Pyrogens Specifically Disrupt the Acquisition of a Task Involving Cognitive Processing in the Rat

Aubert, Arnaud; Vega, Carolina; Dantzer, Robert; Goodall, Glyn

doi:10.1006/brbi.1995.1013

Cited by 108 publications

(48 citation statements)

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“…By using later time points for treatment (after the acquisition phase) in the matching-to-place version of the task, we were able to demonstrate that LPS is capable of disrupting cognitive performance independent of generalized effects on memory consolidation. We do not expect that LPS disrupts the retrieval of previously learned information, because LPS has not been shown to disrupt behavior in a previously learned task (Aubert et al, 1995;Sparkman et al, 2005a). We suggest that LPS-treated animals demonstrate an inability to effectively incorporate the new platform position into the old schema.…”

Section: Discussionmentioning

confidence: 85%

Interleukin-6 Facilitates Lipopolysaccharide-Induced Disruption in Working Memory and Expression of Other Proinflammatory Cytokines in Hippocampal Neuronal Cell Layers

et al. 2006

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Proinflammatory cytokines inhibit learning and memory but the significance of interleukin-6 (IL-6) in acute cognitive deficits induced by the peripheral innate immune system is not known. To examine the functional role of IL-6 in hippocampus-mediated cognitive impairments associated with peripheral infections, C57BL6/J (IL-6 ϩ/ϩ ) and IL-6 knock-out (IL-6 Ϫ/Ϫ ) mice were trained in a matching-to-place version of the water maze. After an acquisition phase, IL-6 ϩ/ϩ mice injected intraperitoneally with lipopolysaccharide (LPS) exhibited deficits in working memory. However, IL-6 Ϫ/Ϫ mice were refractory to the LPS-induced impairment in working memory. To determine the mechanism by which IL-6 deficiency conferred protection from disruption in working memory, plasma IL-1␤ and tumor necrosis factor ␣ (TNF␣), c-Fos immunoreactivity in the nucleus of the solitary tract (NTS), and steady-state levels of IL-1␤ and TNF␣ mRNA in neuronal layers of the hippocampus were determined in IL-6 ϩ/ϩ and IL-6 Ϫ/Ϫ mice after injection of LPS. Plasma IL-1␤ and TNF␣ and c-Fos immunoreactivity in the NTS were increased similarly in IL-6 ϩ/ϩ and IL-6 Ϫ/Ϫ mice after LPS, indicating high circulating levels of IL-1␤ and TNF␣ and activation of vagal afferent pathways were not sufficient to disrupt working memory in the absence of IL-6. However, the LPS-induced upregulation of IL-1␤ and TNF␣ mRNA that was evident in hippocampal tissue of IL-6 ϩ/ϩ mice was greatly attenuated or entirely absent in IL-6 Ϫ/Ϫ mice. Collectively, these data suggest that humoral and neural immune-to-brain communication pathways are intact in IL-6-deficient mice but that, in the absence of IL-6, the central cytokine compartment is hyporesponsive.

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Section: Discussionmentioning

confidence: 85%

Interleukin-6 Facilitates Lipopolysaccharide-Induced Disruption in Working Memory and Expression of Other Proinflammatory Cytokines in Hippocampal Neuronal Cell Layers

et al. 2006

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“…In an autoshaping task, rats injected with IL-1 (4 g, i.p.) show learning impairment, compared with the salineinjected controls [31] . In the three-panel runway task, intrahippocampal injection of IL-1 (32 and 100 ng/side, but not 10 ng/side) is shown to impair the working memory of rats [32,33] .…”

Section: Introductionmentioning

confidence: 81%

Interleukin-1β with learning and memory

Huang

Sheng²

2010

Neurosci. Bull.

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Abstract:Interleukin-1 (IL-1) is one of the first cytokines ever described. It has long been recognized to play an important role in mediating inflammation and orchestrating the physiological and behavioral adjustments that occur during sickness.Recently, accumulating evidence has indicated that IL-1 also adversely affects cognitive function. Nevertheless, there are also some reports showing no effects or even beneficial effects of IL-1 on learning and memory. The relationship between IL-1 and cognitive impairment has not been clearly elucidated. Here we reviewed the evidence of both negative and positive effects of IL-1 on learning and memory, and the key factors that may affect the effects of IL-1 on learning and memory were discussed.

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“…It was reported that IL-1R1 knockout mice display slower rate of learning in the spatial memory paradigm and impaired short-term and long-term plasticity in the hippocampus (Avital et al, 2003). On the other hand, administration of IL-1 produces detrimental effects on learning and memory processes (Oitzl et al, 1993;Gibertini et al, 1995;Aubert et al, 1995;Pugh et al, 1999) and inhibits long-term potentiation (Katsuki et al, 1990;Bellinger et al, 1993;Cunningham et al, 1996;O'Connor and Coogan, 1999;Vereker et al, 2000) though the mechanisms are largely unknown. Maternal infection is proposed to cause cytokine imbalance in fetal brain as well as maternal serum and alter fetal development and subsequent behavior and/or cognitive function in the offspring (Deverman and Patterson, 2009;Patterson, 2009).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-1 Receptor Accessory Protein Organizes Neuronal Synaptogenesis as a Cell Adhesion Molecule

et al. 2012

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Pyrogens Specifically Disrupt the Acquisition of a Task Involving Cognitive Processing in the Rat

Cited by 108 publications

References 0 publications

Interleukin-6 Facilitates Lipopolysaccharide-Induced Disruption in Working Memory and Expression of Other Proinflammatory Cytokines in Hippocampal Neuronal Cell Layers

Interleukin-6 Facilitates Lipopolysaccharide-Induced Disruption in Working Memory and Expression of Other Proinflammatory Cytokines in Hippocampal Neuronal Cell Layers

Interleukin-1β with learning and memory

Interleukin-1 Receptor Accessory Protein Organizes Neuronal Synaptogenesis as a Cell Adhesion Molecule

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