Dual effects of TNFα on nerve fiber formation from ventral mesencephalic organotypic tissue cultures

Marschinke, Franziska; Strömberg, Ingrid

doi:10.1016/j.brainres.2008.03.070

Cited by 11 publications

(13 citation statements)

References 36 publications

(48 reference statements)

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“…Previously, we and others have demonstrated in organotypic dorsal root ganglia cultures that TNF-alpha reduces neurite outgrowth in the peripheral nervous system (15,24). In organotypic mesencephalic brain slices TNF-alpha has been shown to support glia-dependent neurite growth (28). In the present study we have demonstrated that TNF-alpha increases neurite outgrowth in brain slices by nearly 45%, thus, at a level comparable with the stimulatory effects of hypothermia.…”

Section: Discussionsupporting

confidence: 76%

Hypothermia‐Induced Neurite Outgrowth is Mediated by Tumor Necrosis Factor‐Alpha

et al. 2010

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Systemic or brain-selective hypothermia is a well-established method for neuroprotection after brain trauma. There is increasing evidence that hypothermia exerts beneficial effects on the brain and may also support regenerative responses after brain damage. Here, we have investigated whether hypothermia influences neurite outgrowth in vitro via modulation of the post-injury cytokine milieu. Organotypic brain slices were incubated: deep hypothermia (2 h at 17 degrees C), rewarming (2 h up to 37 degrees C), normothermia (20 h at 37 degrees C). Neurite density and cytokine release (IL 1beta, IL-6, IL-10, and TNF-alpha) were investigated after 24 h. For functional analysis mice deficient in NT-3/NT-4 and TNF-alpha as well as the TNF-alpha inhibitor etanercept were used. Hypothermia led to a significant increase of neurite outgrowth, which was independent of neurotrophin signaling. In contrast to other cytokines investigated, TNF-alpha secretion by organotypic brain slices was significantly increased after deep hypothermia. Moreover, hypothermia-induced neurite extension was abolished after administration of the TNF-alpha inhibitor and in TNF-alpha knockout mice. We demonstrate that TNF-alpha is responsible for inducing neurite outgrowth in the context of deep hypothermia and rewarming. These data suggest that hypothermia not only exerts protective effects in the CNS but may also support neurite outgrowth as a potential mechanism of regeneration.

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Section: Discussionsupporting

confidence: 76%

Hypothermia‐Induced Neurite Outgrowth is Mediated by Tumor Necrosis Factor‐Alpha

et al. 2010

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“…Conversely, the deficiency of BDNF or NGF is believed to be a cause or a trigger of neurodegeneration [43,44]. Thus, NGF and BDNF, or their receptor agonists, have been used to treat AD and other neurodegenerative diseases [12,45,46]. Dr O’Banion’s team has recently demonstrated that chronic over expression of IL-1 impairs adult hippocampal neurogenesis in the above mentioned mouse model [47].…”

Section: Discussionmentioning

confidence: 99%

“…Even though many studies have reported that increased IL-1 release contributes to neurodegeneration in both acute and chronic brain conditions, findings from acute ischemia, stroke and brain injuries show that the release of IL-1 and other pro-inflammatory cytokines, such as TNF-α, may protect neurons [8-12]. However, many studies have demonstrated that blocking IL-1 or reducing inflammation could reduce neuron death and symptoms of disability as well as save patients’ lives [13].…”

Section: Introductionmentioning

confidence: 99%

Acute and subacute IL-1β administrations differentially modulate neuroimmune and neurotrophic systems: possible implications for neuroprotection and neurodegeneration

Song

Zhang

Dong

2013

J Neuroinflammation

101

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BackgroundIn Alzheimer’s disease, stroke and brain injuries, activated microglia can release proinflammatory cytokines, such as interleukin (IL)-1β. These cytokines may change astrocyte and neurotrophin functions, which influences neuronal survival and induces apoptosis. However, the interaction between neuroinflammation and neurotrophin functions in different brain conditions is unknown. The present study hypothesized that acute and subacute elevated IL-1β differentially modulates glial and neurotrophin functions, which are related to their role in neuroprotection and neurodegeneration.MethodRats were i.c.v. injected with saline or IL-1β for 1 or 8 days and tested in a radial maze. mRNA and protein expressions of glial cell markers, neurotrophins, neurotrophin receptors, β-amyloid precursor protein (APP) and the concentrations of pro- and anti-inflammatory cytokines were measured in the hippocampus.ResultsWhen compared to controls, memory deficits were found 4 days after IL-1 administrations, however the deficits were attenuated by IL-1 receptor antagonist (RA). Subacute IL-1 administrations increased expressions of APP, microglial active marker CD11b, and p75 neurotrophin receptor, and the concentration of tumor necrosis factor (TNF)-α and IL-1β, but decreased expressions of astrocyte active marker glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF) and TrK B. By contrast, up-regulations of NGF, BDNF and TrK B expressions were found after acute IL-1 administration, which are associated with the increase in both glial marker expressions and IL-10 concentrations. However, TrK A was down-regulated by acute and up-regulated by subacute IL-1 administrations. Subacute IL-1-induced changes in the glial activities, cytokine concentrations and expressions of BDNF and p75 were reversed by IL-1RA treatment.ConclusionThese results indicate that acute and subacute IL-1 administrations induce different changes toward neuroprotection after acute IL-1 administrations but neurodegeneration after subacute ones.

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“…This suggestion is strengthened by the fact that the length of these neurites was comparable, independent of treatment. Interestingly, to date, nothing but time in culture has improved the length of these non‐glial‐associated nerve fibers as long as they are present (af Bjerkén et al, 2007; Marschinke and Strömberg, 2008). Thus, regarding studies on effects of for instance neurotrophic factors on cultured dopamine neurons, survival time is then an important factor, since the non‐glial‐ and the glial‐associated growths might be affected differently.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of astrocytes promotes long‐distance growing nerve fibers in ventral mesencephalic cultures

Bjerkén

Marschinke²,

Strömberg³

2008

Intl J of Devlp Neuroscience

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Tyrosine hydroxylase-positive nerve fiber formation occurs in two diverse morphological patterns in rat fetal ventral mesencephalic slice cultures; one is non-glial-associated and the other is glial-associated. The aim of this study was to characterize the non-glial-associated nerve fibers and its relation to migration of astrocytes. Organotypic slice cultures were prepared from embryonic days 12, 14, and 18 rat fetuses and maintained for 5, 7 or 14 days in vitro. Inhibition of cell proliferation using cytosine beta-D-arabinofuranoside was conducted in embryonic day 14 ventral mesencephalic cultures. The treatment impaired astrocytic migration at 7 and 14 days in vitro. The reduced migration of astrocytes exerted a negative effect on the glial-associated tyrosine hydroxylase-positive nerve fibers, reducing the outgrowth from the tissue slice. The non-glial-associated outgrowth was, however, positively affected by reduced astrocytic migration, reaching distances around 3mm in 2 weeks, and remained for longer time in culture. Co-cultures of fetal ventral mesencephalon and frontal cortex revealed the cortex as a target for the non-glial-associated tyrosine hydroxylase-positive outgrowth. The age of the fetal tissue at plating affected the astrocytes such that older tissue increased the length of astrocyte migration. Younger tissue at plating promoted the presence of non-glial-associated outgrowth and long radial-glia-like processes, while older tissue promoted migration of neurons instead of formation of nerve fiber network. In conclusion, inhibition of astrocytic proliferation promotes the persistence of long-distance growing tyrosine hydroxylase-positive nerve fibers in ventral mesencephalic slices cultures. Furthermore, the long-distance growing nerve fibers target the frontal cortex and are absent in cultures derived from older tissue.

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Dual effects of TNFα on nerve fiber formation from ventral mesencephalic organotypic tissue cultures

Cited by 11 publications

References 36 publications

Hypothermia‐Induced Neurite Outgrowth is Mediated by Tumor Necrosis Factor‐Alpha

Hypothermia‐Induced Neurite Outgrowth is Mediated by Tumor Necrosis Factor‐Alpha

Acute and subacute IL-1β administrations differentially modulate neuroimmune and neurotrophic systems: possible implications for neuroprotection and neurodegeneration

Inhibition of astrocytes promotes long‐distance growing nerve fibers in ventral mesencephalic cultures

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