Fig. 1

Transcriptomic analysis of Grm3 deregulation associated with neonatal neuroinflammation in rats. a Functional network enrichment in microglial cells magnetically sorted from P4 animals under basal conditions (CTRL) and following LPD/IL-1β challenge inducing neonatal neuroinflammation. The 20 most enriched molecular functions are reported in the graph, sorted by increasing enrichment score. The ontologies associated with glutamate receptor activity are underlined in red. b Description of the number of genes mapped and their respective FDR values for each molecular function. In red are reported the gene ontology pathways that were associated with glutamate receptor activity. c Grm gene expression in microglia cells sorted from CTRL and LPD/IL-1β animals at P4 according to a Gene Set Enrichment Analysis against the Gene Ontology Database. Data (mean ± SEM) are relative to Grm1 expression in CTRL animals. Multiple t test; ^#p < 0.05. d Grm3 gene expression in microglial cells just sorted from CTRL and LPD/IL-1β animals at P4 analyzed by quantitative RT-PCR. Data (mean ± SEM) are relative to Grm3 expression in CTRL animals. Unpaired t test; ^##p < 0.01. e Grm3 gene expression assessed in primary microglia from CTRL and LPD/IL-1β animals at P4 after 48 h cell culture. Data (mean ± SEM) are relative to Grm3 expression in CTRL animals. Unpaired t test; ^####p < 0.0001. f Minimal Grm3 network showing the centrality of Grm3 gene deregulation following LPD/IL-1β exposure, selecting deregulated genes that are connected to more than 10 genes. Betweenness centrality of hub genes is quantified by the circle size, and the number of connections among genes by the color code. The figure shows that Grm3 has a central position in the network. g The same Grm3 minimal network as in f showing the expression of Grm3 and Grm3-associated genes. The blue color vs the red color intensity is associated with down- and upregulation, respectively