Astrocytes, oligodendroglia, extracellular space volume and geometry in rat fetal brain grafts

Syková, Eva; Roitbak, Tamara; Mazel, Tomáš; Šimonová, Zuzana; Harvey, Alan R.

doi:10.1016/s0306-4522(98)00603-4

Cited by 37 publications

(26 citation statements)

References 61 publications

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“…While we did not see changes in astrocyte number or GFAP expression following partial transection (Blaugrund et al, 1992;Kalla et al, 2001;Selles-Navarro et al, 2001), we did observe hypertrophy of immunostained astrocytic processes spreading beyond tissue affected by the primary injury to intact tissue vulnerable to secondary degeneration, which has been implicated in inhibition of neuroregeneration (Wilhelmsson et al, 2004). Such hypertrophy is associated with rapid changes in the physicochemical characteristics of the extracellular space (Sykova, 2001;Sykova et al, 1999). Furthermore, these reactive astrocytes have increased MnSOD immunoreactivity, indicating increased exposure to superoxide (Aucoin et al, 2005;Levkovitch-Verbin et al, 2000;Lieven and Levin, 2007).…”

Section: Rapid Spread Of Immunoreactivity Of An Oxidative Stress Markmentioning

confidence: 73%

Early Events of Secondary Degeneration after Partial Optic Nerve Transection: An Immunohistochemical Study

Fitzgerald¹,

Bartlett²,

Harvey

et al. 2010

Journal of Neurotrauma

118

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Secondary degeneration in the central nervous system involves indirect damage to neurons and glia away from the initial injury. Partial transection of the dorsal optic nerve (ON) results in precise spatial separation of the primary trauma from delayed degenerative events in ventrally placed axons and parent somata. Here we conduct an immunohistochemical survey of secondary cellular changes in and around axons and their parent retinal ganglion cell (RGC) somata during the first 3 days after a restricted, dorsal ON transection. This is before the secondary loss of RGCs and axons projecting through the uninjured, ventral portion of the ON. Within 5 min, manganese superoxide dismutase (MnSOD; a marker of oxidative stress) co-localizes within the astrocytic network across the entire profile of the ON. Secondary astrocyte hypertrophy of immunofluorescent labeling was evident from 3 h, with sustained increases in myelin basic protein immunoreactivity across the nerve by 24 h. Increases in NG-2-positive oligodendrocyte precursor cells, ED-1-positive activated microglia/macrophages, and Iba1-positive reactive resident microglia/macrophage numbers were only seen in ON vulnerable to secondary degeneration by 3 days. Changes within RGC somata exclusively vulnerable to secondary degeneration were detected at 24 h, as evidenced by increases in MnSOD immunoreactivity, followed by increases in c-jun immunoreactivity at 3 days. Treatment with the voltage-gated calcium channel blocker lomerizine did not alter any measured outcome. We conclude that oxidative stress spreading via the astrocytic network and from injured axons to parent RGC somata is an early event during secondary degeneration, and containment is likely to be required in order to prevent further damage to the nerve.

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Section: Rapid Spread Of Immunoreactivity Of An Oxidative Stress Markmentioning

confidence: 73%

Early Events of Secondary Degeneration after Partial Optic Nerve Transection: An Immunohistochemical Study

Fitzgerald¹,

Bartlett²,

Harvey

et al. 2010

Journal of Neurotrauma

118

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“…It was also observed in grafted neural tissue that showed severe astrogliosis (Syková et al, 1999a) and in spinal cord when astrogliosis was evoked by a 45 min application of 50 mM K ϩ (Syková et al, 1999b). Two possible mechanisms may account for the higher tortuosity.…”

Section: Discussionmentioning

confidence: 94%

Diffusion barriers evoked in the rat cortex by reactive astrogliosis

Roitbak

Syková

1999

Glia

188

142

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Changes in extracellular space (ECS) diffusion parameters in astrogliotic tissue around a unilateral cortical stab wound were determined from concentrationtime profiles of tetramethylammonium (TMA ϩ ) using TMA ϩ -selective microelectrodes. Three diffusion parameters-ECS volume fraction ␣ (␣ ϭ ECS volume/ total tissue volume), tortuosity ( 2 ϭ D/ADC; where D is the free and ADC is the apparent diffusion coefficient of TMA ϩ in the brain), and nonspecific TMA ϩ uptake kЈ-were determined at 3, 7, 21, and 35 days postwounding (dpw), in the hemispheres ipsilateral and contralateral to the lesion. Following diffusion experiments, tissue sections were immunostained for glial fibrillary acidic protein (GFAP) and chondroitin-sulphate proteoglycans (CSPG). In the area 300-1000 µm around the wound, ␣ was increased at 3, 7, and 21 dpw by about 20% but returned to control values at 35 dpw; was increased at all four intervals, reaching a maximum at 7 dpw. kЈ was lower than in the contralateral hemisphere at 7, 21, and 35 dpw. Measurements 1,500-2,000 µm from the wound revealed only an increase in at 7 dpw. The time course of changes in ECS diffusion parameters closely correlated with increased staining for GFAP and CSPG. Our results show that astrogliosis significantly changes the diffusion properties of nervous tissue, making it less permissive. Both hypertrophied astrocytic processes and an enhanced formation of some extracellular matrix molecules could affect, through changes in the diffusion of molecules in the ECS, neuron-glia communication, ''cross-talk'' between synapses, extrasynaptic transmission, and regenerative processes.

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“…Consequently, changes in ECM with age, such as a particular splicing pattern of fibronectin (Pagani et al, 1991) or highly regulated proteoglycan expression (Bandtlow and Zimmermann, 2000), could disrupt cell-ECM molecule interactions and thus disrupt the neural precursor behavior, including their response to growth factors (Garcion et al, 2001). Moreover, the aging brain undergoes reduction in glial volume and extracellular space (Sykova et al, 1999), suggesting that the aged CNS medium could constitute a nonpermissive environment for cell recruitment in the parenchyma by mechanically preventing the emergence of cells from the RMS to the parenchyma in old animals under pathological conditions. The involvement of the ECM is supported by recent experiments showing a lower rate of oligodendrocyte progenitor recruitment in demyelinated lesions in old rats compared with young ones, although the number of oligodendrocyte progenitors available is the same in both groups of animals (Sim et al, 2001).…”

Section: Consequences Of Age On the Capacity Of Neural Precursors To mentioning

confidence: 99%

Growth factor treatment promotes mobilization of young but not aged adult subventricular zone precursors in response to demyelination

Decker

Picard-Riéra

Lachapelle

et al. 2002

J of Neuroscience Research

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Precursor cells of the adult mouse subventricular zone (SVZ) are mobilized and recruited by a lysolecithin (LPC)-induced demyelination of the corpus callosum. Because age decreases the proliferation of the SVZ neural precursors as well as the potential for myelin repair of the adult central nervous system, we have compared the ability of young and aged adult neural precursors to respond to LPC-induced demyelination. With age, the SVZ cells lost their capacity to proliferate and to be recruited by the lesion. Whereas a single injection of fibroblast growth factor-2 or transforming growth factor-␣ stimulated the proliferation of SVZ and rostral migratory stream precursors in both groups of animals after demyelination, they favored recruitment at the lesion in young mice but not in aged ones. In vitro experiments using neurospheres derived from young and aged animals indicated that both populations have the same migratory performances. Our in vivo data thus suggest that aged neural precursors may loose their intrinsic capacities to respond to demyelination-induced signals. Alternatively, their function may be altered by modification of the aged extracellular environment.

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Astrocytes, oligodendroglia, extracellular space volume and geometry in rat fetal brain grafts

Cited by 37 publications

References 61 publications

Early Events of Secondary Degeneration after Partial Optic Nerve Transection: An Immunohistochemical Study

Early Events of Secondary Degeneration after Partial Optic Nerve Transection: An Immunohistochemical Study

Diffusion barriers evoked in the rat cortex by reactive astrogliosis

Growth factor treatment promotes mobilization of young but not aged adult subventricular zone precursors in response to demyelination

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