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      Effects of neurointermediate pituitary lobectomy on humoral and cell-mediated immune responses in the rat.

      Neuroimmunomodulation
      Animals, Antibody Formation, immunology, Dermatitis, Contact, Dinitrochlorobenzene, Drinking, physiology, Ear, External, Edema, Erythrocytes, Extremities, Female, Hemagglutinins, metabolism, Immunity, Cellular, Irritants, Organ Size, Pituitary Gland, Anterior, pathology, surgery, Rats, Rats, Wistar, Sheep, Weight Gain

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          Abstract

          Chronic stress is characterized by an increased activity of the hypothalamic-pituitary-adrenocortical axis and decreased humoral and cell-mediated immune responses. In the rat, corticosterone is the principal natural immune suppressor. Neurointermediate pituitary lobectomy (NIL) in rats induces diabetes insipidus and protracted increases in basal adrenocorticotropin and corticosterone plasma levels, a situation that resembles chronic stress. In this paper, we evaluated the effects of NIL on humoral (hemagglutinin titers and footpad swelling to sheep red blood cells--SRBC) and cell-mediated immune responses (contact hypersensitivity to dinitrochlorobenzene). The studies were conducted on NIL Wistar rats (body weight 150-200 g) 3 weeks after surgery. For comparisons, nonoperated control rats were used. NIL resulted in an increased water intake. Body weight gain and adrenal, thymus, and spleen weights were within the range of nonoperated controls. Eight days after SRBC immunizations a second SRBC injection into the footpad resulted in a decreased swelling response in NIL rats. The hemagglutinin titers were also reduced in the NIL rats. These results indicate that: (1) NIL reduces humoral immune responses and decreases the cell-mediated immune response; (2) the immune alterations are most likely due to the increased activity of the hypothalamic-pituitary-adrenocortical axis induced by NIL, and (3) NIL animals constitute a valuable paradigm to study hypothalamic-pituitary-immune interactions. Copyright 2004 S. Karger AG, Basel

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          Corticotropin-releasing hormone and pituitary-adrenocortical responses in chronically stressed rats.

          Brain corticotropin-releasing hormone (CRH) concentration and pituitary adreno-cortical responses were examined in chronically stressed rats: body restraint stress (6 h/day) for 4 or 5 weeks. Stressed rats showed a reduction in weight gain. CRH concentration in the median eminence and the rest of the hypothalamus were not different between control and chronically immobilized rats. The anterior pituitary adenocorticotropic hormone (ACTH) concentration was elevated in chronically stressed rats, whereas plasma ACTH and corticosterone levels did not differ from the control values. The median eminence CRH concentration was reduced to the same extent at 5 min after onset of ether exposure (1 min) in chronically immobilized rats and controls. However, plasma ACTH and corticosterone showed greater responses to ether stress in chronically immobilized rats than in control rats. Plasma ACTH and corticosterone responses to exogenous CRH were not different between control and chronically immobilized rats, while the response to arginine vasopressin (AVP) was significantly greater in chronically immobilized rats. These results suggest that chronic stress caused an increase in the ACTH-secreting mechanism and that pituitary hypersensitivity to vasopressin might at least be partly responsible for this.
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            Paradoxical responses of hypothalamic corticotropin-releasing factor (CRF) messenger ribonucleic acid (mRNA) and CRF-41 peptide and adenohypophysial proopiomelanocortin mRNA during chronic inflammatory stress

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