Chapter 38 Inhibition of regeneration: the ultrastructure of reactive astrocytes and abortive axon terminals in the transition zone of the dorsal root

Stensaas, L. J.; Partlow, Lester M.; Burgess, P. R.; Horch, K.W.

doi:10.1016/s0079-6123(08)61846-4

Cited by 65 publications

(29 citation statements)

References 23 publications

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“…Astrocyte proliferation may be in part beneficial, because the cells produce trophic factors that promote neuron survival and neuritic growth (Manthorpe et al, 1986) and secrete components of basal lamina that may guide regenerating axons (Bernstein et al, 1985). By regulating ions and neurotransmitters (Kimelberg, 1983), astrocytes may also help to maintain the normal extracellular environment 01989 Alan R. Liss, Inc. in the immediate vicinity of neurons in CNS injury; however, by facilitating gliosis, astrocyte proliferation may contribute to the formation of a physical barrier between the lesioned area and the intact nervous system and thereby prevent reestablishment of circuitry (Reier, 1986;Stensaas et al, 1987). A better understanding of the proliferative properties of astrocytes is essential in elucidating the role of this reactive phenomenon in events that promote or impede successful regeneration in the CNS.…”

Section: Introductionmentioning

confidence: 99%

Trauma‐induced proliferation of astrocytes in the brains of young and aged rats

Topp

Faddis

Vijayan

1989

Glia

106

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The time-course and magnitude of astrocyte proliferation following neural trauma was evaluated in young adult (3 months) and mid-aged (16-19 months) male Fischer 344 rats. One to 4 days after a needle wound was made through the cortex and the hippocampus, rats received three intraperitoneal injections of 3H-thymidine at 8 hour intervals and were sacrificed 1 hour after the last injection. For astrocyte quantification, 3H-thymidine autoradiography was combined with immunohistochemical staining for glial fibrillary acidic protein followed by semithin sectioning. In areas of the cortex and hippocampus adjacent to the wound, astrocytes were categorized as unlabeled or labeled with silver grains over the nuclei. Labeling index and numerical density of astrocytes were determined using stereological methods. The results showed that in both young and older rats, astrocyte proliferation is an early glial response to neural trauma, occurring during the first 4 postlesion days and contributing to an increase in astrocyte population. Regional differences in labeling index and numerical density suggest heterogeneity in the proliferative capacity of astrocyte subpopulations in the rat brain. Compared with young animals, older rats demonstrated greater labeling in the cortex but not in the hippocampus. Thus, aging is associated with region-specific increase in astrocyte reactivity to trauma possibly due to increased availability of mitogens or enhanced sensitivity of astrocytes to mitogenic signals.

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Section: Introductionmentioning

confidence: 99%

Trauma‐induced proliferation of astrocytes in the brains of young and aged rats

Topp

Faddis

Vijayan

1989

Glia

106

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“…The majority ofthe regenerating dorsal root axons stop among these astrocytic processes and form stable axo-glial endings (Liuzzi and Lasek, 1987a;Stensaas et al, 1987). Those few axons that are not stopped at the DRTZ either penetrate into the spinal cord (Liuzzi and Lasek, 1987b) or grow back toward the DRG.…”

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confidence: 99%

Axo-glial interactions at the dorsal root transitional zone regulate neurofilament protein synthesis in axotomized sensory neurons

Liuzzi

Tedeschi

1992

J. Neurosci.

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After dorsal root crush, dramatic ultrastructural differences are observed between regenerated dorsal root axonal endings that are physically blocked at a ligation neuroma and those that are allowed to form axo-glial endings among the astrocytes at the dorsal root transitional zone (DRTZ). Physically blocked axonal endings swell immensely with membranous organelles and neurofilaments (NFs) while axo-glial endings do not, suggesting that DRTZ astrocytes stop axonal growth by activating a physiological stop pathway within those endings. Since protease-dependent NF degradation at axonal endings is a part of this pathway, this study addresses the question of whether NF subunit synthesis in the dorsal root ganglion (DRG) is regulated by the pathway. Lumbar dorsal roots were crushed and, at various postinjury times, the attached DRGs were removed and pulse-labeled in vitro with 35S-methionine for subsequent analysis of protein synthesis by electrophoresis and fluorography. Within 24 hr of axotomy, there was a down-regulation of the 68 kDa (NF-L) and 145 kDa (NF-M) NF subunits. At 14 d postcrush, a time when most of the regenerating axons have reached and been stopped by DRTZ astrocytes, NF protein synthesis returned to control levels. By contrast, when the axons were prevented from reaching the DRTZ by ligating or removing segments of the roots, NF synthesis failed to return to normal levels. These data suggest that activation of the physiological stop pathway by DRTZ astrocytes regulates NF protein synthesis in the DRG.

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“…This is also where axonal growth is inhibited because the axons either turn around along the dorsal root or form swollen end bulbs abutting the astrocytes. 18 Full explanation is not only far beyond the scope of this report but also unavailable based on existing scientific data. Raisman and colleagues 19,20 are working on using olfactory ensheathing cells to overcome the barrier after spinal cord injury.…”

Section: Discussionmentioning

confidence: 96%

The clinical study of repairing cauda equina fibres with fibrin glue after lumbar fracture and dislocation

Sun

Liu

et al. 2010

Spinal Cord

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Study design: A retrospective study. Objectives: To study the outcome of repair of cauda equina fibres with fibrin glue after lumbar fracture and/or dislocation. Methods: Seven acute cases and one chronic case of L2 or L3 fracture and/or dislocation complicated with complete cauda equina injury were selected. Sural nerve or ventral roots of injured cauda equina were chosen to repair the motor cauda equina fibres with fibrin glue after open reduction and internal fixation of the unstable vertebrae. The functional recovery after surgery was observed. Results: Recovery of the strength of thigh muscles (iliopsoas, quadriceps femoris, gluteus maximus, adductors) was observed in all seven acutely injured patients (t ¼ 3.74, Po0.05), but not in the chronic one. Neither recovery of leg muscles nor sensation of the lower extremities was observed in any case. Conclusions: The cauda equina ventral roots injured after lumbar fracture and/or dislocation can be repaired with fibrin glue and motor recovery is expected.

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Chapter 38 Inhibition of regeneration: the ultrastructure of reactive astrocytes and abortive axon terminals in the transition zone of the dorsal root

Cited by 65 publications

References 23 publications

Trauma‐induced proliferation of astrocytes in the brains of young and aged rats

Trauma‐induced proliferation of astrocytes in the brains of young and aged rats

Axo-glial interactions at the dorsal root transitional zone regulate neurofilament protein synthesis in axotomized sensory neurons

The clinical study of repairing cauda equina fibres with fibrin glue after lumbar fracture and dislocation

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