MODULATION OF BRAIN INFLAMMATION DURING RABIES INFECTION BY IMMUNOSSUPPRESSIVE TREATMENTS: IONIZING RADIATION, CYCLOSPORINE AND CYCLOPHOSPHAMIDE

International audienceRabies virus is a highly neurotropic agents which invades the central nervous system (CNS) via the anterograde axonal transport. The infection is accompanied by a weak cytopathic effect but induces severe neural dysfunctions. However, the mechanisms that underly rabies pathogenesis are still poorly understood. One of the main features of rabies pathogenesis to be investigated was the central inflammatory reaction and its role in the neural and immune dysfunctions observed during rabies infection. Thus, the present paper will focus on the central nervous system (CNS) inflammation process that follows rabies virus infection, using a mouse model of infection with fixed pathogenic or non-pathogenic rabies virus strains, with emphasis on the effect of different immunosuppressive agents on the course of infection

Enriched but not depleted uranium affects central nervous system in long-term exposed rat

Uranium is well known to induce chemical toxicity in kidneys, but several other target organs, such as central nervous system, could be also affected. Thus in the present study, the effects on sleep-wake cycle and behavior were studied after chronic oral exposure to enriched or depleted uranium. Rats exposed to 4% enriched uranium for 1.5 months through drinking water, accumulated twice as much uranium in some key areas such as the hippocampus, hypothalamus and adrenals than did control rats. This accumulation was correlated with an increase of about 38% of the amount of paradoxical sleep, a reduction of their spatial working memory capacities and an increase in their anxiety. Exposure to depleted uranium for 1.5 months did not induce these effects, suggesting that the radiological activity induces the primary events of these effects of uranium. © 2005 Elsevier Inc. All rights reserved

Changes in sleep-wake cycle after chronic exposure to uranium in rats

International audienceUranium is a heavy metal known to induce toxicity in kidneys. It is also known to enter the central nervous system, thus inducing neurophysiological effects, after exposure to relatively high concentrations. The effect of chronic uranium exposure (40 mg l(-1) in drinking water, for 90 days) on electroencephalographic architecture has been studied on freely moving rats using a telemetry technique. The main effects of uranium on the sleep-wake cycle were an increase in rapid eye movement sleep (REM-sleep) and theta band power during the light period, as early as Day 30 after exposure commenced. The most probable explanation for these effects is that uranium directly affects the brain. This increase in REM-sleep was previously described in human depression or models of chronically stressed rats and it may be assimilated with some protective or compensatory mechanisms

Acute ileal inflammatory cytokine response induced by irradiation is modulated by subdiaphragmatic vagotomy.

International audienceNeural involvement plays a role in the genesis of the peripheral inflammatory process that contributes to the irradiation intestinal disorders. However, little is known about the role of vagus nerve in modulating inflammatory process in rat. Here, we have shown that the NF-kappaB activation was consistent with the acute overexpression of pro-inflammatory cytokines (IL- 1beta, TNF-alpha, IL-6) at 3, 6, and 12 h induced by whole-body irradiation (8 Gy). Subdiaphragmatic vagotomy reduced NF-kappaB activation and cytokine transcription in the early period post-irradiation. In contrast, vagotomy amplified overexpression of irradiation-induced anti-cytokines (IL-10, IL-1Ra) and of receptors involved in anti-inflammatory effects (IL- 1RII, TNFRII). These results show that the vagus nerve is a pro-inflammatory pathway in early irradiation-induced intestinal inflammation