Interactions Between the Brain and the Immune System in Pain and Inflammation.
Main Author: | |
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Format: | eBook |
Language: | English |
Published: |
Linköping :
Linkopings Universitet,
2019.
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Edition: | 1st ed. |
Series: | Linköping University Medical Dissertations Series
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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.