The role of oligodendroglia and astroglia in wallerian degeneration of the optic nerve

Cook, R. D.; ́niewski, Henryk M. Wis

doi:10.1016/0006-8993(73)90527-1

Cited by 153 publications

(31 citation statements)

References 11 publications

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“…One well-characterized response occurs at the site of injury (Amaducci et al, 198 1;Mathewson and Berry, 1985;Schiffer et al, 1986). There are also wellcharacterized examples of increases in GFAP within glial cells at a distance from the site of injury, for example, within degenerating nerves (Vaughn et al, 1970;Cook and Wisniewski, 1973), in areas undergoing retrograde degeneration after axotomy (Graeber and Kreutzberg, 1986;Tetzlaff et al, 1988), or, as in the present study, in areas that would be denervated by the lesion (Rose et al, 1976;Barret et al, 1981;Gage et al, 1988).…”

Section: Discussionsupporting

confidence: 58%

The process of reinnervation in the dentate gyrus of adult rats: An ultrastructural study of changes in presynaptic terminals as a result of sprouting

Steward

Vinsant

Davis

1988

J of Comparative Neurology

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The present study was undertaken to define the ultrastructure of synapses of the crossed temporodentate pathway after they had sprouted to reinnervate the dentate gyrus following the destruction of the normal ipsilateral temporodentate pathway. The synapses of the sprouted crossed temporodentate pathway were identified at the EM level by using autoradiographic techniques and by evaluating the degeneration of the pathway following secondary lesions. Both EM autoradiography and EM degeneration revealed that the terminals of the sprouted crossed temporodentate pathway formed asymmetric synapses on spines; individual terminals appeared to make more synaptic contacts per terminal (multiple synapses) than in the case of the normal crossed pathway. In the two lesioned animals exhibiting the best labeling, labeled terminals made an average of 3.0 ± 2.2 and 2.0 ± 1.3 contacts per terminal. In contrast, labeled terminals in normal animals exhibited only one contact per terminal. The terminals of the sprouted pathway were also larger than those of the normal crossed pathway. The synapses of the crossed temporodentate pathway that degenerated after a secondary lesion of the entorhinal cortex exhibited both electron‐lucent and electron‐dense forms of degeneration at 2 days postlesion. In two animals that were quantitatively analyzed, the density of degenerating synaptic terminals was 281 and 218/10,000 μm2 in the terminal field of the sprouted crossed pathway. These values are much higher than in normal animals, where the density of degenerating synaptic terminals was only 2.12/10,000 μm2 at 2 days postlesion. Because degenerating terminals were evident at 2 days postlesion, the sprouted crossed pathway does not appear to exhibit the very rapid degeneration that is characteristic of the normal crossed pathway. We conclude that sprouting in this pathway involves terminal proliferation (an increase in the number of presynaptic elements), and terminal hypertrophy (an increase in the size of presynaptic terminals, together with an increase in the number of synaptic contacts formed by individual terminals).

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Section: Discussionsupporting

confidence: 58%

The process of reinnervation in the dentate gyrus of adult rats: An ultrastructural study of changes in presynaptic terminals as a result of sprouting

Steward

Vinsant

Davis

1988

J of Comparative Neurology

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“…Wallerian degeneration in mammalian CNS reportedly proceeds over the course of months or years following an injury. 22 We hypothesize that IFN␤-1a had therapeutic effects in the first year of treatment that were evident on the atrophy measure only in the second treatment year. Ongoing disease activity before study entry may have resulted in brain atrophy during the first year of the study irrespective of the treatment arm assignment, while reduced disease activity in IFN␤-1a recipients may have reduced brain atrophy during the second year of observation.…”

Section: Results Patients Included In This Studymentioning

confidence: 97%

Use of the brain parenchymal fraction to measure whole brain atrophy in relapsing-remitting MS

Rudick¹,

Fisher²,

Lee³

et al. 1999

Neurology

655

251

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Article abstract-Background: Episodic inflammation in the CNS during the early stages of MS results in progressive disability years later, presumably due to myelin and axonal injury. MRI demonstrates ongoing disease activity during the early disease stage, even in some patients who are stable clinically. The optimal MRI measure for the destructive pathologic process is uncertain, however. Methods: In this post-hoc study, MRI scans were analyzed from patients with relapsing MS participating in a placebo-controlled trial of interferon ␤-1a. The brain parenchymal fraction, defined as the ratio of brain parenchymal volume to the total volume within the brain surface contour, was used to measure whole brain atrophy. The relationship between disease features and brain atrophy and effect of interferon ␤-1a were determined. Results: MS patients had significant brain atrophy that worsened during each of 2 years of observation. In many patients, brain atrophy worsened without clinical disease activity. Baseline clinical and MRI abnormalities were not strongly related to the rate of brain atrophy during the subsequent 2 years. Treatment with interferon ␤-1a resulted in a reduction in brain atrophy progression during the second year of the clinical trial. Conclusions: Patients with relapsing-remitting MS have measurable amounts of whole brain atrophy that worsens yearly, in most cases without clinical manifestations. The brain parenchymal fraction is a marker for destructive pathologic processes ongoing in relapsing MS patients, and appears useful in demonstrating treatment effects in controlled clinical trials. Key words: MS-MRI-Brain atrophyInterferon beta. NEUROLOGY 1999;53:1698-1704 Individual MS patients face an unpredictable future during the relapsing-remitting stage of the disease, because severity is highly variable and accurate predictors of long-term outcome are lacking. Recurrent inflammation in optic nerves, brain, and spinal cord damages myelin and axons, leading to intermittent neurologic symptoms initially, and progressive disability later in the disease. Over 50% of patients with relapsing-remitting MS (RRMS) enter the secondary progressive disease stage, which is associated with more continuous physical, neuropsychologic, and socioeconomic decline. Clinical features during the early relapsing-remitting stage are not very accurate in predicting when an individual patient will enter the secondary progressive disease stage.The poor predictive value of clinical features during RRMS may relate to ongoing subclinical disease activity, evident on MRI. Serial MRI scans demonstrate that new lesions occur 5 to 10 times as often as clinical relapses.1-3 The predictive value of MRIbased disease markers has been studied for T2 hyperintense lesions. It was shown that the volume of T2 hyperintense lesions seen on cranial MRI scans at the time of first symptoms predicted subsequent clinical disease progression. 4 This supports the use of MRI as a surrogate marker in MS, but the optimal MRI measure is unknown.Recent studie...

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“…This may reflect the slow Wallerian degeneration in the CNS compared with the PNS (Bignami and Ralston, 1969;Cook and Wisniewski, 1973). However, 6 months after injury the GFR␣-1 immunoreactivity in degenerating white matter was still weak and not as high as in Schwann cells.…”

Section: Slow Increase Of Gfr␣-1 and Truncated Trkb Levels In Degenermentioning

confidence: 91%

Neurotrophic Factors and Receptors in the Immature and Adult Spinal Cord after Mechanical Injury or Kainic Acid

et al. 2001

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Delivery of neurotrophic factors to the injured spinal cord has been shown to stimulate neuronal survival and regeneration. This indicates that a lack of sufficient trophic support is one factor contributing to the absence of spontaneous regeneration in the mammalian spinal cord. Regulation of the expression of neurotrophic factors and receptors after spinal cord injury has not been studied in detail. We investigated levels of mRNAencoding neurotrophins, glial cell line-derived neurotrophic factor (GDNF) family members and related receptors, ciliary neurotrophic factor (CNTF), and c-fos in normal and injured spinal cord. Injuries in adult rats included weight-drop, transection, and excitotoxic kainic acid delivery; in newborn rats, partial transection was performed. The regulation of expression patterns in the adult spinal cord was compared with that in the PNS and the neonate spinal cord. After mechanical injury of the adult rat spinal cord, upregulations of NGF and GDNF mRNA occurred in meningeal cells adjacent to the lesion. BDNF and p75 mRNA increased in neurons, GDNF mRNA increased in astrocytes close to the lesion, and GFR␣-1 and truncated TrkB mRNA increased in astrocytes of degenerating white matter. The relatively limited upregulation of neurotrophic factors in the spinal cord contrasted with the response of affected nerve roots, in which marked increases of NGF and GDNF mRNA levels were observed in Schwann cells. The difference between the ability of the PNS and CNS to provide trophic support correlates with their different abilities to regenerate. Kainic acid delivery led to only weak upregulations of BDNF and CNTF mRNA. Compared with several brain regions, the overall response of the spinal cord tissue to kainic acid was weak. The relative sparseness of upregulations of endogenous neurotrophic factors after injury strengthens the hypothesis that lack of regeneration in the spinal cord is attributable at least partly to lack of trophic support.

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The role of oligodendroglia and astroglia in wallerian degeneration of the optic nerve

Cited by 153 publications

References 11 publications

The process of reinnervation in the dentate gyrus of adult rats: An ultrastructural study of changes in presynaptic terminals as a result of sprouting

The process of reinnervation in the dentate gyrus of adult rats: An ultrastructural study of changes in presynaptic terminals as a result of sprouting

Use of the brain parenchymal fraction to measure whole brain atrophy in relapsing-remitting MS

Neurotrophic Factors and Receptors in the Immature and Adult Spinal Cord after Mechanical Injury or Kainic Acid

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