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Text
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<a href="http://doi.org/10.1006/brbi.1994.1023" target="_blank" rel="noreferrer">http://doi.org/10.1006/brbi.1994.1023</a>
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Title
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Intermittent but not continuous inescapable footshock stress affects immune responses and immunocyte beta-endorphin concentrations in the rat
Publisher
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Brain, Behavior, And Immunity
Date
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1994
Subject
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Male; Time Factors; Animals; Acute Disease; Rats; Comparative Study; Receptors; beta-Endorphin/analysis; Corticosterone/blood; Corticotropin-Releasing Hormone/antagonists & inhibitors; Corticotropin-Releasing Hormone/blood/pharmacology/physiology; Electroshock/adverse effects; Foot; Helplessness; Killer Cells; Learned; Lymphocyte Activation; Lymphoid Tissue/chemistry; Natural/immunology; Neuroimmunomodulation/physiology; Peptide Fragments/pharmacology; Spleen/immunology; Sprague-Dawley; Stress/etiology/immunology
Creator
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Sacerdote P; Manfredi B; Bianchi M; Panerai AE
Description
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It is well known that a variety of stressors influence immune responses. The opioid peptide-beta-endorphin (BE) is deeply involved in stress responses, is synthesized in cells of the immune system, and participates in the modulation of immune function. We analyzed the ability of two different stress paradigms to modulate the beta-endorphin concentrations in the immune cells and the immune response in the rat. Two and 24 h after the exposure to inescapable intermittent footshock (1.6 mA, 60 Hz, 1 s, every 5 s for 20 min) the concentrations of beta-endorphin in splenocytes, peripheral blood mononuclear cells and lymph node cells were significantly increased. In contrast, the exposure to a continuous footshock for 3 min did not affect the concentrations of the opioid peptide. Similarly, phytohemoagglutinin-induced proliferation of splenocytes and natural killer activity were significantly impaired only after the exposure to intermittent footshock stress. On the contrary, plasma corticosterone levels were similarly elevated after both paradigms of stress. The pretreatment with the corticotropin-releasing hormone (CRH) receptor antagonist prevented both the stress-induced increase of immunocyte BE and immunosuppression. In conclusion, our data suggest that intermittent and continuous footshock stressors activate different neuroendocrine responses and that CRH plays a central role in mediating the immune effects of the intermittent footshock stress. The possible relationship between the beta-endorphin changes and immunosuppression is discussed.
1994
Identifier
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<a href="http://doi.org/10.1006/brbi.1994.1023" target="_blank" rel="noreferrer">10.1006/brbi.1994.1023</a>
Rights
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Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
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Journal Article
1994
Acute Disease
Animals
Backlog
beta-Endorphin/analysis
Bianchi M
Brain, Behavior, And Immunity
Comparative Study
Corticosterone/blood
Corticotropin-Releasing Hormone/antagonists & inhibitors
Corticotropin-Releasing Hormone/blood/pharmacology/physiology
Electroshock/adverse effects
Foot
Helplessness
Journal Article
Killer Cells
Learned
Lymphocyte Activation
Lymphoid Tissue/chemistry
Male
Manfredi B
Natural/immunology
Neuroimmunomodulation/physiology
Panerai AE
Peptide Fragments/pharmacology
Rats
Receptors
Sacerdote P
Spleen/immunology
Sprague-Dawley
Stress/etiology/immunology
Time Factors