↗
PubMed2004

Rubrospinal neurons fail to respond to brain-derived neurotrophic factor applied to the spinal cord injury site 2 months after cervical axotomy.

Numerous experimental therapies to promote axonal regeneration have shown promise in animal models of acute spinal cord injury, but their effectiveness is often found to diminish with a delay in administration. We evaluated whether brain-derived neurotrophic factor (BDNF) application to the spinal cord injury site 2 months after cervical axotomy could promote a regenerative response in chronically axotomized rubrospinal neurons. BDNF was applied to the spinal cord in three different concentrations 2 months after cervical axotomy of the rubrospinal tract. The red nucleus was examined for reversal of neuronal atrophy, GAP43 and Talpha1 tubulin mRNA expression, and trkB receptor immunoreactivity. A peripheral nerve transplant paradigm was used to measure axonal regeneration into peripheral nerve transplants. Rubrospinal axons were anterogradely traced and trkB receptor immunohistochemistry performed on the injured spinal cord. We found that BDNF treatment did not reverse rubrospinal neuronal atrophy, nor promote GAP-43 and Talpha1 tubulin mRNA expression, nor promote axonal regeneration into peripheral nerve transplants. TrkB receptor immunohistochemistry demonstrated immunoreactivity on the neuronal cell bodies, but not on anterogradely labeled rubrospinal axons at the injury site. These findings suggest that the poor response of rubrospinal neurons to BDNF applied to the spinal cord injury site 2 months after cervical axotomy is not related to the dose of BDNF administered, but rather to the loss of trkB receptors on the injured axons over time. Such obstacles to axonal regeneration will be important to identify in the development of therapeutic strategies for chronically injured individuals.

Animals↗
PubMed2006

CD4+CD25+ regulatory T cells and CD1-restricted NKT cells do not mediate facial motoneuron survival after axotomy.

CD4+ T cells rescue facial motoneurons (FMN) from axotomy-induced cell death. The objective of this study is to determine if the CD4+ T regulatory subsets, CD4+CD25+ T or CD1d-restricted NKT cells are critical for FMN survival after facial nerve axotomy. Surviving FMN within facial motor nuclei from axotomized and control sides 4 weeks after axotomy were counted to determine percent FMN survival. Data generated by applying this paradigm to recombination activating gene-2-deficient mice reconstituted with CD4+ T cells depleted of CD4+CD25+ T cells and to CD1-/- mice, deficient in CD1d-restricted NKT cells, suggest that neither regulatory CD4+ T subset is critical for FMN survival.

Animals↗
PubMed2004

Distribution of the galectin-1 mRNA in the rat nervous system: its transient upregulation in rat facial motor neurons after facial nerve axotomy.

Galectin-1 is a member of the animal lectin family that displays conserved consensus sequences and similar carbohydrate binding specificities. Recent analyses revealed that galectin-1 plays an important role in the process of nerve regeneration. We analyzed the topological expression of galectin-1 mRNA in adult rat nervous system. Galectin-1 mRNA was predominantly observed in the cell bodies of neurons such as oculomotor nucleus (III), trochlear nucleus (IV), trigeminal motor nucleus (V), abducens nucleus (VI), facial nucleus (VII), hypoglossal nucleus (XII), red nucleus, and locus ceruleus. Neurons in pineal gland and dorsal root ganglia expressed galectin-1 mRNA. We next tested whether the axotomy of facial nerve altered the expression of galectin-1 mRNA in motor neurons. In the adult rats, the axotomy of facial nerve induced transient upregulation of galectin-1 mRNA around 6 h after axotomy. These results indicate that galectin-1 may play roles in the early event of the nerve injury and regeneration through the transient change of its expression level.

Animals↗
PubMed2006

Immunohistochemical analysis of acid-sensing ion channel 2 expression in rat dorsal root ganglion and effects of axotomy.

Several studies have suggested that acid-sensing ion channel 2 (ASIC2) plays a role in mechanoperception and acid sensing in the peripheral nervous system. We examined the expression and distribution of ASIC2 in the rat dorsal root ganglion, the co-localization of ASIC2 with tropomyosin-related kinase (trk) receptors, and the effects of axotomy on ASIC2 expression. ASIC2 immunoreactivity was observed in both neurons and satellite cells. ASIC2-positive neurons accounted for 16.5 +/- 2.4% of the total neurons in normal dorsal root ganglion. Most ASIC2-positive neurons were medium-to-large neurons and were labeled with neurofilament 200 kD (NF200). Within these neurons, ASIC2 was not evenly distributed throughout the cytoplasm, but rather was accumulated prominently in the cytoplasm adjacent to the axon hillock and axonal process. We next examined the co-localization of ASIC2 with trk receptors. trkA was expressed in few ASIC2-positive neurons, and trkB and trkC were observed in 85.2% and 53.4% of ASIC2-positive neurons, respectively, while only 6.9% of ASIC2-positive neurons were co-localized with trkC alone. Peripheral axotomy markedly reduced ASIC2 expression in the axotomized dorsal root ganglion neurons. On the other hand, intense ASIC2 staining was observed in satellite cells. These results show that ASIC2 is expressed in the distinct neurochemical population of sensory neurons as well as satellite cells, and that peripheral axotomy induced marked reductions in ASIC2 in neurons.

Acid Sensing Ion Channels↗
PubMed2005

Effects of amitriptyline and gabapentin on bilateral hyperalgesia observed in an animal model of unilateral axotomy.

Nociceptive responses in an animal model of peripheral nerve injury were studied. The left common sciatic nerve was exposed, tightly ligated at two locations and transected between the ligatures. A bilateral decrease in the nociceptive threshold to mechanical stimulation was observed within 3 h after the operation. The skin of the lateral dorsal part of the injured paw was hypoalgesic, while the medial dorsal paw innervated by the intact saphenous nerve and the contralateral dorsal paw exhibited hyperalgesia. Amitriptyline, an antidepressant, at 25, 50 and 100 mg/kg per day, p.o., and gabapentin, an anticonvulsant, at 30, 100 and 300 mg/kg per day, p.o., significantly inhibited the decrease in the mechanical nociceptive threshold in the injured and uninjured paws. The effects of amitriptyline at 25 and 50 mg/kg were evident at doses that did not cause neurologic deficits as assessed by the inclined screen test. Indomethacin, a cyclooxygenase inhibitor, and morphine (except at the highest dose of 30 mg/kg, s.c.) showed no analgesic effects in this model. The tail-flick latency was also significantly decreased compared with intact rats. Similar bilateral hyperalgesia was observed when axotomy was performed using silk thread instead of chromic gut. When this axotomy model was applied to mice, the nociceptive thresholds in both paws immediately showed a significant decrease in the same manner as in rats. The bilateral and systemic hyperalgesia observed in this axotomy model, which resembles the clinical features of chronic neuropathic pain, suggests the involvement of the central nervous system in the maintenance of the chronic pain state.

Amines↗
PubMed2003

Neurotrophin-3 and TrkC in the frog visual system: changes after axotomy.

Neurotrophins are potent regulators of the survival of different neuronal populations in the CNS. Little is known of the immunodistribution of neurotrophin-3 (NT-3) and tyrosine kinase C (TrkC) receptor in the frog visual system, which can successfully regenerate and recover vision after injury. In this study we show that both NT-3 and TrkC are present in the frog retina and tectum, and that their distribution changes after optic nerve transection. Both NT-3 and TrkC are present in the ganglion cell layer, inner nuclear layer, nerve fiber layer and outer plexiform layer, and in Müller cells of control retinas. Quantification of identified RGCs shows that there are only small changes in the proportion, or intensity, of NT-3 immunostained cells surviving after axotomy and regeneration. Müller cell staining, however, is increased. TrkC staining in the retina does not change after axotomy. In the tectum, NT-3 immunoreactivity is present in the retinorecipient layer 9, and in radial processes of neurons and ependymoglia. TrkC is present in ependymoglia and in tectal neurons. After axotomy or colchicine treatment fewer NT-3-immunoreactive processes are present in layer 9 and there is decreased staining of tectal neurons. These data are consistent with the hypothesis that NT-3 is synthesized in the retina and anterogradely transported to the tectum. TrkC immunostaining, on the other hand, increases in tectal cells after optic nerve transection, suggesting that it may be regulated by the supply of NT-3 from the retina.

Animals↗
PubMed1997

The effects of axotomy and preganglionic denervation on the expression of pituitary adenylate cyclase activating peptide (PACAP), galanin and PACAP type 1 receptors in the rat superior cervical ganglion.

The effects of axotomy, chemical sympathectomy and preganglionic denervation on the expression of the neuropeptides, pituitary adenylate cyclase-activating peptide (PACAP), galanin (GAL), and the PACAP type 1 receptor in the rat superior cervical ganglion (SCG) were investigated by immunocytochemistry, in situ hybridization and receptor autoradiography. An antibody recognizing the rat vesicular acetylcholine transporter (VAChT) was used for the detection of preganglionic cholinergic fibers. In the normal SCG, PACAP-immunoreactivity (-IR) was present in numerous, basket-forming, preganglionic nerve fibers, while very few SCG neurons expressed PACAP. GAL-IR was restricted to occasional neurons, and a few nerve fibers, most of which were, in addition, PACAP-IR. PACAP type 1 receptors were expressed in all nerve cell bodies. Axotomy resulted in a rapid and prominent upregulation of PACAP in a large number of nerve cell bodies. There was a large increase also in GAL expression in many nerve cell bodies. In contrast, there was a marked decline in PACAP type 1 receptor expression. Chemical sympathectomy by administration of the catcholaminergic neurotoxin, 6-hydroxydopamine (6-OHDA), gave rise to similar changes. Preganglionic denervation led to the disappearance of PACAP- and VAChT-IR baskets and to the upregulation of PACAP and GAL expression in neurons located close to the entrance of the sympathetic chain, whereas PACAP type 1 receptor expression was not affected. PACAP and GAL were coexpressed in most neurons after axotomy and chemical sympathectomy. Taken together, these results indicate that disruption of target contact and/or the infliction of an injury to the axons of the sympathetic neurons, rather than the preganglionic output, regulates the expression of PACAP, GAL and the PACAP type 1 receptor.

Animals↗
PubMed1998

Differential expression of calbindin and calmodulin in motoneurons after hypoglossal axotomy.

Axotomy induces a profound modification of Ca2+ homeostasis in injured neurons which may lead to neuronal death. Remarkably, after axotomy and resection of the hypoglossal nerve, 65-75% of the hypoglossal motoneurons survive in the long term and this suggests some adaptive mechanisms compensating the massive calcium influx. As potential components of this adaptation, we have examined calmodulin and calbindin-D28k by in situ hybridisation and immunohistochemistry in motoneurons of the rat after hypoglossal nerve transection. Neuronal calbindin mRNA and protein content was low in normal state, transiently increased to 200% of the basal expression at 8 days post-operation (dpo), then declined to normal again until 28 dpo. Calmodulin mRNA was highly expressed in normal hypoglossal motoneurons and remained constant after axotomy. Calmodulin protein immunoreactivity, however, was transiently decreased in axotomised motoneurons suggesting post-transcriptional modification. The upregulation of calbindin expression may facilitate the survival of injured motoneurons.

Animals↗
PubMed1998

Galanin induced in sympathetic neurons after axotomy is anterogradely transported toward regenerating nerve endings.

Peripheral neurons begin to express galanin after axotomy. When neurons in the superior cervical ganglion were axotomized near (about 2 mm) from the ganglion, galanin-like immunoreactivity (IR) was maximal within 72 h. Axotomy of neurons in the middle and inferior cervical ganglion complex (MICG), which could be performed 2 cm from the ganglia, led to an additional galanin increase 7 and 14 days later. This second increase was not accompanied by changes in galanin mRNA or the number of galanin-immunostained neurons. Galanin-IR was detectable in a postganglionic trunk of the MICG 2 days after axotomy. At this time, immunoreactive fibers were only seen near the lesion site, while later they were found throughout the trunk. The data suggest that galanin is actively transported toward the site of nerve crush/transection and that the second increase in galanin-IR found in the MICG may be due to a saturation of the axonal transport system.

Animals↗
PubMed1998

Effect of peripheral axotomy on dorsal root ganglion neuron phenotype and autonomy behaviour in neuropeptide Y-deficient mice.

The lumbar 5 (L5) dorsal root ganglia (DRGs) were studied in neuropeptide tyrosine (NPY)-deficient (-/-) and wild type (+/+) mice after unilateral sciatic nerve transection using in situ hybridization and immunohistochemistry. NPY, galanin and two NPY receptors (Y-Rs) were analyzed as well as self-mutilation behaviour (autotomy) and nociceptive thresholds. No difference between wild type and NPY-deficient mice was seen in the tail-flick or hot plate test. However, -/- mice showed a much stronger autotomy behaviour than wild type mice. NPY was not found in L5 DRGs in -/- mice, not even after axotomy. Galanin was upregulated to the same extent after axotomy in NPY-deficient and wild type mice. Y1- and Y2-R mRNAs were found mainly in small DRG neuron profiles. Both receptor mRNAs were downregulated after axotomy, to about the same extent in NPY-deficient as in wild type mice. In control and contralateral ganglia the mRNA levels of both receptors were lower in NPY-deficient mice than in wild type mice. The contralateral Y2-R mRNA levels did not reach control values in the NPY-deficient mice, as they did in the wild type mice. In both strains the Y1-R protein was decorating the somatic plasmalemma. The present results suggest that lack of NPY may cause exaggerated autotomy, a self-mutilation behaviour possibly related to pain sensation, in agreement with the described analgesic effect of NPY. Although significant differences in levels of Y1- and especially Y2-R mRNAs were observed between wild type and NPY-deficient mice, they were only moderate. These findings suggest that expression, regulation, localization and possible function of Y1- and Y2-Rs are not dependent on presence of the endogenous ligand. Also, deletion of NPY does not seem to influence the expression of the partly coexisting peptide galanin.

Animals↗
PubMed2000

Glutamate transporter GLT-1 is highly expressed in activated microglia following facial nerve axotomy.

Glutamate transporters play an important role in the re-uptake of glutamate after its release from glutamatergic synapses. So far five of such transporters subtypes have been cloned from rodent and human brains. The densities of glutamate transporters are recognised to be developmentally regulated, but the role of glutamate transporters in the mechanisms underlying the occurrence of neuronal traumatic injury has not been widely studied. In the present study quantitative Western blotting and immunohistochemical technique were employed to study the expression of GLT-1/EAAT2 in the facial nuclei of adult rats following unilateral facial nerve axotomy. The total content of GLT-1 protein decreased in the ipsilateral axotomised rat facial nucleus. However, activated microglia surrounding motoneurons showed high expression of GLT-1 after facial nerve axotomy. Parallel studies revealed that primary cultured microglial cells also showed GLT-1-immunoreactivity. To our knowledge, this is the first direct demonstration of the expression of GLT-1 protein in activated microglial cells, suggesting a neuroprotective role of microglia against glutamate excitotoxicity following nerve axotomy.

ATP-Binding Cassette Transporters↗
PubMed2002

Axotomy does not up-regulate expression of sodium channel Na(v)1.8 in Purkinje cells.

Aberrant expression of the sensory neuron specific (SNS) sodium channel Na(v)1.8 has been demonstrated in cerebellar Purkinje cells in experimental models of multiple sclerosis (MS) and in human MS. The aberrant expression of Na(v)1.8, which is normally present in primary sensory neurons but not in the CNS, may perturb cerebellar function, but the mechanisms that trigger it are not understood. Because axotomy can provoke changes in Na(v)1.8 expression in dorsal root ganglion (DRG) neurons, we tested the hypothesis that axotomy can provoke an up-regulation of Na(v)1.8 expression in Purkinje cells, using a surgical model that transects axons of Purkinje cells in lobules IIIb-VII in the rat. In situ hybridization and immunocytochemistry did not reveal an up-regulation of Na(v)1.8 mRNA or protein in axotomized Purkinje cells. Hybridization and immunostaining signals for the sodium channel Na(v)1.6 were clearly present, demonstrating that sodium channel transcripts and protein were present in experimental cerebella. These results demonstrate that axotomy does not trigger the expression of Na(v)1.8 in Purkinje cells.

Animals↗
PubMed1999

Expressed-sequence-tag approach to identify differentially expressed genes following peripheral nerve axotomy.

Gene expression profiles in the rat hypoglossal nucleus after axotomy were demonstrated using expressed-sequence-tag (EST) approach. To demonstrate the gene-expression profiles after axotomy, nerve-transected hypoglossal nuclei were dissected and collected from about 1000 rats, with which a cDNA library was constructed. More than 750 clones were sub-cloned and sequenced from the library. The clones which hit frequently are likely to be associated with mitochondrial respiratory chain, cytoskeletal protein and protein synthesis. One hundred three clones from among the sequenced clones were further processed for histological screening using unilateral-hypoglossal nerve-transected brain sections by in situ hybridization histochemistry. In situ hybridization study revealed that 26% of clones examined showed upregulated expression of mRNA in response to axotomy. They included genes encoding proteins associated with glucose, lipid and protein metabolism, cytoskeleton, neurotransmission and immune reaction. The present EST analysis may have an advantage in targeting genes which are associated with nerve injury with a good efficacy, as compared with other methods such as differential display and subtraction.

Animals↗