Cell division in injured spinal cord

Adrian, Erle K.

doi:10.1002/aja.1001230307

Cited by 42 publications

(6 citation statements)

References 29 publications

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“…This latter observation implies a rapid local transformation of the resident microglial population into brain macrophages which then become indistinguishable from macrophages derived from infiltrating monocyte precursors. Other studies using autoradiographic and immunohistochemical techniques have reached similar conclusions regarding the dual nature of the macrophage response after CNS injury (Adrian, Jr. and Walker, 1962;Adrian, Jr. 1968;Morshead and van der Kooy, 1990;Milligan et al, 1991). A more vigorous response of recruited macrophages has been reported after neural trauma in sites capable of significant anatomical plasticity and regeneration, i.e., the peripheral nervous system (PNS) and the CNS of neonates (Perry et al, 1987a;Milligan et al, 1991).…”

Section: Origin Of Microglial and Macrophage Reactions In The Injuredmentioning

confidence: 63%

Cellular inflammatory response after spinal cord injury in sprague-dawley and lewis rats

1997

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The distribution of microglia, macrophages, T-lymphocytes, and astrocytes was characterized throughout a spinal contusion lesion in Sprague-Dawley and Lewis rats by using immunohistochemistry. The morphology, spatial localization, and activation state of these inflammatory cells were described both qualitatively and quantitatively at 12 hours, 3, 7, 14, and 28 days after injury. By use of OX42 and ED1 antibodies, peak microglial activation was observed within the lesion epicenter of both rat strains between three and seven days post-injury preceding the bulk of monocyte influx and macrophage activation (seven days). Rostral and caudal to the injury site, microglial activation plateaued between two and four weeks post-injury in the dorsal and lateral funiculi as indicated by morphological transformation and the de-novo expression of major histocompatibility class II (MHC II) molecules. Similar to the timing of microglial reactions, T-lymphocytes maximally infiltrated the lesion epicenter between three and seven days post-injury. Reactive astrocytes, while present in the acute lesion, were more prominent at later survival times (7-28 days). These cells were interspersed with activated microglia but appeared to surround and enclose tissue sites occupied by reactive microglia and phagocytic macrophages. Thus, trauma-induced central nervous system (CNS) inflammation, regardless of strain, occurs rapidly at the site of injury and involves the activation of resident and recruited immune cells. In regions rostral or caudal to the epicenter, prolonged activation of inflammatory cells occurs preferentially in white matter and primarily consists of activated microglia and astrocytes. Differences were observed in the magnitude and duration of macrophage activation between Sprague-Dawley (SD) and Lewis (LEW) rats throughout the lesion. Increased expression of complement type 3 receptors (OX42) and macrophage-activation antigens (ED1) persisted for longer times in LEW rats while expression of MHC class II molecules was attenuated in LEW compared to SD rats at all times examined. Variations in the onset and duration of T-lymphocyte infiltration also were observed between strains with twice as many T-cells present in the lesion epicenter of Lewis rats by 3 days post-injury. These strain-specific findings potentially represent differences in corticosteroid regulation of immunity and may help predict a range of functional neurologic consequences affected by neuroimmune interactions.

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Section: Origin Of Microglial and Macrophage Reactions In The Injuredmentioning

confidence: 63%

Cellular inflammatory response after spinal cord injury in sprague-dawley and lewis rats

1997

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“…The earliest injection of 3H-thymidine in the present study was at 31 hours after wounding, and labeling was seen in these animals at 48 hours, suggesting an early proliferative response of astrocytes. Adrian (1968), Altman (1962), Huntington and Terry (19651, and Mori (1972) have also demonstrated astrocyte labeling as early as postlesion day 1.…”

Section: Astrocyte Proliferation In Neural Traumamentioning

confidence: 94%

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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“…In contrast, neuronal differentiation does occur when NSCs are grafted into one of the few neurogenic areas of the adult brain (15,45,48). For example, NSCs present in the adult spinal cord do not generate new neurons in situ, normally or after injury (1,17). Likewise, spinal cord NSCs transplanted back into the adult spinal cord generate only glial cells (45).…”

Section: Introductionmentioning

confidence: 99%