Microglia mediated responses to neuronal damage in the form of neuroinflammation is a common thread propagating neuropathology. In this study, we investigated the microglial alterations occurring as a result of sphingosine 1‐phosphate (S1P) accumulation in neural cells. We evidenced increased microglial activation in the brains of neural S1P‐lyase (SGPL1) ablated mice (SGPL1fl/fl/Nes) as shown by an activated and deramified morphology and increased activation markers on microglia. In addition, an increase of pro‐inflammatory cytokines in sorted and primary cultured microglia generated from SGPL1 deficient mice was noticed. Further, we assessed autophagy, one of the major mechanisms in the brain that keeps inflammation in check. Indeed, microglial inflammation was accompanied by defective microglial autophagy in SGPL1 ablated mice. Rescuing autophagy by treatment with rapamycin was sufficient to decrease interleukin 6 (IL‐6) but not tumor necrosis factor (TNF) secretion in cultured microglia. Rapamycin mediated decrease of IL‐6 secretion suggests a particular mechanistic target of rapamycin (mTOR)‐IL‐6 link and appeared to be microglia specific. Using pharmacological inhibitors of the major receptors of S1P expressed in the microglia, we identified S1P receptor 2 (S1PR2) as the mediator of both impaired autophagy and proinflammatory effects. In line with these results, the addition of exogenous S1P to BV2 microglial cells showed similar effects as those observed in the genetic knock out of SGPL1 in the neural cells. In summary, we show a novel role of the S1P‐S1PR2 axis in the microglia of mice with neural‐targeted SGPL1 ablation and in BV2 microglial cell line exogenously treated with S1P.

A feeding trial was conducted to determine the maximum substitution limits of poultry by-product meal (PBM; 66% crude protein) protein for fish meal (FM; 59% crude protein) protein in the diet of juvenile Black Sea Bass Centropristis striata (family Serranidae). Eight isonitrogenous (44% crude protein) and isolipidic (13% crude lipid) diets were formulated to replace FM protein with PBM protein at 0 (control), 40%, 50%, 60%, 70%, 80%, 90%, and 100% in Black Sea Bass diets. Diets were fed twice daily to triplicate groups of juveniles (initial mean weight = 1.2 g) to apparent satiation for 8 weeks in a recirculating aquaculture system. Final survival was excellent (95-100%) in all diet treatments, with no significant differences. No significant differences in body weight gain (BWG) were observed in fish fed the 40-90% PBM protein diets (1,136-1,357%) compared with the control diet (1,307%). However, BWG of fish fed the 100% PBM protein diet (1,045%) was significantly lower than in the control group. Regression analysis with BWG indicated that PBM protein can replace FM protein in Black Sea Bass diets at levels as high as 81.8%, with no reduction in fish growth performance. For fish fed diets with up to 90% PBM protein, feed conversion (1.08-1.17) and protein efficiency ratios (2.01-2.14) were not significantly different from fish fed a control 100% FM-protein-based diet (0.99 and 2.29, respectively). Apparent digestibility coefficients of dietary protein remained high (81.6-87.0%) under all levels of FM replacement with PBM protein. After the feeding trial, whole body and muscle protein content and the concentrations of whole body n-3 polyunsaturated fatty acids showed no significant differences among the treatments at FM protein replacement levels up to 90%. Poultry by-product meal is a promising alternative protein source for sustainable diet development in Black Sea Bass. a Melick Aquafeed, Catawissa, Pennsylvania; 59.5% protein, 12% lipid. b Melick Aquafeed; 67% protein, 15% lipid. g Calculated value based on carbohydrates, proteins, and lipids at 17.2, 23.6, and 39.5 kJ/g, respectively (Blaxter 1989). 76 DAWSON ET AL.

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A 70‐day feeding experiment was conducted to assess the dietary vitamin A (VA) requirements of juvenile Japanese flounder (Paralichthys olivaceus). Six semi‐purified diets with VA supplementations of 0, 5000, 10 000, 15 000, 20 000 and 25 000 IU kg−1 were fed twice a day to triplicate groups of 20 juveniles per tank with an initial weight of 1.59 ± 0.01 g (mean ± SE). Weight gain (WG) and specific growth rate (SGR) increased as dietary VA increased up to 10 000 IU kg−1. Significantly lower WG and SGR were observed for the 0 IU kg−1 treatment than for treatments of 5000, 10 000 and 15 000 IU kg−1. Highest WG and SGR were observed in fish fed 10 000 IU kg−1; slightly lower values were recorded in fish fed 15 000, 20 000 or 25 000 IU kg1. No significant difference was observed in survival rate among treatments. Whole body total lipid was significantly higher in fish fed 0 and 5000 IU kg−1 than for other levels. Reduced growth and small livers were observed as signs of VA deficiency in fish fed 0 IU kg−1. Slightly reduced growth and pale fragile livers were observed as effects of VA excess in fish fed 25 000 IU kg−1. Total retinol contents in liver and eyes increased with increasing levels of dietary VA. No retinol was detected in livers, and significantly lower total retinol content was observed in eyes, of fish fed 0 IU kg−1. WG analysed by the broken line method indicated that an optimum dietary VA requirement of 9000 IU kg−1.

Three experiments were conducted to determine the extent to which menhaden fish meal protein (FMP) can be replaced by solvent‐extracted soybean meal protein (SBP) in the diet of juvenile black sea bass Centropristis striata. Diets were formulated replacing FMP by SBP at 0, 10, 20, 30, 40, 50, and 60% (experiment 1) and 0, 60, 70, 80, 90, and 100% (experiment 2), with supplementation with squid meal, krill meal, and attractants in both experiments. Experiment 3 was designed to replace FMP by SBP at 40, 50, 60, 70, and 80% without supplemental squid and krill meal and at 60% and 70% with supplemental methionine and lysine. Diets were fed twice daily to triplicate groups of fish (N = 15 per group) in 75‐L tanks containing recirculating seawater. Fish were fed for 6, 10, and 8 weeks in experiments 1, 2, and 3, respectively. No significant differences in body weight gain, feed efficiency, and survival were observed among treatments in experiment 1. In experiment 2, no significant differences in percent weight gain were observed among fish fed diets replacing FMP at 0, 60, and 70%. In experiment 3, body weight gain was not significantly different for fish fed supplemental methionine and lysine in 70% SBP diets compared with fish fed 0% SBP diets. No significant differences were observed in whole‐body n‐3 polyunsaturated fatty acids among treatments in experiment 2. Broken‐line regression of the specific growth rate data suggested that the maximum level of FMP replacement with SBP in black sea bass diets was 67.6–68.4% with 75 g/kg squid meal and 50 g/kg krill meal in the diet and 57.2–58.0% without squid and krill meal supplementation.