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Circumventricular organs of rats that experimental hydrocephalus and subarachnoidal hemorrhage carried out: an anaglyphic SEM study  [PDF]
Tatar I,Akpinar G,Acikgoz B,Tunali S
Neuroanatomy , 2004,
Abstract: It is known that circumventricular organs that are located around the ventricular system ofthe brain are lack of blood-brain barrier and support the body water-salt balance. They alsoeffect many physiological events such as some neuroendocrine and reproduction mechanisms.In different pathological conditions their results and the step in which the circumventricularorgans are affected are unknown. Although circumventricular organs do not have a bloodbrainbarrier, they do not completely show the same characteristics.In pathological conditions they show their own effects by means of mediators. It is necessaryto research their structural changes, also the changes in the neurotransmitters that areaffected by circumventricular organs.Hydrocephalus was induced in rats by injecting kaolin into the subarachnoidal space at thecranial convexity. Subarachnoidal hemorrhage was realized with a puncture of the basilarartery through transclival route. We took and studied images using a JEOL SEM ASID-10(Japan) electron microscope. We examined slices of subfornical organ, organum vasculosum,lamina terminalis, area postrema and median eminence.The purpose of this study is to view three-dimensional scanning electron microscopicimages of the circumventricular organs using the anaglyph technique that records images asstereopairs (converted as a red-blue images and viewed with special glasses).
Hypertension effects on p73 expression in the rat circumventricular organs and cerebrospinal fluid  [PDF]
Emilia M. Carmona-Calero, Ibrahim González-Marrero, Manuela Casta?eyra-Martin, Juan M. González-Toledo, Leandro Casta?eyra-Ruiz, Héctor de Paz-Carmona, Agustín Casta?eyra-Ruiz, Lidia Ruiz-Mayor, Agustín Casta?eyra-Perdomo
World Journal of Neuroscience (WJNS) , 2012, DOI: 10.4236/wjns.2012.22010
Abstract: It has been reported that spontaneously hypertensive rats (SHR) show ventricular dilation, changes in CSF proteins and variations in the circumventricular organs (CVO) such as: the subcommissural organ (SCO), the subfornical organ (SFO) and the area postrema (AP) which are located in the walls of the third and fourth ventricles. On the other hand, p73 proteins are present in cells of the central nervous system (CNS) such as circumventricular structures and the neuroepithelium which are altered in ventricular dilation. The purpose of the present work is to study the TAp73 isoform expression in the circumventricular organs (CVO) and their variations in ventricular dilatation and arterial hypertension. Brains and cerebrospinal fluid (CSF) from control Wistar-Kyoto rats (WKY) and SHR were used. The paraffin sections containing the CVO were immunohistochemically proc-essed with anti-TAp73 and by western blot, p73 bands in the CSF and circumventricular organ extract were also identified. The western blot study showed bands marked with p73 in the CSF and CVO, the p73 band expression was bigger in the SHR than in the WKY rats. We also found stronger markings in the SFO, SCO and AP of the hypertensive rats than in the WKY rats. It could be concluded that hypertension in the SHR produces altera-tions in the relationship between the p73 protein, circumventricular structures and CSF.
Roles and Mechanism of Interleukin-1 on Sickness Behavior

Yang Hongyu,Lin Wenjuan,

心理科学进展 , 2004,
Abstract: Interleukin-1 is a key molecular factor involved in the process of brain-immune interactions. Many stressful stimuli may increase IL-1 bioactivity, and administering IL-1 produces sickness behavior. Peripherally released IL-1 acts on the brain via a fast transmission pathway involving primary afferent nerve innervating the bodily site of inflammation and a slow transmission pathway involving slowly diffusing IL-1 from the circumventricular organs and choroids plexus to brain targets.
The circumventricular organs participate in the immunopathogenesis of experimental autoimmune encephalomyelitis
Martina Schulz, Britta Engelhardt
Fluids and Barriers of the CNS , 2005, DOI: 10.1186/1743-8454-2-8
Abstract: We performed an extensive immunohistological study on the area postrema (AP), the subfornical organ (SFO), the organum vasculosum of the lamina terminalis (OVLT) and the median eminence (ME) in frozen brain sections from healthy SJL mice and mice suffering from EAE. Expression of cell adhesion molecules, the presence of leukocyte subpopulations and the detection of major histocompatibility complex antigen expression was compared.Similar changes were observed for all four CVOs included in this study. During EAE significantly increased numbers of CD45+ leukocytes were detected within the four CVOs investigated, the majority of which stained positive for the macrophage markers F4/80 and Mac-1. The adhesion molecules ICAM-1 and VCAM-1 were upregulated on the fenestrated capillaries within the CVOs. A considerable upregulation of MHC class I throughout the CVOs and positive immunostaining for MHC class II on perivascular cells additionally documented the immune activation of the CVOs during EAE. A significant enrichment of inflammatory infiltrates was observed in close vicinity to the CVOs.Our data indicate that the CVOs are a site for the entry of immune cells into the CNS and CSF and consequently are involved in the inflammatory process in the CNS during EAE.In multiple sclerosis and in its animal model, experimental autoimmune encephalomyelitis (EAE), inflammatory cells obtain access to the central nervous system (CNS) parenchyma and the cerebrospinal fluid (CSF) and initiate the events leading to signs of paralysis. The endothelial blood-brain barrier (BBB) has been considered the obvious place for entry for circulating lymphocytes into the CNS. Therefore most investigations have focused on defining the molecular mechanisms involved in leukocyte recruitment from the circulating blood across the endothelial BBB. The adhesion molecules, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), both members of the immunoglobulin superfam
Minocycline attenuates lipopolysaccharide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia
Christopher J Henry, Yan Huang, Angela Wynne, Mark Hanke, Justin Himler, Michael T Bailey, John F Sheridan, Jonathan P Godbout
Journal of Neuroinflammation , 2008, DOI: 10.1186/1742-2094-5-15
Abstract: In the first set of experiments the effect of minocycline pretreatment on LPS-induced microglia activation was assessed in BV-2 microglia cell cultures. In the second study, adult (3–6 m) BALB/c mice received an intraperitoneal (i.p.) injection of vehicle or minocycline (50 mg/kg) for three consecutive days. On the third day, mice were also injected (i.p.) with saline or Escherichia coli LPS (0.33 mg/kg) and behavior (i.e., sickness and anhedonia) and markers of neuroinflammation (i.e., microglia activation and inflammatory cytokines) were determined. In the final study, adult and aged BALB/c mice were treated with the same minocycline and LPS injection regimen and markers of neuroinflammation were determined. All data were analyzed using Statistical Analysis Systems General Linear Model procedures and were subjected to one-, two-, or three-way ANOVA to determine significant main effects and interactions.Minocycline blocked LPS-stimulated inflammatory cytokine secretion in the BV-2 microglia-derived cell line and reduced LPS-induced Toll-like-receptor-2 (TLR2) surface expression on brain microglia. Moreover, minocycline facilitated the recovery from sickness behavior (i.e., anorexia, weight loss, and social withdrawal) and prevented anhedonia in adult mice challenged with LPS. Furthermore, the minocycline associated recovery from LPS-induced sickness behavior was paralleled by reduced mRNA levels of Interleukin (IL)-1β, IL-6, and indoleamine 2, 3 dioxygenase (IDO) in the cortex and hippocampus. Finally, in aged mice, where exaggerated neuroinflammation was elicited by LPS, minocycline pretreatment was still effective in markedly reducing mRNA levels of IL-1β, TLR2 and IDO in the hippocampus.These data indicate that minocycline mitigates neuroinflammation in the adult and aged brain and modulates the cytokine-associated changes in motivation and behavior.The bi-directional communication between the immune system and the central nervous system (CNS) is necessary for m
Gadofluorine M-enhanced MRI shows involvement of circumventricular organs in neuroinflammation
Eva Wuerfel, Carmen Infante-Duarte, Robert Glumm, Jens T Wuerfel
Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-70
Abstract: In a longitudinal study we investigated in vivo alterations of CVO during neuroinflammation, applying Gadofluorine M- (Gf) enhanced magnetic resonance imaging (MRI) in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. SJL/J mice were monitored by Gadopentate dimeglumine- (Gd-DTPA) and Gf-enhanced MRI after adoptive transfer of proteolipid-protein-specific T cells. Mean Gf intensity ratios were calculated individually for different CVO and correlated to the clinical disease course. Subsequently, the tissue distribution of fluorescence-labeled Gf as well as the extent of cellular inflammation was assessed in corresponding histological slices.We could show that the Gf signal intensity of the choroid plexus, the subfornicular organ and the area postrema increased significantly during experimental autoimmune encephalomyelitis, correlating with (1) disease severity and (2) the delay of disease onset after immunization. For the choroid plexus, the extent of Gf enhancement served as a diagnostic criterion to distinguish between diseased and healthy control mice with a sensitivity of 89% and a specificity of 80%. Furthermore, Gf improved the detection of lesions, being particularly sensitive to optic neuritis. In correlated histological slices, Gf initially accumulated in the extracellular matrix surrounding inflammatory foci and was subsequently incorporated by macrophages/microglia.Gf-enhanced MRI provides a novel highly sensitive technique to study cerebral BBB alterations. We demonstrate for the first time in vivo the involvement of CVO during the development of neuroinflammation.The central nervous system (CNS) may no longer be considered immune privileged but rather a site of selective immune activity [1,2]. This so-called restricted immunity is warranted by the barrier function of capillary endothelium, which channels the entry of serum proteins and immune cells from the blood to the CNS or the cerebrospinal fluid (CSF), respectively [1
Sickness behaviour pushed too far – the basis of the syndrome seen in severe protozoal, bacterial and viral diseases and post-trauma
Ian A Clark, Alison C Budd, Lisa M Alleva
Malaria Journal , 2008, DOI: 10.1186/1475-2875-7-208
Abstract: The idea of acute infectious illness being caused by rampant overproduction of inflammatory cytokines that, in lower concentrations, mediate innate immunity, was first argued a quarter of a century ago [1], and has generated a large literature. Once recombinant tumour necrosis factor (TNF) and interleukin-1 (IL-1) became available in the late 1980s, and assays based on them replaced earlier methods, the concept spread to other pro-inflammatory cytokines, and from malaria and sepsis to viral and certain autoimmune diseases. It is now also well-entrenched in the literature of the post-trauma syndrome. Clearly, different triggers for cytokine generation and release can be expected to generate different foci, profiles, concentrations and kinetics of these mediators – now numerous enough to form superfamilies – and thus clinical variation within the same general principle is to be expected. But an accepted fundamental pattern has emerged.At a time of shifting perceptions on the interaction between sickness and host activity (reviewed by Dantzer [2]), Hart [3] argued that the distinctive behaviour of sick humans and animals (lethargy, anorexia, depressed motor activity etc.) was not simply another untoward aspect of being ill. Instead, it was reasoned to be an adaptive syndrome that had evolved as a protective mechanism to maximize chances of survival through encouraging the sick animal to seek out and remain in a safe resting place, and not search for food, until a survivable infectious episode had passed. Hart also proposed that sickness behaviour was caused by the inflammatory cytokines, TNF and IL-1. This was later confirmed by others [4], and investigated further through showing that IL-1 contributes significantly to the anorexia caused by both endotoxin and influenza infection [5,6]. The literature on this field is now considerable. Indeed, Cavadini and co-workers [7] note that this link between TNF and IL-1 and sickness behaviour induced them to investigate if thes
Renal hemodynamics and the mediators in sepsis  [cached]
Erciyes Medical Journal , 2002,
Abstract: Sepsis is a clinical emergency with increasing incidence and mortality. The incidence of acute renal failure are 19% in sepsis, 27 % in severe sepsis, and 51% in septic shock. For the pathogenesis of acute renal failure during sepsis local and systemic mediators, renal hypoperfusion, reperfusion injury, neutrophil-endothel associations, microvascular thromboses are the involved mechanisms. Norepinephrine, Angiotensine II, and vasopressin are the systemic mediators. Local mediators are Tumor necrosis factor alpha, Interleukin-1, Prostoglandin-E2, Prostoglandin I2, Thromboxane-A2, adhesion molecules, leucotrienes, platelet derived growth factor, endothelin, and adenosine. Renal blood flow and renal hemodynamics during sepsis are the leading factors of “septic” clinic features and renal failure. Understanding the pathogenesis of sepsis and renal failure will lead to treatment of septic patients that have renal dysfunction.
Mediators of Pruritus in Psoriasis  [PDF]
Adam Reich,Jacek C. Szepietowski
Mediators of Inflammation , 2007, DOI: 10.1155/2007/64727
Abstract: The pathogenesis of pruritus in psoriasis remains unclear. Many possible mediators were implicated to transmit or modulate this sensation in psoriasis, but none has been clearly proven to be a causative agent of itching. The most often discussed theory mentioned the importance of impaired innervations and neuropeptides imbalance in psoriatic skin. Other possible causes of itching might be increased expression of interleukin 2 or vascular abnormalities. Recent data indicated that pruritus could be also evoked by opioid system, prostanoids, interleukin 31, serotonin, or proteases. Whether these mechanisms are also involved in pruritus accompanying psoriasis requires further investigation. Limited knowledge of pruritus origin in psoriasis is responsible for the lack of the effective antipruritic treatments for psoriatics. Here, we summarize the current knowledge about the pathogenesis of pruritus in psoriasis and point out possible directions of future studies aiming the pathogenesis of this symptom in psoriasis.
Sickness Behaviour: Causes and Effects
M Viljoen, A Panzer
South African Family Practice , 2003,
Abstract: This paper discusses sickness behaviour as a central motivational state. It deals with the adaptational value and underlying mechanisms of sickness behaviour and with the consequences of the body's failure to terminate the activity of the symptoms-producing cytokines. SA Fam Pract 2003;45(10):15-18
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