Close Axonal Injury of Rubrospinal Neurons Induced Transient Perineuronal Astrocytic and Microglial Reaction That Coincided with Their Massive Degeneration

Liu, Pei‐Hsin; Wang, Yueh-Jan; Tseng, Guo‐Fang

doi:10.1006/exnr.2002.8057

Cited by 12 publications

(31 citation statements)

References 36 publications

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“…Detailed procedures had been described in a preceding paper (Liu et al 2003). Four days before being killed, animals were subjected to unilateral dorsolateral funiculus lesion and Fast blue application at the C2 level on the same side of the brainstem lesion to check for the presence of RS neurons spared by the brainstem lesion.…”

Section: Brainstem Rs Tractotomymentioning

confidence: 99%

“…Four days before being killed, animals were subjected to unilateral dorsolateral funiculus lesion and Fast blue application at the C2 level on the same side of the brainstem lesion to check for the presence of RS neurons spared by the brainstem lesion. Brainstem lesion sites of all animals presented in this paper were examined as described before (Liu et al 2003) and were found to locate 1.2-1.5 mm caudal to the red nucleus (RN). This lesion transected the axons of most, if not all, RS neurons and did not involve the rubro-olivary tract or the superior cerebellar peduncle in which the excitatory afferents to RS neurons traveled (Wang et al 2000).…”

Section: Brainstem Rs Tractotomymentioning

confidence: 99%

“…l-NAME treatment To find out whether the upregulation of nNOS is related to neuronal death we examined the effect of blocking NO synthesis following brainstem RS axotomy since this lesion was known to cause largescale cell loss of RS neurons (Liu et al 2003). Five rats were treated with daily intraperitoneal injection of l-NAME (Sigma, 100 mg/kg b.w.…”

Section: Brainstem Rs Tractotomymentioning

confidence: 99%

“…However, upper cervical axotomy resulted in a 15% loss of the axotomized neurons and the surviving neurons showed dramatic shrinkage of their cell bodies 10 weeks post-lesion (Liu et al 2003;Wang and Tseng, 2004a). When the lesion was moved closer to their cell bodies at the brainstem, 75% of them died within 10 weeks (Liu et al 2003). It is of interest to learn how RS neurons regulate the expression of neuronal nitric oxide synthase (nNOS) over time after axonal injuries at these three locations for the following two rationales.…”

Section: Introductionmentioning

confidence: 99%

“…In rat rubrospinal (RS) neurons, lower thoracic axotomy was found to cause a relatively minor effect to RS neurons . However, upper cervical axotomy resulted in a 15% loss of the axotomized neurons and the surviving neurons showed dramatic shrinkage of their cell bodies 10 weeks post-lesion (Liu et al 2003;Wang and Tseng, 2004a). When the lesion was moved closer to their cell bodies at the brainstem, 75% of them died within 10 weeks (Liu et al 2003).…”

Section: Introductionmentioning

confidence: 99%

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The proximity of the lesion to cell bodies determines the free radical risk induced in rat rubrospinal neurons subjected to axonal injury

Liu

Tsai

Chung

et al. 2004

Anatomy and Embryology

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To find out whether close axonal injury resulted in greater free radical risk to cord-projection central neurons than distant ones, we studied the expressions of nitric oxide synthase, calcineurin, and superoxide dismutase in rat rubrospinal neurons following brainstem, C2 and T10 axotomies using immunohistochemical methods. We found that nitric oxide synthase expression was upregulated more following brainstem than C2 lesion while T10 lesion triggered no detectable changes. This response peaked at 1 week and returned to control level by 8-week-post-injury. At the same time, calcineurin, which activated nitric oxide synthase, was increased 1 week following brainstem and C2 axotomies. These suggest that close, but not distant, axotomy enhanced NO production, which appeared to be cytotoxic since blocking NO synthesis with N-nitro- l-arginine methyl ester reduced brainstem axotomy-induced rubrospinal cell loss. On the other hand, the mitochondrial Mn-superoxide dismutase, which competes with NO to prevent the formation of the cytotoxic free radical peroxynitrite, was notably reduced after brainstem but almost unaltered following C2 axotomy. Meanwhile, the cytosolic Cu/Zn-superoxide dismutase was not altered following C2 but increased after brainstem axotomy. Ultrastructurally, in rubrospinal neurons more mitochondria became swollen following brainstem than C2 axotomy. Based on these, we proposed that besides the NO-overproduction-induced toxicity, superoxide-loading-induced mitochondrial damage also added to hampering the survival of the closely axotomized neurons.

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Section: Brainstem Rs Tractotomymentioning

confidence: 99%

Section: Brainstem Rs Tractotomymentioning

confidence: 99%

Section: Brainstem Rs Tractotomymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

The proximity of the lesion to cell bodies determines the free radical risk induced in rat rubrospinal neurons subjected to axonal injury

Liu

Tsai

Chung

et al. 2004

Anatomy and Embryology

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Interaction of olfactory ensheathing cells with astrocytes may be the key to repair of tract injuries in the spinal cord: The ‘pathway hypothesis’

Liu

Raisman

2005

J Neurocytol

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Transplantation of cultured adult olfactory ensheathing cells has been shown to induce anatomical and functional repair of lesions of the adult rat spinal cord and spinal roots. Histological analysis of olfactory ensheathing cells, both in their normal location in the olfactory nerves and also after transplantation into spinal cord lesions, shows that they provide channels for the growth of regenerating nerve fibres. These channels have an outer, basal lamina-lined surface apposed by fibroblasts, and an inner, naked surface in contact with the nerve fibres. A crucial property of olfactory ensheathing cells, in which they differ from Schwann cells, is their superior ability to interact with astrocytes. When confronted with olfactory ensheathing cells the superficial astrocytic processes, which form the glial scar after lesions, change their configuration so that their outer pial surfaces are reflected in continuity with the outer surfaces of the olfactory ensheathing cells. The effect is to open a door into the central nervous system. We propose that this formation of a bridging pathway may be the crucial event by which transplanted olfactory ensheathing cells allow the innate growth capacity of severed adult axons to be translated into regeneration across a lesion so that functionally valuable connections can be established.

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Remote Neurodegeneration: Multiple Actors for One Play

Viscomi

Molinari

2014

Mol Neurobiol

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Remote neurodegeneration significantly influences the clinical outcome in many central nervous system (CNS) pathologies, such as stroke, multiple sclerosis, and traumatic brain and spinal cord injuries. Because these processes develop days or months after injury, they are accompanied by a therapeutic window of opportunity. The complexity and clinical significance of remote damage is prompting many groups to examine the factors of remote degeneration. This research is providing insights into key unanswered questions, opening new avenues for innovative neuroprotective therapies. In this review, we evaluate data from various remote degeneration models to describe the complexity of the systems that are involved and the importance of their interactions in reducing damage and promoting recovery after brain lesions. Specifically, we recapitulate the current data on remote neuronal degeneration, focusing on molecular and cellular events, as studied in stroke and brain and spinal cord injury models. Remote damage is a multifactorial phenomenon in which many components become active in specific time frames. Days, weeks, or months after injury onset, the interplay between key effectors differentially affects neuronal survival and functional outcomes. In particular, we discuss apoptosis, inflammation, oxidative damage, and autophagy-all of which mediate remote degeneration at specific times. We also review current findings on the pharmacological manipulation of remote degeneration mechanisms in reducing damage and sustaining outcomes. These novel treatments differ from those that have been proposed to limit primary lesion site damage, representing new perspectives on neuroprotection.

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Close Axonal Injury of Rubrospinal Neurons Induced Transient Perineuronal Astrocytic and Microglial Reaction That Coincided with Their Massive Degeneration

Cited by 12 publications

References 36 publications

The proximity of the lesion to cell bodies determines the free radical risk induced in rat rubrospinal neurons subjected to axonal injury

The proximity of the lesion to cell bodies determines the free radical risk induced in rat rubrospinal neurons subjected to axonal injury

Interaction of olfactory ensheathing cells with astrocytes may be the key to repair of tract injuries in the spinal cord: The ‘pathway hypothesis’

Remote Neurodegeneration: Multiple Actors for One Play

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