Norepinephrine inhibits gamma-interferon-induced MHC class II (Ia) antigen expression on cultured brain astrocytes
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Substances of abuse and the blood brain barrier: Interactions with physical exercise
2020, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Physical activity both improves antioxidant defenses and lowers lipid peroxidation levels in all age groups (Bouzid et al., 2018). During physical exercise, peripherally circulating norepinephrine (NE) is reported to suppress the inflammatory gene transcription, an anti-inflammatory effect that is mediated via the β2- adrenergic receptors (Frohman et al., 1988; Sanders, 2012). NE can promote a shift of Th1/Th2 balance toward Th2 response by activating the β2-receptor (Huang et al., 2014).
Treatment with the noradrenaline re-uptake inhibitor atomoxetine alone and in combination with the α2-adrenoceptor antagonist idazoxan attenuates loss of dopamine and associated motor deficits in the LPS inflammatory rat model of Parkinson's disease
2018, Brain, Behavior, and ImmunityCitation Excerpt :In support, many groups have reported a NA dependent enhancement of DA loss in various animal models of PD (Bing et al., 1994; Fornai et al., 1995; Marien et al., 1993; Mavridis et al., 1991), however the precise mechanism following LC lesion leading to potentiation of DAergic cell loss remains unknown (Szot et al., 2010). A number of in vitro studies implicate a role for NA and β2-ARs in promoting anti-inflammatory actions via communication with microglial, astrocytic and neuronal cell types (Ballestas and Benveniste, 1997; Braun et al., 2014; Feinstein, 1998; Frohman et al., 1988; Madrigal et al., 2005; McNamee et al., 2010a; Russo et al., 2004; and Willis and Nisen, 1995). Stimulation of astrocytic α1 and/or β-adrenoceptors the subsequent increase in cAMP and protein kinase A, may also provide neuroprotection through secretion of neurotrophic factors including NGF (Furukawa et al., 1989), BDNF (Jurič et al., 2006) and NT-3 (Mele et al., 2010).
Noradrenaline, Astroglia, and Neuroinflammation
2017, Noradrenergic Signaling and AstrogliaAstrocytes as potential targets to suppress inflammatory demyelinating lesions in multiple sclerosis
2010, Neurochemistry InternationalCitation Excerpt :These DNA-binding proteins serve as a scaffold for CIITA, which is required for IFNγ-inducible MHC class II expression (Harton and Ting, 2000; Moreno et al., 1999; Nikodemova et al., 2007; Steimle et al., 1994). Norepinephrine normally tightly suppresses the expression of IFNγ-induced MHC class II molecules on astrocytes via the stimulation of β2 adrenergic receptors, which activate adenylate cyclase with the consequent increase of intracellular cAMP (Frohman et al., 1988a,b). In MS lesions and the surrounding normal appearing white matter, astrocytes were found to be deficient in β2 adrenergic receptors (De Keyser et al., 1999; Zeinstra et al., 2000a).
Astrocytic β<inf>2</inf>-adrenergic receptors: From physiology to pathology
2010, Progress in NeurobiologyNorepinephrine-Mediated Suppression of Phagocytosis by Wound Neutrophils
2009, Journal of Surgical ResearchCitation Excerpt :While there is considerable interpatient variability in the degree of response to NE infusion because of disparate age, renal function, and hepatic function, it is clear that NE administration further increases circulating catecholamine levels, often to a degree that far exceeds physiological levels 7]. A growing body of literature indicates that NE and other adrenergic agonists can modulate many aspects of the immune response (initiative, proliferative, and effector phases), altering production of and cellular responses to cytokines, lymphocyte proliferation, antibody secretion, and inflammatory gene expression [8–12]. Additionally, the presence of α- and β-adrenoreceptors on neutrophils is well documented [13, 14].