Time-dependent sensitization of corticotropin-releasing hormone, arginine vasopressin and c-fos immunoreactivity within the mouse brain in response to tumor necrosis factor-α
Section snippets
Experimental procedures
Adult male CD-1 mice (3–4 months of age), obtained from Charles River Inc. (Laprairie, QC, Canada) were housed in groups of four in standard propylene cages. After arrival, mice were given at least 2 weeks to acclimate to the laboratory. Animals were maintained on a 12-h light–dark cycle (lights on 08.00–20.00 h), and all experimental procedures were conducted between 09.00 h and 12.00 h in order to avoid variations due to diurnal rhythms. An ad libitum diet of Ralston Purina (St. Louis, MO,
Results
At the time of killing, mice acutely treated with TNF-α showed few signs of illness. However, as we previously observed (Hayley et al., 1999), mice re-exposed to TNF-α 14 or 28 days following initial exposure to this cytokine generally displayed marked sickness, characterized by reduced motor activity and social exploration, curled body posture, piloerection, and ptosis. In addition, mice showed clear signs of cyanosis of the ears, nose and tail, and hypovolemia reflected by a pronounced
Median eminence colocalization of AVP and CRH
Over time following acute stressor or IL-1β treatment, phenotypic changes occur within CRH neurons terminating in the external zone of the median eminence, such that AVP and CRH expression increases (Schmidt et al., 1995). In the present investigation, a single dose of TNF-α likewise provoked a time-dependent shift towards increased AVP/CRH co-immunoreactive terminals within this site, largely attributable to increased AVP within CRH terminals. This effect peaked 7–14 days following cytokine
Acknowledgements
This research was supported by Grant MT-13124 from the Medical Research Council of Canada. H.A. is an Ontario Mental Health Senior Research Fellow and S.H. was supported by a scholarship from the Canadian Institutes of Health Research. The technical assistance of Babben Tinner, Amy Peaire and Dr. Jerzy Kulczyski is greatly appreciated.
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Comparison of CRF-immunoreactive neurons distribution in mouse and rat brains and selective induction of Fos in rat hypothalamic CRF neurons by abdominal surgery
2011, Brain ResearchCitation Excerpt :CRF-ir fibers in naïve mice were prominent in the median eminence, BST and CeA and moderately stained in the medial preoptic area and several midbrain nuclei while observed less in the pontine and medullary nuclei except the medial parabrachial nucleus, ventrolateral medulla and inferior olivary nuclei. These data expand previous reports in mice focused on individual brain nuclei detecting the presence of CRF immunoreactivity in fibers and/or cell bodies in the median eminence (Hayley et al., 2001), PVN (Westberg et al., 2009; Workman et al., 2008), BST, CeA (Asan et al., 2005; Costine et al., 2010), LPB or medial vestibular nucleus (Westberg et al., 2009). In addition, the locations of CRF-ir neurons overlap mostly with areas containing CRF mRNA in wild type mice and CRF-green fluorescent protein transgenic mice (Alon et al., 2009).
Interferon-gamma deficiency modifies the effects of a chronic stressor in mice: Implications for psychological pathology
2010, Brain, Behavior, and ImmunityCitation Excerpt :For instance, among cancer and hepatitis C patients, immunotherapeutic application of the pro-inflammatory cytokine, interferon-alpha (IFN-α), provoked a depression-like syndrome amenable to antidepressant treatment (Capuron et al., 2001; Musselman et al., 2001; Raison et al., 2005). Additionally, members of the interleukin family of cytokines, including IL-1β, IL-6 and IL-2 (and their respective soluble receptors), as well as the pro-inflammatory cytokine, tumor necrosis factor-alpha (TNF-α), promote anxiety- and depressive-like pathology in rodents (Hayley et al., 2001, 2005; Anisman et al., 2008b). Importantly, stressors can elevate peripheral and central cytokine expression (Anisman et al., 2005; Buchanan et al., 2008), and pro-inflammatory cytokines, such as IL-1β, contribute to or exacerbate the behavioral and neurochemical effects of psychological stressors (Gibb et al., 2008; Goshen et al., 2008).
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2008, Journal of Psychiatric ResearchCitation Excerpt :This effect was proposed to be mediated by neuroendocrine and neurotransmitter systems involved in vulnerability to affective disorders (Maes, 1999). In this respect it has been demonstrated that IL-1β and TNF-α stimulate the expression/release of corticotrophin-releasing hormone (CRH) in the paraventricular nucleus (PVN) of the hypothalamus (Hayley et al., 2001; Tilders and Schmidt, 1998), the control center of the HPA axis and alters the turnover of norepinephrine and serotonin (5-HT) in the hypothalamus, amygdala, prefrontal cortex, and hippocampus (Ando and Dunn, 1999; Brebner et al., 2000; Dunn et al., 1999; Hayley et al., 1999). Further evidence for the role of pro-inflammatory cytokines in depression was gathered from studies with TNF receptors (TNFR) knock-out mice, in which it was shown that both TNFR1−/− and TNFR2−/− mice were more active in the FST than wild-type animals (Simen et al., 2006).