Effects of chronic intrahippocampal infusion of lipopolysaccharide in the rat

Szczepanik, Ann Marie; Fishkin, R.J.; Rush, Douglas K.; Wilmot, Carly

doi:10.1016/0306-4522(95)00296-u

Cited by 37 publications

(23 citation statements)

References 42 publications

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“…The kinetics of the inflammatory reaction following intracerebral LPS infusion have been previously described in murine (Andersson et al,l992b) and rat (Bourdiol et al, 1991;Montero-Menei et al, 1994Szczepanik et al, 1996) CNS. Similarly, the aim of our study was to determine whether glial activation by a single LPS injection into the SN could have any effect on the viability of the dopaminergic neurons in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…Taking into account that intracerebral injection of LPS activates glial cells in vivo (Bourdiol et al, 1991;Andersson et al, 1992b;Montero-Menei et al, 1994Szczepanik at al., 1996) and that, recently, in vitro studies (Bronstein et al, 1995) have described that dopaminergic neurons were twice as sensitive to the toxic effects of LPS as were tyrosine hydroxylase (TH)-negative neurons, we consider that LPS provides an interesting model to study the re-sponse of the dopaminergic system to inflammation and to help clarify how brain cells can be involved in neurotoxic processes.…”

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confidence: 99%

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Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

Castaño

Herrera

Cano

et al. 1998

Journal of Neurochemistry

365

270

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Abstract:The pathogenesis of Parkinson's disease is still poorly understood. To address the hypothesis that immunemediated events, such as microglial activation, may be involved in the dopaminergic neurodegeneration, we have studied the effect that intranigral injection of the immunostimulant lipopolysaccharide has on monoaminergic neurotransmitters in rats. Activation of microglial cells, visualized by immunohistochemistry with a specific monoclonal antibody, was already obvious 2 days after injection. In relation to the biochemical parameters studied, we found a significant decrease of dopamine levels in both the substantia nigra and striatum up to at least 21 days after intranigral injection of lipopolysaccharide. This result was supported by the decrease in tyrosine hydroxylase activity and the loss of tyrosine hydroxylase-positive neuronal bodies, shown by immunohistochemistry. These alterations of the dopaminergic system did not reverse during the interval studied (21 days); conversely, the serotoninergic system suffered only transient damage. In addition, we found that the neurotoxic effect of lipopolysaccharide was not mediated by nitric oxide. Based on our results we suggest that the nigrostriatal dopaminergic system is susceptible to damage by inf lammatory events and that these may be implicated in neurodegeneration processes such as Parkinson's disease.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

Castaño

Herrera

Cano

et al. 1998

Journal of Neurochemistry

365

270

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show abstract

“…Intrahippocampal LPS injections enhanced ␤-amyloid clearance in aged transgenic mice that develop Alzheimer's disease-like pathology (DiCarlo et al, 2001;Malm et al, 2005), although contradictory results were obtained in younger mice (Qiao et al, 2001). In contrast, direct injection of TLR ligands into the healthy brain or spinal cord induced robust inflammation that caused tissue damage and, in some cases, behavioral deficits (Szczepanik et al, 1996;Fitch et al, 1999;Popovich et al, 2002). TLR4 and TLR9 ligands may mediate neuronal and oligodendrocyte injury indirectly, via effects on microglia (Lehnardt et al, 2002(Lehnardt et al, , 2003Iliev et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Toll-Like Receptor 2 Signaling in Response to Brain Injury: An Innate Bridge to Neuroinflammation

Babcock

Wirenfeldt²,

Holm³

et al. 2006

J. Neurosci.

177

179

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Reactive gliosis is a prominent feature of neurodegenerative and neuroinflammatory disease in the CNS, yet the stimuli that drive this response are not known. There is growing appreciation that signaling through Toll-like receptors (TLRs), which is key to generating innate responses to infection, may have pathogen-independent roles. We show that TLR2 was selectively upregulated by microglia in the denervated zones of the hippocampus in response to stereotactic transection of axons in the entorhinal cortex. In mice lacking TLR2, there were transient, selective reductions in lesion-induced expression of cytokines and chemokines. Recruitment of T cells, but not macrophages, was delayed in TLR2-deficient mice, as well as in mice lacking TNFR1 (tumor necrosis factor receptor 1). TLR2 deficiency also affected microglial proliferative expansion, whereas all of these events were unaffected in TLR4-mutant mice. Consistent with the fact that responses in knock-out mice had all returned to wild-type levels by 8 d, there was no evidence for effects on neuronal plasticity at 20 d. These results identify a role for TLR2 signaling in the early glial response to brain injury, acting as an innate bridge to neuroinflammation.

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“…Administration of the TLR 2 ligand zymosan promoted regeneration after optic nerve crush injury [16], and systemic injection of the TLR 4 ligand -LPS accelerated myelin clearance in the injured spinal cord [30]. Direct injection of TLR ligands into the healthy brain or spinal cord induced robust inflammation that caused tissue damage [11,24].…”

Section: O -Lack Of Antigen In Tissue Sections; + -< 10%; ++ -25-40%;mentioning

confidence: 99%

Original article Toll-like receptors as an innate immunity bridge to neuroinflammation in medulloblastoma

Maślińska¹,

Laure‐Kamionowska²,

Maślinska³

2012

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Effects of chronic intrahippocampal infusion of lipopolysaccharide in the rat

Cited by 37 publications

References 42 publications

Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

Toll-Like Receptor 2 Signaling in Response to Brain Injury: An Innate Bridge to Neuroinflammation

Original article Toll-like receptors as an innate immunity bridge to neuroinflammation in medulloblastoma

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