Neonatal sciatic nerve transection induces TUNEL labeling of neurons in the rat spinal cord and DRG

Oliveira, Alexandre Leite Rodrigues de; Risling, Mårten; Deckner, M.; Lindholm, Tomas; Langone, Francesco; Cullheim, Staffan

doi:10.1097/00001756-199709080-00006

Cited by 55 publications

(30 citation statements)

References 8 publications

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“…Several lines of evidence that indicate that both developing neurones and glial cells die by apoptosis following injury to a peripheral nerve or to the spinal cord (Lawson and Lowrie, 1998;Liu et al, 1997;Oliviera et al, 1997), although some necrotic cell death does take place (Li et al, 1998). In this study, we found that hsp27 immunoreactive motoneurones did not co-express markers of apoptosis.…”

Section: Discussioncontrasting

confidence: 41%

The Effect of Neonatal Nerve Injury on the Expression of Heat Shock Proteins in Developing Rat Motoneurones

Kalmár¹,

Burnstock

Vrbová

et al. 2002

Journal of Neurotrauma

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The expression of the heat shock proteins hsp27 and hsp70 was examined in the spinal cord and sciatic nerves of developing rats. Using immunohistochemistry, we found that hsp27 is present in many motoneurones at birth. With development, the intensity of staining increases, reaching adult levels by 21 days, when all sciatic motoneurones express hsp27. In the sciatic nerve, hsp27 is strongly expressed throughout postnatal development. In contrast, hsp70 immunoreactivity in motoneurones and the sciatic nerve is weak at birth and does not change with development. The expression of heat shock proteins has been shown to increase in cells under conditions of stress, where they have beneficial effects on cell survival. The effect of neonatal nerve injury on hsp27 and hsp70 expression was also examined in this study. Four days after injury, staining for hsp27 increases in motoneurones, whereas hsp70 does not change. However, there is a significant increase in hsp70 staining in glial cells surrounding the injured motor pool, predominantly in astrocytes. Since neonatal nerve injury induces apoptotic motoneurone death, we also studied the co-expression of hsp27 with markers of apoptosis. No hsp27-positive motoneurones were found to be apoptotic, as assessed by both TUNEL and caspase-3 immunoreactivity. Therefore, it is possible that the upregulation of hsp27 observed in injured motoneurones may play a role in protecting motoneurones from apoptotic cell death following nerve injury.

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Section: Discussioncontrasting

confidence: 41%

The Effect of Neonatal Nerve Injury on the Expression of Heat Shock Proteins in Developing Rat Motoneurones

Kalmár¹,

Burnstock

Vrbová

et al. 2002

Journal of Neurotrauma

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“…16 Another major risk factor is the immaturity of the individual; motoneuron cell death is much more prevalent following axotomy in newborn rodents. 41,42 Neonatal nerve injury-induced motoneuron loss is mediated by excitotoxic mechanisms and is apoptotic in nature. 27 The time course of apoptotic cell death following spinal nerve root avulsion evolves relatively rapidly, within several days, 27,32 and therefore can be partially reversed by prompt infusion of growth factors and neurotrophins.…”

Section: Cell Death Of Motoneuron After Nerve Injuriesmentioning

confidence: 99%

Motoneuron survival after chronic and sequential peripheral nerve injuries in the rat

Forden

Walsh

et al. 2010

JNS

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“…We have shown that apoptotic death may underlie the loss of spinal motoneurons, DRG neurons, and interneurons in the spinal cord after neonatal sciatic nerve transection (Oliveira et al, 1997). In this situation, the loss of interneurons coincides with the programmed apoptotic death of such neurons, which occurs from birth up to the sixth postnatal day in the rat (Lawson et al, 1997), whereas PCD of motoneurons and DRG neurons takes place prenatally (Harris and McCaig, 1984;Oppenheim, 1991;Coggeshall et al, 1994).…”

mentioning

confidence: 93%

Apoptosis of spinal interneurons induced by sciatic nerve axotomy in the neonatal rat is counteracted by nerve growth factor and ciliary neurotrophic factor

Oliveira

Risling

Negro

et al. 2002

J of Comparative Neurology

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We have previously shown that not only motoneurons and dorsal root ganglion cells but also small neurons, presumably interneurons in the spinal cord, may undergo apoptotic cell death as a result of neonatal peripheral nerve transection in the rat. With the aid of electron microscopy, we have here demonstrated that apoptosis in the spinal cord is confined to neurons and does not involve glial cells at the survival time studied (24 hours). To define the relative importance of the loss of a potential target (motoneuron) and a potential afferent input (dorsal root ganglion cell) for the induction of apoptosis in interneurons in this situation, we have compared the distributions and time courses for TUNEL labeling, which detects apoptotic cell nuclei, in the L5 segment of the spinal cord and the L5 dorsal root ganglion after sciatic nerve transection in the neonatal (P2) rat. In additional experiments, we studied the effects on TUNEL labeling of interneurons after treatment of the cut sciatic nerve with either ciliary neurotrophic factor (CNTF) to rescue motoneurons or nerve growth factor (NGF) to rescue dorsal root ganglion cells. The time courses of the TUNEL labeling in motoneurons and interneurons induced by the lesion show great similarities (peak at 8-48 hours postoperatively), whereas the labeling in dorsal root ganglion cells occurs later (24-72 hours). Both CNTF and NGF decrease the number of TUNEL-labeled interneurons, but there is a regional difference, in that CNTF preferentially saves interneurons in deep dorsal and ventral parts of the spinal cord, whereas the rescuing effects of NGF are seen mainly in the superficial dorsal horn. The results are interpreted as signs of a trophic dependence on both the target and the afferent input for the survival of interneurons neonatally.

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Neonatal sciatic nerve transection induces TUNEL labeling of neurons in the rat spinal cord and DRG

Cited by 55 publications

References 8 publications

The Effect of Neonatal Nerve Injury on the Expression of Heat Shock Proteins in Developing Rat Motoneurones

The Effect of Neonatal Nerve Injury on the Expression of Heat Shock Proteins in Developing Rat Motoneurones

Motoneuron survival after chronic and sequential peripheral nerve injuries in the rat

Apoptosis of spinal interneurons induced by sciatic nerve axotomy in the neonatal rat is counteracted by nerve growth factor and ciliary neurotrophic factor

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