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A degree of brain inflammation is required for repair of damaged tissue, but excessive inflammation causes neuronal cell death. Here, we observe that IL-10 is expressed in LPS-injected rat cerebral cortex, contributing to neuronal survival. Cells immunopositive for IL-10 were detected as early as 8 h post-injection and persisted for up to 3 d, in parallel(More)
Present study demonstrated that fibrillar β-amyloid peptide (fAβ 1-42) induced ATP release, which in turn activated NADPH oxidase via the P2X 7 receptor (P2X 7 R). Reactive oxygen species (ROS) production in fAβ1-42-treated microglia appeared to require Ca 2+ influx from extracellular sources, because ROS generation was abolished to control levels in the(More)
Previously we demonstrated that ATP released from LPS-activated microglia induced IL-10 expression in a process involving P2 receptors, in an autocrine fashion. Therefore, in the present study we sought to determine which subtype of P2 receptor was responsible for the modulation of IL-10 expression in ATP-stimulated microglia. We found that the patterns of(More)
Recent studies have reported that the " cholinergic anti-inflammatory pathway " regulates peripheral in-flammatory responses via α 7 nicotinic acetylcholine receptors (α 7 nAChRs) and that acetylcholine and nicotine regulate the expression of proinflammatory mediators such as TNF-α and prostaglandin E 2 in micro-glial cultures. In a previous study we showed(More)
The formation of glial scars impedes growth of regenerating axons after CNS injuries such as spinal cord injury (SCI). Hepatocyte growth factor (HGF), originally identified as a mitogen for hepatocytes, exerts pleiotropic functions in the nervous system. HGF has been implicated in peripheral wound healing via regulation of the transforming growth factor(More)
Recent studies have reported that the cholinergic anti-inflammatory pathway regulates peripheral inflammatory responses via alpha7 nicotinic acetylcholine receptors (alpha7 nAChRs) and that acetylcholine and nicotine regulate the expression of proinflammatory mediators such as TNF-alpha and prostaglandin E2 in microglial cultures. In a previous study we(More)
The possibility that P2X₇ receptor (P2X₇R) expression in microglia would mediate neuronal damage via reactive oxygen species (ROS) production was examined in the APPswe/PS1dE9 mouse model of Alzheimer's disease (AD). P2X7R was predominantly expressed in CD11b-immunopositive microglia from 3 months of age before Abeta plaque formation. In addition, gp91phox,(More)
We investigated the distribution of calcium/calmodulin-dependent protein kinase II (CaM kinase II) in the brains of mice infected with ME7 scrapie strain. CaM kinase II is an enzyme that plays a major role in the regulation of long-term potentiation, a form of synaptic plasticity associated with learning and memory. Immunoreactivity of CaM kinase II alpha,(More)
The possibility that P2X7 receptor (P2X7R) expression in microglia would mediate neuronal damage via re-active oxygen species (ROS) production was examined in the APPswe/PS1dE9 mouse model of Alzheim-er's disease (AD). P2X 7 R was predominantly expressed in CD11b-immunopositive microglia from 3 months of age before Aβ plaque formation. In addition, gp91(More)
Doppel protein (Dpl) is a paralog of the cellular form of prion protein (PrP(C)). Its ectopic expression in the CNS elicits significant cerebellar Purkinje cell degeneration in some lines of PrP knockout mice. However, little is known about the Dpl-mediated neurodegenerative mechanism. To understand the molecular and intracellular pathways underlying(More)
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