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. 2021 May 29;11(6):723. doi: 10.3390/brainsci11060723

Figure 2.

Figure 2

Schematic model of multilevel interactions between inflammatory and redox pathways under toxic stress exposure. AP-1: activator protein-1; BBB: blood-brain-barrier; Ca: calcium; DAMPs: damage-associated molecular patterns; GAD-67: glutamic acid decarboxylase-67; GC: glucocorticoid; GLU: glutamate; GSH: glutathione; HPA-axis: hypothalamic-adrenal-pituitary axis; JNK: c-Jun N-terminal kinase; KMO: kynurenine 3-monooxygenase; MAPK: mitogen-activated protein kinase; MLT: melatonin; NAD: nicotinamide adenine dinucleotide; NFkB: nuclear factor kappa beta; nAMPK: neuronal 5′-adenosine monophosphate-activated protein kinase; NLRP-3: nod-like receptor protein-3; NMDA-R: N-methyl-D-aspartate receptor; NO: nitric oxide; NOS: nitric oxide synthase; NOX: nicotinamide adenine dinucleotide phosphate (NADPH) oxidase; Nrf2: nuclear related factor-2; p-38: protein-38 MAPK; PAMPs: pathogen-associated molecular patterns; PG: prostaglandins; PNS: parasympathetic nervous system; PVI: GABAergic parvalbumin interneurons; QLA: quinolinic acid; RNS: reactive nitrogen species; ROS: reactive oxygen species; SNS: sympathetic nervous system; TLR: toll-like receptors; TRY: tryptophan; ↑: induction; ↓: inhibition; Ø: no change.