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We used quantitative autoradiography to determine whether the development of glutamate receptors correlates with the plastic period for monocular deprivation in rat visual cortex. To study glutamate receptors, we incubated sections of rat visual cortex with tritiated (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10imin e maleate (MK-801), tritiated kainate, and tritiated amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA). [3H]MK-801 is a noncompetitive ligand for the N-methyl-D-aspartate (NMDA) receptor. [3H]kainate and [3H]AMPA are competitive ligands for non-NMDA receptors. To compare glutamate binding sites with a nonglutamate binding site, we studied [3H]muscimol, which binds to gamma-aminobutyric acid (GABA)A receptors. [3H]MK-801 binding was maximal at postnatal day 26 (P26) and decreased in adulthood. [3H]AMPA binding was maximal at P18. [3H]kainate binding and [3H]muscimol binding were not age dependent. Dark rearing partially prevented the age-dependent decrease in [3H]MK-801 binding but had no effect on [3H]kainate or [3H]AMPA binding. Dark rearing decreased muscimol binding in adult animals. These results suggest that NMDA receptors, but not other glutamate receptors or GABAA receptors, are likely to be critical for developmental plasticity in rat visual cortex.

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Itaconate is a promising new candidate for anti-inflammatory and metabolic reprogramming, and 4-octyl itaconate (OI) is a cell-permeable itaconate derivative. To investigate the effect of OI in inflammatory response and glycolipid metabolism, we fed gibel carp with a 40% dietary soybean meal diet containing 0.1% OI (SBM + 0.1OI) or not (SBM) and compared these with fishmeal (FM) as reference. Compared with FM, dietary SBM decreased the growth performance, induced inflammation in the intestine and liver, and decreased the glucose utilization ability of the liver. However, 0.1% OI supplementation in SBM significantly increased the growth performance (from 20.11 ± 0.77 to 23.33 ± 0.45 g, P < 0.05), reduced inflammation in different organs through Nrf2 activation, and alleviated SBM-induced high plasma glucose (from 6.06 ± 0.23 to 4.37 ± 0.14 g, P < 0.05) and low crude body lipid (from 4.08 ± 0.17 to 4.91 ± 0.10 g, P < 0.05). Multi-omics revealed that OI had obvious effects on carbohydrate metabolism. OI regulates peroxisome proliferator-activated receptor gamma (ppar-γ), and its target genes (glut2 and gk) enhance liver glycolysis and lipid de novo lipogenesis, which are also dependent on Nrf2 activation. To conclude, dietary 0.1% OI can promote the growth of gibel carp and alleviate foodborne intestinal and hepatic inflammation and abnormal glycolipid metabolism by Nrf2regulated Pparγ expression.