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Department
Neuroscience
Course Code
NROC61H3
Professor
Le Boutillier

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Sharif Alkatib
Eskandari: Neural-Immune Interactions in Health and Disease
Cytokines produce signals read by the brain to indicate a site of inflammation
leading to a fever and sickness-behaviors
CNS
Glucorticoids
CRH
Paraventricular nucleus hypophyseal portal blood
supply
Argine vasopressin
Stimulate the release of adrenocorticotropin (ACTH) from
AP
Causes adrenal glands to release glucorticoids
Modulated by serotonergic, cholinergic and
catecholaminergic systems
Negative feedback HPA axis
GABA/BZD
Inhibit serotonin-induced CRH secretion
Inflammatory response, cytokine expression, IC trafficking,
immune cell maturation and differentiation
Low levels
Shift from pro-inflammatory (increased interleukins) and
tumor necrosis factor alpha to anti-inflammatory and
increased interleukin receptor antagonists
Hypothalamic-pituitary-gonadal axis
Higher risk for lupus, rheumatoid arthritis, and MS (in
women)
Mediation between the HPA and HPG so that the fetus is
not rejected
Estrogen R for alpha and beta important for thymus
development
SNS (catecholamines)
Thymus, lymph nodes and spleen
Inhibit TNF, IL-12 and interferon-gamma and inflammatory cytokines
Stimulate anti-inflammatory cytokines (IL-10) and transforming growth
factor beta
Inhibit cellular immunity (Th1) and strengthen humoral response (Th2)
PNS
Local dealings with inflammation with substance P, CRH and
vasoactive intestinal polypeptide
Usually pro-inflammatory
Opiods
Suppress killer t cells
Increases plasma levels of catecholamines
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