Interactions Between the Brain and the Immune System in Pain and Inflammation.

Intro -- Abstract -- Acknowledgments -- Contents -- List of Figures -- Abbreviations -- List of Papers -- Background -- Cytokines and prostaglandins -- Immune-to-brain signalling -- Local inflammation -- Pain pathways -- The sensory and affective components of pain -- The parabrachial-amygdaloid pathway in pain processing -- Systemic inflammation and the sickness syndrome -- Inflammation-induced anorexia -- The parabrachial-amygdaloid pathway in food intake control -- Brain-to-immune signalling -- Modulation of immune response through the autonomous nervous system -- Modulation of immune response through the HPA-axis -- Methods -- Mouse models -- Cell-type specific manipulations: Cre/loxP system -- EP3RSertCre -- Vector-based manipulations -- Chemogenetics -- Global gene deletions: CGRP-KO -- Inflammatory pain model: Formalin injections -- Assessing the affective component of pain: Conditioned Place Aversion -- Assessing the sensory component of pain: Nociceptive scoring -- Systemic inflammation model: Intraperitoneal lipopolysaccharide injections -- LPS-induced anorexia -- Conditioned Taste Avoidance -- Inflammatory challenge in presence or absence of the dam -- Ex vivo studies -- Immunofluorescence -- Quantitative Polymerase Chain Reaction (qPCR) -- Sex of animals used -- Statistical analysis -- Aim and significance -- Results and discussion -- Paper I: Prostaglandin-mediated inhibition of serotonin signaling controls the affective component of inflammatory pain -- Activation of EP3 receptors by PGE2 of neural origin influences the affective component of inflammatory pain -- The EP3 receptors mediating the affective component of inflammatory pain are located on serotonergic cells -- Inhibition of the serotonergic neurons of the dorsal raphe mediates the affective component of pain.

Paper II: Calcitonin gene related peptide is dispensable for many danger-related motivational responses -- CGRP is absent in the projections to the central amygdala in CGRP-KO mice -- CGRP signaling is not necessary for inflammation induced anorexia and conditioned taste aversion -- CGRP signaling is not necessary for pain-related behaviors -- Paper III: Acute maternal separation potentiates the gene expression and corticosterone response induced by inflammation -- Maternal separation slightly attenuates proinflammatory gene induction one hour after inflammatory challenge without affecting CORT levels -- Maternal separation potentiates proinflammatory gene induction and CORT response three hours after inflammatory challenge -- A warm and soft object attenuates some of the effects of separation stress -- Corticosterone levels correlate with IL-6, Ccl2 and hepatic IL-1 expression -- Conclusions -- Paper I: Prostaglandin-mediated inhibition of serotonin signaling controls the affective component of inflammatory pain -- Paper II: Calcitonin gene related peptide is dispensable for many danger-related motivational responses -- Paper III: Acute maternal separation potentiates the gene expression and corticosterone response induced by inflammation -- Bibliography.

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Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, 2023. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries.