Anatomical and physiological experiments in the lamprey reveal the neural circuit involved in transforming olfactory inputs into motor outputs, which was previously unknown in a vertebrate.

Although four different primary olfactory pathways have been described in tetrapod vertebrates, polymorphic olfactory sensory neurons comingle in the olfactory epithelium and project axons into separate bulbar regions in teleost fish. However, spatially segregated neurons may exist in the peripheral olfactory organ of lampreys, extant representatives of ancestral jawless vertebrates. In lampreys, the caudoventral portion of the peripheral olfactory organ contains tubular diverticula, named the accessory olfactory organ (AOO). Short, ciliated AOO cells were retrogradely labelled following application of biocytin or carbocyanine dyes to the medial region of the olfactory bulb. Tracer application to eight radial locations within the layer of glomeruli with mitral cells, of the olfactory bulb, showed that AOO projections were restricted to the medial region of the olfactory bulb. The outer boundary of the AOO projection extended to the ventromedial region of glomerular neuropil in 43% of the specimens. The olfactory sensory neurons in the main olfactory epithelium projected to glomerular neuropil throughout the olfactory bulb, including sparse projections to the medial region of the olfactory bulb. This study shows that these AOO neurons and their projections in the medial region of the olfactory bulb are anatomically distinct regions of the primary olfactory pathway in the sea lamprey.

Cyanidin-3-O-glucoside (C3G), an anthocyanin belonging to the flavonoid family and commonly present in food and vegetables in human diet, has exhibited anti-inflammatory and anti-oxidant effects. This study aimed to investigate the protective ability of C3G against inflammatory and oxidative injuries, as well as to clarify the possible mechanism in lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) in vitro and acute respiratory distress syndrome mouse model in vivo. HUVECs or male Kunming mice were pretreated with C3G 1 h before LPS stimulation. C3G significantly inhibited the production of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin (IL) -6, and IL-1β) in cell supernatants and bronchoalveolar lavage fluid (BALF) as determined by enzyme-linked immunosorbent assay. Histopathologic examination with hematoxylin and eosinstaining showed that C3G pretreatment substantially suppressed inflammatory cell infiltration, alveolar wall thickening, and interstitial edemain lung tissues. C3G markedly prevented LPS-induced elevation of malondialdehyde and myeloperoxidase levels in lung tissue homogenates, wet to dry ratio of lung tissues, total cells, and inflammatory cells (neutrophils and macrophages) in BALF. Moreover, C3G reduced superoxide dismutase activity in the lung tissue homogenates. Western blot assay also showed that C3G pretreatment significantly suppressed LPS-induced activation of nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways by blocking the phosphorylation of inhibitor κB-α, NF-κB/P65, extracellular signal-regulated kinase, p38, and c-Jun NH2-terminal kinase in the lung tissues. In summary, C3G may ameliorate LPS-induced injury, which results from inflammation and oxidation, by inhibiting NF-κB and MAPK pathways and playing important anti-inflammatory and anti-oxidative roles.

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