Reduced Reelin expression induces memory deficits through Dab-1/ NMDAR signaling pathway: Cronobacter sakazakii infection in a rat model of experimental meningitis

The purpose of this study was to examine whether the Cronobacter sakazakii infection induced inflammation alters the Reelin signaling pathway that involving in learning and memory. To test this, postnatal day (PND) -15 rat pups were either treated with Luria Bertani broth / Escherichia coli OP50 / C. sakazakii through oral gavage or maintained as control and allowed to stay with their mothers until PND-24. Experimental groups ’ rats were subjected to long-term novel object recognition (NOR) test during their adolescent age PND-30-32. Observed behavioural data showed that C. sakazakii infection causes a deficit in recognition of novel objects from known objects. Further, our analysis showed that C. sakazakii infection mediated inflammation decreases the Reelin expression by proteolytic cleavage and alter its receptor apolipoprotein E-receptor (ApoER)-2 splice variants ApoER2 (ex-19) and ApoER2 (Δ). Subsequently, down-regulated Reelin alters the phosphorylation of disabled adapter protein (Dab) -1 and lead to differential expression of N-methyl-D-asparate (NMDA) receptor subunits 2A and 2B. Further, the NMDA receptor influences the expression of post-synaptic density (PSD)-95 protein and brain derived neurotrophic factor (BDNF). Observed results suggest a deficit in recognition of novel object possibly due the alternation in Reelin signaling pathway.
Source: Developmental Neuroscience - Category: Neuroscience Source Type: research