The influence of restraint stress on the expression of mRNAs for IL-6 and the IL-6 receptor in the hypothalamus and midbrain of the rat

Shizuya, Koji; Komori, Teruhisa; Fujiwara, Ryoichi; Miyahara, Satoru; Ohmori, Masaki; Nomura, Junichi

doi:10.1016/s0024-3205(97)00608-5

Cited by 52 publications

(29 citation statements)

References 14 publications

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“…Stress not only can increase cytokine levels (Black, 2002;Deak et al, 2005;Minami et al, 1991;Nguyen et al, 1998;O'Connor et al, 2003;Shintani et al, 1995a, b;Shizuya et al, 1997;Suzuki et al, 1997) but also can augment the effects of a subsequent increase in cytokines by LPS or stress (Johnson et al, 2004;Munhoz et al, 2006;Takemura et al, 1997). These findings led to the hypothesis that cytokines are involved in depressive illness (Anisman and Merali, 2003;Dunn et al, 2005;Hayley et al, 2005;Raison et al, 2006;Simen et al, 2006) and addictive behavior (Crews et al, 2006;Friedman and Eisenstein, 2004).…”

Section: Discussionmentioning

confidence: 99%

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Breese

Knapp

Overstreet

et al. 2007

Neuropsychopharmacol

100

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Previous investigations demonstrated that repeated stresses before an ethanol exposure sensitize ethanol withdrawal-induced anxietylike behavior ('anxiety'). In addition to activating the hypothalamic-pituitary-adrenal axis, acute stress also elevates cytokines in brain. Initially, to test possible cytokine involvement in this stress/withdrawal protocol, cytokines were increased in brain with 2 weekly repeated lipopolysaccharide (LPS) administrations (1000 m/kg) (LPS/withdrawal protocol) or with twice weekly intracerebroventricular (i.c.v.) administrations of the cytokines IL-1b, CCL2 (MCP-1) or TNFa (cytokine/withdrawal protocol) before exposure and withdrawal from a 5-day cycle of chronic ethanol diet. Both protocols sensitized withdrawal-induced anxiety and confirm cytokine involvement in the sensitized anxiety response. Testing of various doses of LPS (16-1000 mg/kg) and TNFa (3-100 ng, i.c.v.) demonstrated the dose-related nature of these protocols to sensitize withdrawal-induced anxiety. The sensitized anxiety was not produced by a single 5-day ethanol diet cycle or by repeated LPS or cytokine treatments alone. Likewise, sensitized anxiety in these protocols could not be attributed to differences in ethanol ingestion. When challenged with a subsequent re-exposure to a 5-day ethanol diet cycle 16 days after completion of the LPS/withdrawal or cytokine/withdrawal protocols, an increase in withdrawal-induced anxiety was observedFan indication of induction of an underlying persistent adaptive change. Finally, just as found previously with the stress/withdrawal protocol, administration of the benzodiazepine receptor antagonist flumazenil before the LPS or TNF treatments prevented anxiety sensitization. Together, these findings indicate that increased cytokine activity induces adaptive change that supports sensitization of ethanol withdrawal-induced anxiety that may be linked to GABA A -receptor function.

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Section: Discussionmentioning

confidence: 99%

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Breese

Knapp

Overstreet

et al. 2007

Neuropsychopharmacol

100

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“…31,32 We observed that the basal level of TNF-␣ in plasma was markedly elevated in aged mice and obese mice, 33 as well as substantial increases in the plasma level of TNF-␣ antigen, which may be inducibly produced by adipose tissues, 33,34 after 20 hours of restraint stress in these mice (Figure 8). TNF-␣ promotes a hypercoagulable state because this cytokine was shown experimentally to increase TF expression 35 by activation of AP-1 and NF-B sites.…”

Section: Discussionmentioning

confidence: 86%

Aging and obesity augment the stress-induced expression of tissue factor gene in the mouse

Yamamoto

Shimokawa

et al. 2002

Blood

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“…In addition, our results demonstrate that the stress-induced plasma IL-6 elevation lags behind the plasma ACTH elevation. Now there is overwhelming evidence that IL-1 and IL-6 are synthesized within the brain and that their synthesis increases in a variety of central nervous system pathologies including stress [22][23][24]. The above findings thus suggest that these cytokines are produced in the brain, but not in the periphery, and thus may mainly react to activate the HPA axis when animals are exposed to restraint stress.…”

Section: Discussionmentioning

confidence: 96%

The Restraint Stress-Induced Elevation in Plasma Interleukin-6 Negatively Regulates the Plasma TNF-α Level

Nukina

Sudo²,

Kobashi

et al. 1998

Neuroimmunomodulation

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Although a considerable amount of evidence has shown that physical and psychological stress elevates the plasma interleukin 6 (IL-6) levels, the physiological significance of such an elevation remains to be elucidated. In this study, in order to determine whether the restraint stress-induced elevation of plasma IL-6 contributes to the activation of the hypothalamic-pituitary-adrenal axis, and whether or not such elevation can affect the inflammatory processes, the plasma levels of ACTH, corticosterone, interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α) in mice pretreated with anti-IL-6 antibody (MP5-20F3 monoclonal antibody) were compared with those in mice pretreated with rat IgG (control antibody) both during and after stress. Both the anti-IL-6-antibody- and control-antibody-pretreated mice showed the same extent of plasma ACTH and corticosterone increases during stress, and no significant difference was found between the two groups of animals. On the other hand, the level of plasma TNF-α in the anti-IL-6-treated animals was also significantly higher than that in the control animals both immediately after cessation of stress and 60 min after the cessation of the 120-min period of restraint. Plasma IL-1 activity, however, did not reach a detectable level in either group of animals at any time point examined. These results thus indicate that the restraint-stress-induced elevation of plasma IL-6 negatively regulates the plasma TNF-α levels and may thus contribute to the maintenance of homeostasis.

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The influence of restraint stress on the expression of mRNAs for IL-6 and the IL-6 receptor in the hypothalamus and midbrain of the rat

Cited by 52 publications

References 14 publications

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Aging and obesity augment the stress-induced expression of tissue factor gene in the mouse

The Restraint Stress-Induced Elevation in Plasma Interleukin-6 Negatively Regulates the Plasma TNF-α Level

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