Subdiaphragmatic vagotomy does not block intraperitoneal lipopolysaccharide-induced fever

Hansen, Michael K.; Daniels, Stephanie; Goehler, Lisa E.; Gaykema, Ronald P.; Maier, Steven F.; Watkins, Linda R.

doi:10.1016/s1566-0702(00)00224-1

Cited by 52 publications

(29 citation statements)

References 20 publications

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“…Even after vagotomy, i.p. LPS increases IL-1 levels within the brain (Van Dam et al, 2000) and vagotomy does not attenuate the ability of LPS to increase circulating cytokine levels Hansen et al, 2000). When it was found that circulating cytokines could enter the brain by active transport, that cytokines could be produced at the BBB in response to circulating PAMPs and that cytokines could enter the brain by volume diffusion at the circumventricular organs (Fig.4) (Quan and Banks, 2007) Approximately half recognize viral PAMPs, either lipids or nucleotides.…”

Section: Pathways That Mediate Inflammation-induced Behaviormentioning

confidence: 99%

“…All TLRs shown (TLR10 cooperates with TLR2 to recognize triacylated lipoproteins but does not activate typical TLR signaling) (Guan et al, 2010), except TLR3, directly induce the expression of TNF, IL-1 and IFN whereas TLR3, 4, 7 and 9 activation results primarily in IFN and IFN expression (Hanke and Kielian, 2011 response to i.p. challenges have a humoral component even after vagotomy Hansen et al, 2000). It is clear, however, that all behavioral responses to infection have a cytokine basis, as even i.p.…”

Section: Pathways That Mediate Inflammation-induced Behaviormentioning

confidence: 99%

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Immune–neural connections: how the immune system’s response to infectious agents influences behavior

McCusker

Kelley

2013

Journal of Experimental Biology

354

259

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Sickness and depressionOver the past 30years, it has become clear that the immune system plays a critical role in animal behavior. This role is tightly linked to the obvious role that immune cell activation plays in the clearance of pathogenic organisms. Systemic or central infections elicit a group of symptoms that are necessary for the organism to conserve resources, reorganize priorities and limit the spread of the infection to other members of the community. This sickness behavior is a motivational state that is common to most pathogeninduced infections ranging from viruses to multicellular parasites, but, because of its ubiquitous nature, is frequently accepted as an unavoidable and non-specific consequence of infection. However, considering the broad spectrum of symptoms -fever, nausea, decreased appetite, malaise, fatigue and achiness -it seems clear that a highly organized, although not pathogen-specific, response is being manifested to aid in the fight against infection (Dantzer, 2001;Ericsson et al., 1995).We are all familiar with the human symptoms of sickness but, to investigate changes in behavior associated with sickness, it is critical to have reliable animal measurements that relate to changes in the affective state. Using preclinical animal models, sickness behavior is best evaluated when the test involves a means to assess motivation. Sickness behavior is frequently assessed as social exploration/investigation (in rodent models, this response is frequently reported as a decrease in time actively seeking interaction with a novel animal as a result of diminished motivation for social exploration or neophobia). Social exploration is a naturalistic behavior and all animals have a strong motivation, whether driven by curiosity or sexual desire. With this strong motivational stimulus, infections cause a strong differential between time of exploration of healthy and sick animals, with less time of exploration being observed with sick animals. Another simpler but effective model is exploration of the environment [often referred to as locomotor activity (LMA), representing some level of physical movement in a novel environment such as rearing, quadrant entry, line crossings or total distance traveled; all of which are highly correlated]. LMA is best conducted in a novel environment, as the motivation to explore is stronger in this

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Section: Pathways That Mediate Inflammation-induced Behaviormentioning

confidence: 99%

Section: Pathways That Mediate Inflammation-induced Behaviormentioning

confidence: 99%

Immune–neural connections: how the immune system’s response to infectious agents influences behavior

McCusker

Kelley

2013

Journal of Experimental Biology

354

259

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“…Subdiaphragmatic section of the vagus nerves (Hansen et al, 2000a;Konsman et al, 2000) together with extensive c-Fos imaging (Konsman et al, 2000) have revealed that the vagal sensory pathway along with its primary (NTS) and secondary (extended amygdala and some hypothalamic structures) projection areas are strongly involved in the behavioral responses to cytokines. The transient pattern of c-Fos protein induction that was observed in the present study is in total agreement with the already available data on the mechanisms of action of cytokines in the brain and in particular the normalization of the LPS-induced expression of brain cytokines within a few hours (Laye et al, 1994;Castanon et al, 2004).…”

Section: Lps Induces Delayed Cellular Activities In the Extended Amygmentioning

confidence: 99%

“…We tested this hypothesis by submitting mice to well-accepted tests of depressive-like behavior including the tail suspension test, the forced swim test and the sucrose consumption test (Cryan et al, 2002(Cryan et al, , 2005. At the neuroanatomical level, activation of the peripheral innate immune system has already been shown to induce the expression of cFos in a rapid and transient manner in a number of brain areas that have been proposed to underlie the different behavioral and metabolic components of cytokine-induced sickness behavior (e.g., Hansen et al, 2000a;Konsman et al, 2000). To determine the neuroanatomical substrates of LPS-induced depressive-like behavior, we decided to map the brain distribution of Delta FosB in addition to c-Fos since this truncated splice variant of FosB is characterized by a long half-life leading to its accumulation during repeated or long lasting stimulation (Nestler et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide induces delayed FosB/DeltaFosB immunostaining within the mouse extended amygdala, hippocampus and hypothalamus, that parallel the expression of depressive-like behavior

Frenois

Moreau²,

O’Connor³

et al. 2007

Psychoneuroendocrinology

386

287

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Proinflammatory cytokines induce both sickness behavior and depression, but their respective neurobiological correlates are still poorly understood. The aim of the present study was therefore to identify in mice the neural substrates of sickness and depressive-like behavior induced by lipopolysaccharide (LPS, 830 μg/kg, intraperitoneal). LPS-induced depressive-like behavior was dissociated from LPS-induced sickness by testing mice either at 6 h (at which time sickness was expected to be maximal) or at 24 h post-LPS (at which time sickness was expected to be minimal and not to bias the measurement of depressive-like behavior). Concurrently, the expression of acute and chronic cellular reactivity markers (c-Fos and FosB/ΔFosB respectively) was mapped by immunohistochemistry at these two time points. In comparison to saline, LPS decreased motor activity in a new cage at 6 but not at 24 h. In contrast, the duration of immobility in the tail suspension test was increased at both 6 and 24 h. This dissociation between decreased motor activity and depressive-like behavior was confirmed at 24 h post-LPS in the forced swim test. LPS also decreased sucrose consumption at 24 and 48 h, despite normal food and water consumption by that time. At 24 h post-LPS, LPS-induced depressive-like behavior was associated with a delayed cellular activity (as assessed by FosB/ΔFosB immunostaining) in specific brain structures, particularly within the extended amygdala, hippocampus and hypothalamus, whereas c-Fos labeling was markedly decreased by that time in all the brain areas at 6 h post-LPS. These results provide the first evidence in favor of a functional dissociation between the brain structures that underlie cytokine-induced sickness behavior and cytokine-induced depressive-like behavior, and provide important cues about the neuroanatomical brain circuits through which cytokines could have an impact on affect.

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“…Vagal afferent fibers have been previously suggested to mediate part of the neuroimmune response to low doses of LPS (Romanovsky et al, 1997a;Hansen et al, 2000a;Konsman et al, 2000;Hosoi et al, 2005), but direct or indirect (Visintin et al, 2001;Zarember and Godowski, 2002;Hosoi et al, 2005;Perlik et al, 2005) stimulation of TLR4s to activate vagal afferents does not appear to be involved in the programming response. There was no evidence for early activation of the NTS where vagal afferents terminate, nor did hepatic vagotomy reduce the early corticosterone surge in the postnatal LPS-treated adult.…”

Section: Mediators Of Increased Hpa Axis Activitymentioning

confidence: 99%

Early Life Activation of Toll-Like Receptor 4 Reprograms Neural Anti-Inflammatory Pathways

Mouihate¹,

Galic²,

Ellis³

et al. 2010

Journal of Neuroscience

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A single postnatal exposure to the bacterial endotoxin, lipopolysaccharide (LPS), reduces the neuroimmune response to a subsequent LPS exposure in the adult rat. The attenuated fever and proinflammatory response is caused by a paradoxical, amplified, early corticosterone response to LPS. Here we identify the mechanisms underlying the heightened corticosterone response to LPS in adults after early life exposure to LPS. In postnatal LPS-treated rats, hypothalamic corticotrophin-releasing hormone mRNA, pituitary proopiomelanocortin mRNA, and circulating adrenocorticotrophic hormone were all increased after adult exposure to LPS without significant modification to hippocampal or hypothalamic glucocorticoid receptor mRNA or protein or vagally mediated afferent signaling to the brain. Postnatal LPS administration did cause a persistent upregulation of the LPS Toll-like receptor-4 (TLR4) mRNA in liver and spleen, but not in brain, pituitary, or adrenal gland. In addition, cyclooxygenase-2 (COX-2), which is a prostaglandin biosynthetic enzyme and is normally undetectable in most peripheral tissue, was constitutively expressed in the liver. Adult immune activation of the upregulated TLR4 and COX-2 caused a rapid, amplified rise in circulating, but not brain, prostaglandin E 2 that induced an early, enhanced activation of the hypothalamic-pituitary-adrenal (HPA) axis. Thus, postnatal LPS reprograms the neuroimmune axis by priming peripheral tissues to create a novel, prostaglandin-mediated activation of the HPA axis brought about by increased constitutive expression of TLR4 and COX-2.

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Subdiaphragmatic vagotomy does not block intraperitoneal lipopolysaccharide-induced fever

Cited by 52 publications

References 20 publications

Immune–neural connections: how the immune system’s response to infectious agents influences behavior

Immune–neural connections: how the immune system’s response to infectious agents influences behavior

Lipopolysaccharide induces delayed FosB/DeltaFosB immunostaining within the mouse extended amygdala, hippocampus and hypothalamus, that parallel the expression of depressive-like behavior

Early Life Activation of Toll-Like Receptor 4 Reprograms Neural Anti-Inflammatory Pathways

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