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

Bibliographic Details
Main Author: Zajdel, Joanna.
Format: eBook
Language:English
Published: Linköping : Linkopings Universitet, 2019.
Edition:1st ed.
Series:Linköping University Medical Dissertations Series
Subjects:
Online Access:Click to View
Table of Contents:
  • 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.