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PubMed1989

Prepro-VIP and preprotachykinin mRNAs in the rat dorsal root ganglion cells following peripheral axotomy.

Using in situ hybridization histochemistry, we examined the expression of prepro-vasoactive intestinal polypeptide (VIP) mRNAs and preprotachykinin (PPT) mRNAs which coded for substance P (SP) in the rat dorsal root ganglion (DRG) following spinal nerve transection. VIP mRNAs increased dramatically in the DRG neurons after transection of the peripheral branch of the spinal nerve (sciatic nerve), whereas PPT mRNAs showed a gradual decrease for a few weeks. Dorsal rhizotomy or axotomy of the central branch of DRG cells had little influence on VIP-mRNAs and no effect on PPT mRNA expression. These results demonstrated an activation of VIP biosynthesis in the DRG neurons due to axotomy of the peripheral branch, which was opposite to the reaction of PPT mRNA to the same treatment.

Animals↗

PubMedDate not supplied

Retrograde response to axotomy of motoneurons in the thoracic spinal cord of the aging cat.

The retrograde response of HRP-labelled intercostal motoneurons was compared in adult (1-2 years) and aging (10-15 years) cats, 64-68 days following crush of intercostal nerves or following nerve transection with proximal ligation. A comparison of the neuroglial response to these two lesions was also made. In both adult and aging cats, 64-68 days following nerve crush, most labelled motoneurons had a normal appearance. In contrast, 64-68 days following nerve transection and ligation the Nissl bodies of labelled motoneurons lacked the highly ordered ultrastructure characteristic of normal and control motoneurons. No axotomy-induced neuronal loss was found in aging cats. A three-fold increase in numbers of microglial cells was quantified in the ipsilateral ventral horn of aging cats following nerve transection and ligation. This increase was not seen following nerve crush in aging cats, nor following either type of nerve injury in adult cats. Numbers of astroglia and oligodendroglia were unaffected by axotomy in adult and aging animals.

Aging↗

PubMed1991

Ultrastructural changes in the shape of neurons and related structures in frog sympathetic ganglia after axotomy.

Changes in the shape of neuronal perikarya and other ganglionic structures were observed by electron microscopy in the frog sympathetic ganglia at different times after axotomy. Degenerating and hypertrophic profiles appeared to reflect a remodelling process affecting preganglionic fibres. The shape of neuronal perikarya was modified by the formation of infoldings occupied by preganglionic fibres and/or by that of short winding dendrites often bearing a synapse. The origin of these changes is discussed. In frog sympathetic ganglia, the period of recovery after axotomy was marked by specific reactions which affected neuronal shape and preganglionic fibres, and are not known to occur in the ganglia of mammals.

Animals↗

PubMed1988

Axotomy induces MHC class I antigen expression on rat nerve cells.

Immunomorphological staining demonstrates that class I major histocompatibility complex (MHC)-coded antigen expression can be selectively induced on otherwise class I-negative rat nerve cells by peripheral axotomy. Induction of class I as well as class II antigen expression was simultaneously seen on non-neural cells in the immediate vicinity of the injured nerve cells. As nerve regeneration after axotomy includes growth of new nerve cell processes and formation of new nerve cell contacts, the present findings raise the question of a role for MHC-coded molecules in cell-cell interactions during nerve cell growth.

Animals↗

PubMed1991

Increased neuropeptide Y (NPY)-like immunoreactivity in rat sensory neurons following peripheral axotomy.

The effects of peripheral axotomy (sciatic nerve transection) on the presence and distribution of neuropeptide Y (NPY) in rat dorsal root ganglion (DRG) and spinal grey matter were examined using immunocytochemistry. In normal rats and on the sham-operated side of experimental rats, NPY-like immunoreactivity (NPYir) was observed in all laminae of the lumbar spinal cord, with an especially dense concentration of immunostained axons and axonal varicosities in laminae I-II of the dorsal horn. There was no detectable NPYir in L4-L5 DRG cells from normal rats or from the sham-operated side of experimental rats. At 14 days after axotomy, there was a large ipsilateral increase in the density of NPYir axons and varicosities in the lumbar spinal cord on the side of the nerve injury; this was especially apparent in laminae III-V. In the same rats, NPYir was observed in many small, medium, and large neurons in the L4-L5 DRGs on the side of the severed nerve.

Animals↗

PubMed1993

Reactive changes of glial cells after optic nerve axotomy in adult rats.

We have studied the glial response to optic nerve axotomy in vitro. Glial cells were obtained from normal and crush-axotomized optic nerves. In cultures from axotomized nerves, large numbers of astrocytes, oligodendrocyte progenitors and mature oligodendrocytes were found. Significantly fewer astrocytes and oligodendrocyte progenitors were present in cultures from normal nerves, mature oligodendrocytes did not occur. Proliferation and maturation of oligodendrocyte progenitor cells was only observed in cultures from axotomized nerves, suggesting the regulatory influence of blood-derived factors which are not present in normal nerves after in vitro axotomy. These data show that optic nerve injury enhances the ability of astrocytes, oligodendrocytes and their precursors to survive and/or proliferate in vitro.

Animals↗

PubMed1995

Temporal analysis of neuropeptide Y expression in the rat trigeminal ganglion following peripheral axotomy of the inferior alveolar nerve.

Temporal changes in the appearance and the cell-size spectrum of neuropeptide Y (NPY)-like immunoreactive (IR) cells in the rat trigeminal ganglion (TG) following peripheral axotomy of the inferior alveolar nerve (IAN) were studied by retrograde neuronal tracing with True Blue (TB) and immunohistochemistry for NPY. The number of labeled cells following application of TB to the cut-end of the IAN increased rapidly up to 3 days, and was maintained at a constant level thereafter. The size distribution of cross-sectional areas of TB-labeled cells was similar at 3 days and afterwards. NPY-IR cells, which were not detected in the normal TG, appeared on the first day following axotomy, and increased gradually in number reaching a maximum at 14 days. The frequency histogram of the cross-sectional areas of NPY-IR cells was similar at 3 days and afterwards. The present results indicate that the effect of nerve injury on the levels of NPY expression in the sensory neurons began soon after nerve injury, reaching a maximum around 14 days, and that induction of NPY in the sensory neurons occurred in the same cell size-specific manner for a long period.

Age Factors↗

PubMed1994

Multiple signals underlie the axotomy-induced up-regulation of c-JUN in adult sensory neurons.

We examined the axotomy-induced expression of the immediate-early gene (proto-oncogene) c-jun in the Ola mouse mutant (which exhibits a dramatic delay in Wallerian degeneration) using immunocytochemistry to c-JUN (the protein product of the protooncogene c-jun). c-JUN-like protein immunoreactivity was present in a similar proportion (ca. 60%) of L4 dorsal root ganglion (DRG) neuronal cell bodies from normal (C57/6J/BL) and Ola mice at 1 week following a sciatic nerve crush (axotomy). In normal mice, the intensity and extent of staining declined at 3 weeks, correlating with regeneration. In contrast, Ola mice exhibited a marked reduction (by 77%) in the extent of staining at 2 weeks. At 3 weeks (coinciding to the onset of extensive axonal degeneration in this mutant), staining levels were increased to 1 week levels. Taken together, these findings suggest that multiple signals (both independent and dependent on axonal degeneration) regulate c-jun expression in DRG neuronal cell bodies.

Animals↗

PubMed1994

Critical period for degradation of adult rat retinal ganglion cells and their regeneration capability after axotomy.

The optic nerve (ON) in adult rats was transected intraorbitally followed by retrograde labelling of retinal ganglion cells (RGCs) with fluorescence dye (DiI). A two phase reduction of axotomized RGCs was represented in the retina until 15 days after ON transection. The critical period of RGC loss is around 7 days after axotomy. In this period, the capability of neurite regeneration from RGCs in culture was strongly intensified by ON transection. These findings indicate that the 7th day after axotomy is important for both RGC survival and regeneration.

Animals↗

PubMed1995

Acidic fibroblast growth factor prevents post-axotomy neuronal death of the newborn rat facial nerve.

The death of facial motoneurons after axotomy provides a useful tool for studying neurotrophic factors which could prevent motoneuron loss in vivo. The right facial nerve trunk before the postauricular nerve branching of newborn rats was transected at its extracranial exit, and topically treated, at the axotomy site, with either a vehicle solution containing agarose or sucralfate, or acidic fibroblast growth factor (aFGF). Acidic FGF treatment increased the survival of the facial motoneurons from 18% to 70%. These results suggest that aFGF is a neurotrophic factor for motoneurons in vivo and that this growth factor may provide a new basis for the development of treatments to prevent the loss of damaged motoneurons.

Animals↗

PubMed1996

Multiple projections are unlikely to account for the survival of rat medial septal neurons after axotomy.

Previous studies have demonstrated that numerous septohippocampal neurons survive axotomy disconnecting them from target-derived neurotrophins. One reason for survival could be that these neurons have additional projections to other targets supplying them with neurotrophic factor(s). We show that anterograde tracing indeed labeled additional targets of the medial septum (MS) in controls as well as in experimental animals. However, only very few MS neurons could be double-labeled by retrograde tracer injections into the hippocampus and these targets. Thus, for the majority of septohippocampal neurons multiple projections cannot account for their survival following axotomy.

Animals↗

PubMed1984

Cortically induced postsynaptic potentials in hypoglossal motoneurons after axotomy.

Cortically induced postsynaptic potentials were studied in normal and axotomized cat hypoglossal motoneurons. In normal protruder motoneurons innervating tongue protruder muscles, we have demonstrated that stimulation of the orbital gyrus, at the point optimum for inducing lapping movements of the tongue by repetitive stimuli, produced inhibitory postsynaptic potentials or excitatory postsynaptic potentials followed by predominant inhibitory postsynaptic potentials. The cortically induced excitatory postsynaptic potential in normal protruder motoneurons was composed of only the short-latency component. In protruder motoneurons 30, 40, 60 and 80 days after axotomy, we have demonstrated that the number of protruder motoneurons responding with two components of excitatory postsynaptic potentials (the short- and the long-latency component) to cortical stimulation increased in correspondence with the lapse of days after axotomy and that the amplitude of cortically induced inhibitory postsynaptic potentials in axotomized protruder motoneurons was reduced in size as compared with normal protruder motoneurons.

Animals↗

PubMed1993

Expression of immediate early gene proteins following axotomy and inhibition of axonal transport in the rat central nervous system.

The expression of the immediate early gene-encoded proteins c-Jun, Jun B, Jun D, c-Fos, Fos B and Krox-24 in central neurons following transection of, or inhibition of, axonal transport in their axons was investigated in the rat using immunocytochemistry. Transection of the medial forebrain bundle, which produces an essentially complete axotomy of neurons in the ipsilateral mammillary nucleus, substantia nigra pars compacta, ventral tegmental area and parafascicularis, induced the expression of c-Jun, Jun D and, to a lesser extent, Krox-24, in these nuclei. Microinjection of colchicine into the medial forebrain bundle to chemically inhibit axonal transport similarly induced the expression of these proteins in these areas. The expression of the proteins was first evident 24 h after transection, reached a maximum at 48 h and was still present after 10 days. However, after 30 days the proteins were absent from the substantia nigra, ventral tegmentum and parafascicularis, and were still present only in the mammillary nuclei. The other immediate early genes, Jun B, c-Fos and Fos B, were never expressed above the basal levels seen in untreated rats. Transection of the corpus callosum and the hippocampal commissure, which produces only a partial axotomy of neurons in the cerebral cortex and hippocampus, respectively, did not induce the expression of any of the genes in these neurons. Microinjection of colchicine or vinblastine to produce a localized inhibition of axonal transport in the cerebral cortex, hippocampus, thalamus and cerebellum also induced the expression of c-Jun, Jun D and, again to a lesser extent, Krox-24, in neurons surrounding the injection site. In contrast to this selective expression, administration of the neuronal excitant metrazole induced the expression of all six immediate early gene proteins in central nervous system neurons. These results demonstrate that transection of, or inhibition of, transport in the axons of central neurons induces a particular pattern of expression of transcriptionally operating immediate early genes that may be related to the regenerative competency of the neurons.

Animals↗

PubMed1996

Prevention by lamotrigine, MK-801 and N omega-nitro-L-arginine methyl ester of motoneuron cell death after neonatal axotomy.

Motoneuron cell death was analysed in the rat facial motor nucleus after neonatal facial nerve transection. In situ DNA fragmentation labelling showed that axotomized motoneurons die by an apoptotic mechanism. In order to investigate the existence of excitotoxic mechanisms in this type of neuronal death, rats were treated with several agents known to possess neuroprotective action through a variety of mechanisms. The Na+ channel inhibitor lamotrigine and the antagonist for the N-methyl-D-aspartate-type glutamate receptor, dizocilpine maleate (MK-801) were found to be able to rescue motoneurons from cell death induced by axotomy. The nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester was also able to protect motoneurons from death, but to a lesser extent. The distribution of constitutive and inducible isoforms of nitric oxide synthase was investigated by immunocytochemistry in the facial motor nucleus. No changes were detected in constitutive nitric oxide synthase immunoreactivity in the facial motor nucleus after axotomy. However, in the axotomized facial motor nucleus, inducible nitric oxide synthase showed a positive immunolabelling specifically located in activated astrocytes, but not in microglia. Nitric oxide derived from activated astrocytes may have a role in promoting excitotoxic mechanisms in axotomized motoneurons. We conclude that excitotoxic mechanisms involving apoptotic cell death are present when immature motoneurons die as a consequence of target disconnection.

Animals↗

PubMed1984

Regulation of glycine receptor binding in the mouse hypoglossal nucleus in response to axotomy.

Recent studies have shown that muscarinic receptors in brain hypoglossal nuclei exhibit a loss of specific ligand binding in response to axotomy of the hypoglossal nerve. The mouse hypoglossal nucleus contains a high level of receptors for the inhibitory neurotransmitter, glycine; the ligand [3H]strychnine binds to the glycine receptor with high affinity. In the present study [3H]strychnine binding in mouse hypoglossal nuclei was examined at 1 to 150 days after unilateral lesions of the hypoglossal nerve. Brains were sectioned on a cryostat, thaw-mounted onto microscope slides, incubated with [3H]strychnine and processed for light microscopic autoradiography. Receptor density was assessed by counting silver grains in photomicrographs of operated and control nuclei. During the first 25 days after axotomy grain density fell to 50 percent of that of the control nucleus. After this time grain density slowly increased, returning to control levels by 150 days post lesion. These data indicate that glycine receptors on the axotomized cells of the hypoglossal nucleus are lost when connection with the target muscles of the tongue is interrupted, and that the receptors reappear when the hypoglossal nerve regenerates. It is suggested that excitatory and inhibitory neurotransmitter receptor systems may be regulated in a coordinated fashion by the functional state of the motoneuron.

Animals↗

PubMed1995

Axotomy of rat facial nerve induces TGF-beta and latent TGF-beta binding protein.

Transforming growth factor-beta (TGF-beta) has been found to be abundantly and specifically expressed in the nervous system. However, the function of TGF-beta during nerve regeneration is still unknown. We have examined the expression of TGF-beta isoforms and the latent TGF-beta binding protein (LTBP) by immunohistochemistry in the rat facial nuclei after unilateral axotomy. An increased immunoreactivity for all the TGF-beta isoforms and the LTBP was observed in the facial nuclei of the injured side during the regeneration period examined until Day 24. These differences were tested statistically by nominal logistic regression analysis. When the intensity of the immunoreactivity in the injured side was compared to that of the contralateral side, significantly increasing differences were found for TGF-beta 2 (p < 0.003) and LTBP (p < 0.002). Strong immunostaining was detected in the neuronal perikarya and their axons. No clear immunoreactivity was seen in either microglia or astrocytes. The enhanced immunoreactivity was seen in the operated side already at Day 3, remaining at high level with some fluctuations until Day 12 or 24 after axotomy. These findings suggest that TGF-beta might play a functional role in the regeneration of motor neurons.

Amino Acid Sequence↗

PubMed1987

Axotomy increases the conduction velocity of C-cells in bullfrog sympathetic ganglia.

Axotomy produced an increase in the spike width and a decrease in amplitude of the afterhyperpolarization which followed the action potential in C-cells of bullfrog sympathetic ganglia. Although no change in B-cell conduction velocity was noted, C-cell conduction velocity increased significantly and approached that of B-cells. This change may reflect a process of dedifferentiation prior to the initiation of regrowth following axotomy.

Action Potentials↗

PubMed1997

Astrocytes in the aged rat spinal cord fail to increase GFAP mRNA following sciatic nerve axotomy.

Aging in the brain is associated with specific changes in the astrocyte population. The present study establishes that similar changes occur in the aging spinal cord. The levels of glial fibrillary acidic protein (GFAP) mRNA were significantly increased 0.4-fold in aged 8- to 17-month-old rats compared to young 2-month-old rats. The ability of astrocytes in the aging spinal cord to respond to a non-invasive CNS injury was compared to young rats 4 days following sciatic nerve axotomy. The level of GFAP mRNA was significantly increased 0.5-fold in the young rats in response to axotomy. In contrast, the level of GFAP mRNA in aged rats did not increase following injury above that present in non-axotomized rats of the same age.

Aging↗