作者: Barry McGuinness , Andrew Harkin
DOI: 10.1007/978-3-319-13602-8_3
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摘要: Bi-directional communication between the brain and immune system is a research area gaining in prominence search for biological factors associated with development of number psychiatric disorders. In this regard, animal models make substantial contributions to our understanding these interactions. For instance, long-term adaptive changes system, response stress, have been documented include stress-induced desensitisation cell glucocorticoid receptors (GR) β2-adrenoceptors (AR) which turn can impact on ability elicit their natural anti-inflammatory actions. It interest that psychological stress has reported induce microglial activation pro-inflammatory cytokine expression central nervous (CNS) studies, whilst there little evidence or an increase CNS cytokines depressed humans date, studies are providing important insights into potential role inflammatory events pathophysiology related Stress be linked state, it consider reciprocal peripheral mediators brain. accumulating inflammation plays pathogenesis major depressive illness. To further explore behavioural effects activation, currently use range agents used initiate including bacterial endotoxin lipopolysaccharide (LPS), interferon (IFN) alpha, inoculation Bacille Calmette–Guerin (BCG), experimental autoimmune encephalitis (EAE) administration synthetic double stranded ribonucleic acid (dsRNA) polyinosinic:polycytidylic (poly-IC), viral mimetic. Immune provokes signs depression may ameliorated following treatment antidepressant drugs. Despite findings question as how immunological basis disorder reconciled more traditional hypotheses impairment monoamine transmission functional neurotrophins remains addressed. indoleamine 2,3 dioxygenase (IDO) kynurenine pathway influence transport, receptor neurotrophic factor possibilities. The such systems new avenues develop better find improved therapies address current unmet clinical needs.