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PubMed1994

Decreased immunoreactivity of platelet-derived growth factor B chain-like peptide after axotomy in the dorsal motor nucleus of the vagus nerve.

Platelet-derived growth factor-B chain (PDGF-B) and B chain-specific beta receptor (PDGF-R) were investigated immunohistochemically in the dorsal motor nucleus of the vagus nerve and hypoglossal nucleus after axotomy using antibodies raised against synthetic polypeptides. PDGF-B and PDGF-R immunoreactivity were observed in nerve cell bodies contralateral to the axotomized nerve in both vagal (degenerative) and hypoglossal (regenerative) nuclei. The immunoreactivity for PDGF-B antibody persisted until day 28 after axotomy in the hypoglossal neurons, while that in many neurons in the vagal nucleus diminished after day 3. In the severed vagal nucleus some of the axotomized neurons showed no immunoreactivity for PDGF-B chain, and these changes preceded the decrease in neuronal numbers in the vagal nucleus. The immunoreactivity for PDGF-R antibody showed no marked change in either the vagal or hypoglossal nucleus until day 28 after axotomy. These findings suggest that the decrease in PDGF-B immunoreactivity is not due to a non-specific depletion of cytoplasmic protein in the severed vagal neurons. PDGF, taken up by the nucleus and bound to chromatin, has been reported to exert direct effects on the enhancement of transcription and synthesis of RNA. The decrease in level of PDGF-B chain in the vagal neurons seems to cause the reduction of RNA and protein synthesis, resulting in neuronal degeneration.

Animals↗
PubMed1994

Effects of peripheral axotomy of the inferior alveolar nerve on the levels of neuropeptide Y in rat trigeminal primary afferent neurons.

The effects of peripheral axotomy of the inferior alveolar nerve (IAN) on the presence and distribution of neuropeptide Y (NPY)-like immunoreactivity (IR) in the trigeminal sensory nuclear complex (TSNC) and trigeminal ganglion were investigated in the rat by immunohistochemistry. In the normal trigeminal ganglion, there were no NPY-IR cells, and some perivascular nerve fibres exhibited NPY-IR. In normal TSNC, many NPY-IR axons and nerve terminals were observed in the superficial layers of the subnucleus caudalis (SpVc) and paratrigeminal nucleus (paraV), but were sparse in the other subnuclei of the TSNC. Fourteen days following peripheral axotomy of the IAN, many large- and medium-sized cells in the trigeminal ganglion displayed NPY-IR, and marked increases in the numbers and staining densities of NPY-IR were observed in deeper laminae (laminae III-V) of the dorso-medial region of the SpVc and other nuclei, in addition to the dorso-medial region of the spinal trigeminal tract. Degrees of alterations of the levels of NPY were most marked in the SpVc. The present results indicate that peripheral axotomy of the IAN evokes the appearance of NPY-IR in the trigeminal ganglion and alterations of NPY-IR in the entire IAN projection areas of the TSNC.

Animals↗
PubMed1995

Axotomy transiently down-regulates androgen receptors in motoneurons of the spinal nucleus of the bulbocavernosus.

Testosterone is an important trophic factor for motoneurons in the spinal nucleus of the bulbocavernosus (SNB), and SNB motoneurons are more responsive to testosterone than are other motoneurons. Axonal injury during early postnatal life prevents the normal development of steroid-sensitivity by adult SNB motoneurons. Axonal injury also causes changes in the expression by motoneurons of a wide range of proteins, including the up-regulation of trophic factor receptors. We have used a polyclonal antibody (PG-21; G.S. Prins) to study the expression of androgen receptors in SNB motoneurons after axonal injury. PG-21 labeled motoneuronal nuclei in the lower lumbar spinal cord of rats in a pattern that matched autoradiographic reports of androgen accumulation in this region of the nervous system. A population of numerous, small cells located dorsal to the central canal also showed evidence of androgen receptor expression. Cutting the axons of SNB motoneurons in adulthood or in development caused a decrease in androgen receptor immunoreactivity in SNB motoneurons. This is the first report that a trophic factor receptor in motoneurons is down-regulated after axonal injury, and is interesting in light of reports that testosterone treatment can facilitate motoneuronal regeneration after nerve cut. Androgen receptor levels subsequently returned to normal, regardless of the age at axotomy, providing no evidence for a lasting effect of developmental axotomy on androgen receptor levels in SNB motoneurons. Thus, axotomy-induced down-regulation of androgen receptors does not underlie the inability of SNB motoneurons to respond to androgen treatment several months after pudendal nerve cut in development.

Aging↗
PubMed1996

Perineuronal microglial reactivity following proximal and distal axotomy of rat rubrospinal neurons.

Microglial reactivity in the red nucleus of rats was studied following upper cervical and lower thoracic rubrospinal tractotomy using the lectin binding method. Following axotomy, the contralateral nucleus containing the axotomized neurons was identified using the retrograde tracer Fast blue. It was subdivided into dorsomedial (DM) and ventrolateral (VL) portions known to project to the cervical and lumbar spinal cord, respectively. Lectin-labeled microglial cells and processes on the contralateral as well as in the ipsilateral nucleus were then quantified. An early and a late increase in microglial reactivity was observed in the nucleus at 2-5 days and 2-8 weeks following thoracic and cervical tractotomy with the latter producing a more pronounced reactivity. In rats subjected to thoracic axotomy, a similar microglial increase also occurred in the intact contralateral DM nuclear area suggesting the possible action of diffusable factor(s) that might have triggered the microglial activation from the axotomized VL nuclear area. The uninjured ipsilateral nucleus also exhibited a similar pattern of microglial reactivity irrespective of the number of ipsilaterally projecting neurons following both cervical and thoracic axotomy. This could have been elicited by the retrograde influence from the denervated targets carried by the intact rubrospinal fibers of the opposite side since many of them in fact terminate bilaterally (Antal, M. et al., J. Comp. Neurol., 325 (1992) 22-37). In all the axotomized or intact nucleus, microglial processes did not appear to surround neuronal cell bodies. The characteristic responses of microglial cells in the red nucleus may be related to the failure of rubrospinal neurons to regenerate following the severance of their axons.

Amidines↗
PubMed1983

Role of electrical activity in axotomy-induced increased glucose use.

Glucose use as demonstrated by 2-deoxyglucose autoradiography increases in the hypoglossal nucleus after axotomy of the hypoglossal nerve. There are several possible explanations for this increase, including increased energy metabolism to support increased protein, RNA, and lipid synthesis during regeneration or, alternatively, increased electrical activity associated with the site of nerve transection or alterations in the neurolemma. To evaluate the possible role of electrical activity, we recorded spike activity in the hypoglossal nucleus after axotomy and evaluated glucose uptake in the hypoglossal nucleus after xylocaine application to the proximal nerve stump. There was no evidence from these experiments that an increased number of action potentials is responsible for the increased glucose use after axotomy.

Action Potentials↗
PubMed1989

Testosterone-induced acceleration of recovery from facial paralysis following crush axotomy of the facial nerve in male hamsters.

In this study, the effects of testosterone propionate (TP) on recovery from facial paralysis following crush axotomy of the facial nerve in male hamsters were examined. In the first experiment, TP (5 mg/ml sesame oil; 0.1 ml) was injected subcutaneously and on alternate days in one-half of the animals subjected to crush axotomies of the facial nerve, with the second half receiving vehicle alone. An accelerative effect of TP on recovery from facial paralysis was observed near the end of the first and beginning of the second week after crush axotomy. When the dosage and frequency were doubled in the next experiment, a greater accelerative effect of TP on recovery from facial paralysis was observed. In the last experiment, castrated animals were used in order to eliminate the endogenous source of the hormone and two different modes of hormone administration, TP implants vs TP injections, were compared. The results of that experiment indicate that continuous exposure to the hormone, in the form of subcutaneous implants of 100% crystalline TP, had the most pronounced effect on acceleration of recovery from facial paralysis. In addition, no differences in the responses of the castrated, axotomized animals and the normal, axotomized animals were found. This suggests that the presence of endogenous hormone contributes little to the acceleration of functional recovery observed with TP. Finally, the time course of the accelerative effect of TP suggests that the hormone is acting primarily at the level of the facial neuron, which contains androgen receptors, and perhaps secondarily at the level of the facial muscles, which are also known to contain androgen receptors.

Animals↗
PubMed1986

Non-response of rough endoplasmic reticulum containing intracisternal microtubules to axotomy in the dog.

Responses of the RER containing intracisternal microtubules in the canine ganglion nodosum to axotomy were observed at 3, 7, 14, 30, 50 and 99 days after section of the vago-sympathetic trunk. At 3 days, neurons showed no changes. From 7 days to 50 days, a retrograde reaction occurred in the cell bodies; nuclei were irregular in outline and eccentric in position and flattened RER disintegrated and dispersed. On the other hand, dilated RER containing intracisternal microtubules, which was detected as cytoplasmic inclusions under the light microscope, was present at the opposite pole to the eccentric nucleus. The ratio of areas of cytoplasmic inclusion to cell body significantly decreased. However, there were no changes in the size and arrangement of intracisternal microtubules within the RER. At 99 days, axotomized cell bodies had recovered and the RER containing intracisternal microtubules was indistinguishable from the contralateral controls. These findings indicate that the RER containing intracisternal microtubules is not disrupted by axotomy, though it is compactly packed at the periphery of cell bodies during the retrograde reaction. It appears, therefore, that the RER containing intracisternal microtubules does not respond to axotomy.

Aging↗
PubMed1996

Neuroprotective effect of various cytokines on developing spinal motoneurons following axotomy.

Ciliary neurotrophic factor (CNTF), a multipoietic factor, on a variety of neurons, prevents axotomy-induced motoneuron loss and can improve the outcome of murine motor neuron disease (MND). We carried out a study to determine whether other cytokines rescue spinal motoneurons from axotomy-induced cell death. Unilateral sciatic nerve was transected in neonatal rats. Two doses of recombinant murine cholinergic differentiation factor/leukemia inhibitory factor (CDF/LIF), recombinant rat CNTF, recombinant human granulocyte-colony stimulating factor (G-CSF), recombinant human interleukin-6 (IL-6), recombinant human tumor necrosis factor beta (TNF beta), or vehicle were administered daily for 2 weeks by intraperitoneal injection. After treatment, the number of spinal motoneurons was determined at the level of L4-5 segments. In comparison with vehicle, the higher doses of CDF/LIF, CNTF, and IL-6, and the lower doses of CDF/LIF and IL-6 significantly retarded the loss of motoneurons. G-CSF and TNF beta failed to inhibit motoneuron death. CDF/LIF and IL-6 rescued motoneurons from the retrograde death following axotomy, in a similar manner to CNTF. These results provide evidence that several cytokines may have therapeutic potential in human axonopathy or MND.

Animals↗
PubMed1995

Peripheral axotomy increases the expression of galanin message-associated peptide (GMAP) in dorsal root ganglion cells and alters the effects of intrathecal GMAP on the flexor reflex in the rat.

We have previously reported that galanin message-associated peptide (GMAP), a fragment of galanin precursor protein, occurs in a limited number of dorsal root ganglion (DRG) cells in rats with intact sciatic nerves. In the present study, the localization of GMAP in dorsal root ganglia, dorsal roots and dorsal horn was analyzed immunohistochemically and compared between rats with intact and sectioned sciatic nerves. Furthermore, the effects of intrathecal (i.t.) GMAP on the flexor reflex in rats with intact and sectioned nerves were examined. In rats with intact sciatic nerves, i.t. GMAP elicited a moderate facilitation of the flexor reflex. The facilitation of the flexor reflex induced by conditioning stimulation (CS) of cutaneous C-fibers was strongly blocked by GMAP. GMAP also selectively antagonized the reflex facilitatory effect of i.t. substance P (SP), but not i.t. vasoactive intestinal peptide (VIP). Unilateral sciatic nerve section induced an upregulation of GMAP in the ipsilateral dorsal root ganglia 2 weeks after axotomy. The effect of GMAP on the baseline reflex was similar in normal and axotomized rats, but the blocking effect of GMAP on C-fiber CS-induced facilitation was significantly reduced after axotomy. GMAP did not antagonize the reflex facilitatory effect of SP after axotomy, whereas an antagonism on VIP-induced facilitation was observed. The possible role of GMAP in spinal transmission and comparison with the effects of galanin are discussed.

Animals↗
PubMed1986

Peripheral axotomy of the rat mandibular trigeminal nerve leads to an increase in VIP and decrease of other primary afferent neuropeptides in the spinal trigeminal nucleus.

In the vasoactive intestinal polypeptide (VIP)-rich lumbosacral spinal cord, VIP increases at the expense of other neuropeptides after primary sensory nerve axotomy. This study was undertaken to ascertain whether similar changes occur in peripherally axotomised cranial sensory nerves. VIP immunoreactivity increased in the terminal region of the mandibular nerve in the trigeminal nucleus caudalis following unilateral section of the sensory root of the mandibular trigeminal nerve at the foramen orale. Other primary afferent neuropeptides (substance P, cholecystokinin and somatostatin) were depleted and fluoride-resistant acid phosphatase activity was abolished in the same circumscribed areas of the nucleus caudalis. The rise in VIP and depletion of other markers began 4 days postoperatively and was maximal by 10 days, these levels remaining unchanged up to 1 year postoperatively. VIP-immunoreactive cell bodies were absent from trigeminal ganglia from the unoperated side but small and medium cells stained intensely in the ganglia of the operated side after axotomy. These observations indicate that increase of VIP in sensory nerve terminals is a general phenomenon occurring in both cranial and spinal sensory terminal areas. The intense VIP immunoreactivity in axotomised trigeminal ganglia suggests that the increased levels of VIP in the nucleus caudalis are of peripheral origin, indicating a change in expression of neuropeptides within primary afferent neurons following peripheral axotomy.

Acid Phosphatase↗
PubMed1995

Axotomy-induced regulation of c-Jun expression in regenerating rat retinal ganglion cells.

Antibodies to c-Jun, JunD, JunB, c-Fos, FosB and Krox-24 proteins were used to examine the expression of these transcription factors in identified adult rat retinal ganglion cells with regenerating axons in a peripheral nerve graft. First, expression in ganglion cells 1 month after graft placement was compared to expression in these neurons 5 to 6 months after grafting. Whereas strong c-Jun expression was seen in most ganglion cells one month after grafting, most 5- to 6-month ganglion cells showed only basal expression. The maintained nucleolar expression of FosB in both ganglion cell groups was the only other transcription factor seen. Second, transcription factor expression was examined in these short- and long-term regenerating neurons after a second axotomy caused by graft transection and compared to the effects of a single axotomy on expression in non-regenerating ganglion cells. Only c-Jun was re-expressed in the regenerating ganglion cells after re-axotomy.

Animals↗
PubMed1986

Axotomy affects calcium-sensitive potassium conductance in sympathetic neurones.

Following peripheral nerve section, the cell body and proximal axon undergo various physiological and morphological changes which may be associated with regrowth. We found that axotomy reduced the amplitude and duration of the afterhyperpolarization (AHP) of the action potential (AP) of bullfrog sympathetic neurones. In addition, the repolarization of the AP was slowed. The Ca2+-channel blocker, Cd2+ (200 microM) produced similar effects in normal cells by blocking the Ca2+-sensitive K+ conductances (gK, Ca) which contribute to the AHP and to AP repolarization. Although Ca2+-channel function was preserved after axotomy, Cd2+ did not affect axotomized neurones. This suggests that axotomy promotes a functional loss of gK, Ca which could reflect a regenerative response of the cell to injury.

Action Potentials↗
PubMed1996

Specific up-regulation of the POU domain transcription factor Oct-2 following axotomy.

Peripheral nerve damage causes a dramatic alteration to the gene expression in primary sensory neurons, changes within the neuronal cell body giving rise to an altered phenotype, adapted for axonal regeneration. Such changes suggest an alteration in activity, or levels, of cellular transcription factors. The POU family transcription factor Oct-2 is known to be induced in sensory neurons by nerve growth factor (NGF) and might therefore be affected by the removal of target-derived NGF following axotomy. Paradoxically, however, the expression of Oct-2 showed a transient increase of two- to three-fold 24 h after axotomy. In contrast, axotomy had no effect on the levels of the Brn-3 sub-family of POU proteins, indicating that this effect was specific for Oct-2.

Animals↗
PubMed1990

Expression of beta-preprotachykinin mRNA and tachykinins in rat dorsal root ganglion cells following peripheral or central axotomy.

The changes in gene expression and protein synthesis induced in neurons by axotomy usually lead to increased production of axon constituents and decreased production of molecules related to neurotransmission. Exceptions to this generalization occur, however, and it is unclear whether the injury itself changes the pattern of synthesis or whether individual mechanisms regulate the synthesis of the various axonal components. We used in situ hybridization histochemistry and immunocytochemistry to compare the changes in L4 and L5 rat dorsal root ganglion neuron levels of preprotachykinin mRNA and tachykinin peptides caused by sciatic nerve injury with those caused by dorsal root injury. Both lesions elicit regeneration, although only the axotomized peripheral processes re-establish functional contact with their targets. In the contralateral, intact dorsal root ganglia approximately 17% of neurons contained detectable levels of both mRNAs and peptides. Sciatic nerve section decreased by 70% the number of neurons labeled for preprotachykinin mRNA at three days post-operatively. Not all cells in the ganglion are axotomized by the sciatic nerve lesion; grain counts over the cells spared by the lesion showed an increased level of labeling, possibly a result of collateral sprouting by these spared cells. By two weeks, the number of cells labeled for preprotachykinin mRNA had decreased to 80% of control levels. The numbers of neurons labeled for tachykinin peptides decreased more slowly and reached approximately 50% of control numbers at two weeks. By six months post-operatively, when regeneration is largely complete, the number of neurons containing both mRNAs and peptides returned to normal. In contrast, dorsal root section did not elicit a decrease in the number of neurons labeled either for the mRNAs or the peptides at any of the post-operative intervals examined. These results indicate that axotomy is not the stimulus that elicits changes in the expression of genes coding for tachykinins. Evidence is considered indicating that interruption of the supply of peripherally derived nerve growth factor may be responsible for the changes in gene expression for tachykinins after axotomy.

Animals↗
PubMed1993

Marked increase in cholecystokinin B receptor messenger RNA levels in rat dorsal root ganglia after peripheral axotomy.

It is now well established that the expression of peptides in rat primary sensory neurons is dramatically changed in response to peripheral nerve injury. Thus, as first shown by Jessell et al. peripheral axotomy causes a decrease in substance P levels in the dorsal horn of the corresponding spinal cord segments, and this is due to down-regulation of peptide synthesis in dorsal root ganglion neurons. In contrast, other peptides such as vasoactive intestinal polypeptide and peptide histidine isoleucine, galanin and neuropeptide Y are all markedly upregulated in the rat L4 and L5 dorsal root ganglia after sciatic nerve sectioning. The levels of another peptide, cholecystokinin and its messenger RNA are normally very low or undectable in rat primary sensory neurons, but after peripheral axotomy approximately 30% of the ganglion neurons express cholecystokinin messenger RNA. During the last few years a number of peptide receptors have been cloned, and they all belong to the family of G-protein coupled receptors with seven membrane spanning segments, among them the two cholecystokinin receptors cholecystokininA and cholecystokininB. Ghilardi et al. have recently described presence of cholecystokininB binding sites in rat dorsal root ganglia neurons. In the present study we report that the messenger RNA for the cholecystokininB receptor is present at very low levels in normal dorsal root ganglia of the rat, but axotomy causes a very marked increase in the number of sensory neurons of all sizes expressing cholecystokininB receptor messenger RNA, suggesting an increased sensitivity to cholecystokinin for many primary sensory neurons of different modalities after lesion.

Animals↗
PubMed1995

Ultrastructural studies on peptides in the dorsal horn of the rat spinal cord--IV. Effects of peripheral axotomy with special reference to neuropeptide Y and vasoactive intestinal polypeptide/peptide histidine isoleucine.

Using immunofluorescence histochemistry and pre- and post-embedding immunoelectron microscopy the rat lumbar dorsal horn was analysed in normal rats and 14 days after unilateral transection of the sciatic nerve. A marked increase in neuropeptide Y-like immunoreactivity was observed in the ipsilateral, superficial dorsal horn, especially in laminae III and IV, of the lumbar 4-5 spinal cord segments after peripheral axotomy. In the ipsilateral lamina II two types of neuropeptide Y-immunoreactive, presumably primary afferent terminals could be identified at the ultrastructural level. The first type contained many large dense-core vesicles (100-155 nm in diameter), whereas a second, more common type had only a few and smaller large dense-core vesicles (80-100 nm in diameter), plus synaptic vesicles of varying diameter (50-85 nm), large empty vesicles and tubular structures. Only occasionally were neuropeptide Y-positive terminals in lamina II involved in the formation of axonal labyrinths. In the ipsilateral lamina III, the number of neuropeptide Y-positive nerve terminals markedly increased after axotomy, with a moderate increase in lamina IV. These neuropeptide Y-positive terminals were morphologically similar to the second type of neuropeptide Y-positive terminal in lamina II, i.e. contained many synaptic vesicles (45-50 nm in diameter), a few small large dense-core vesicles (80-100 nm in diameter), electron-dense granular matrix and a few tubular structures. Fusion of synaptic vesicles with the plasma membrane was often observed at these synapses. These terminals frequently formed glomeruli but were not involved in axonal labyrinths. With regard to local neurons, neuropeptide Y-like immunoreactivity was observed in many dendrite-like profiles mostly making synaptic contacts with neuropeptide Y-negative dendrites and only rarely contacting the central terminal of the glomeruli. Neuropeptide Y-positive nerve endings were mainly seen in lamina I and the outer third of lamina II. After peripheral axotomy the number of vasoactive intestinal polypeptide/peptide histidine isoleucine immunoreactive terminals was increased in laminae I and II. They contained many large dense-core vesicles (100-120 nm in diameter), and some of them were positive for vasoactive intestinal polypeptide/peptide histidine isoleucine. Morphologically, the terminals were characterized by a granular matrix, tubular structures, empty vesicles, reduction in synaptic vesicles and absence of postsynaptic densities. Vasoactive intestinal polypeptide/peptide histidine isoleucine-like immunoreactivities were often found in association with labyrinth formation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Galanin expression increases in adult rat sympathetic neurons after axotomy.

Changes in neuropeptide expression occur in sensory, motor, and sympathetic neurons following axotomy. The particular pattern of peptide changes that occurs varies among the three cell types. We have studied the regulation in the rat superior cervical ganglion of the expression of galanin, a peptide previously shown to increase in axotomized sensory and motor neurons. While normally only an occasional neuron exhibiting galanin-like immunoreactivity is found in this ganglion, at two days after transection of the postganglionic internal and external carotid nerves, immunostaining can be observed in many neurons throughout the ganglion. Similar changes are found when ganglia are placed in organ culture for two days. The distribution of immunostained neurons after section of only one of the postganglionic trunks suggests that changes in galanin-like immunoreactivity occur only within neurons whose axons are transected. None the less, even when both nerve trunks are transected, only about half of the neurons in the ganglion exhibit galanin-like immunoreactivity, indicating that only a proportion of the axotomized neurons exhibit a detectable response. The few immunostained neurons seen after section of the cervical sympathetic trunk may also represent axotomized neurons. Galanin-like immunoreactivity extracted from the ganglion co-chromatographs with authentic galanin, and the level of this immunoreactivity increases dramatically after axotomy and explantation, and modestly after decentralization. These same manipulations produce parallel increases in the level of galanin messenger RNA. Together, the findings indicate that the expression of galanin increases in sympathetic neurons after axotomy. Galanin is thus the first neuropeptide whose expression has been shown to increase after transection of all three types of peripheral axons that have been studied.

Animals↗
PubMed1996

Time course of axotomy-induced apoptotic cell death in facial motoneurons of neonatal wild type and bcl-2 transgenic mice.

In neonatal animals, axotomy of facial motoneurons induces cell death. Using the TUNEL technique, which labelled apoptotic DNA breaks in situ, the kinetics of motoneuron death were studied. Lesion of the right facial nerve were performed on two-day-old mice. Then, animals were perfused 8, 12, 16, 20, 24, 28, 32, 48, 72 and 120 h after the lesion. Our results provide direct evidence that, following an axotomy, facial motoneurons die through an apoptotic process. We showed that apoptotic neurons can be detected as early as 16 h after the lesion. Facial motoneurons die within 120 h, with a peak observed 28 h after the lesion. The kinetics of appearance of apoptotic cells were correlated with the loss of Cresyl Violet-stained motoneurons. Furthermore, labelled cells were observed in the contralateral side of the lesion, suggesting that spontaneous apoptotic cell death occurs during the postnatal period. The same study was performed on transgenic mice overexpressing the proto-oncogene bcl-2, a gene repressor of cell death. In these mice, no TUNEL-labelled cells were detected on the lesioned and unlesioned sides. In vivo, Bcl-2 may protect motoneurons from apoptotic death following axotomy and during naturally occurring cell death. These results suggest that these two types of cell death may occur via the same mechanism.

Animals↗