Abstract
It is well established that Cronobacter sakazakii infection cause septicemia, necrotizing enterocolitis and meningitis. In the present study, we tested whether the C. sakazakii infection alter the learning and memory through serotonin transporter (SERT). To investigate the possible effect on SERT, on postnatal day-15 (PND-15), wistar rat pups were administered with single dose of C. sakazakii culture (infected group; 107 CFU) or 100 μL of Luria-Bertani broth (medium control) or without any treatment (naïve control). All the individuals were subjected to passive avoidance test on PND-30 to test their fear memory. We show that single dose of C. sakazakii infection improved fear memory retention. Subsequently, we show that C. sakazakii infection induced the activation of toll-like receptor-3 and heat-shock proteins-90 (Hsp-90). On the other hand, level of serotonin (5-hydroxytryptamine) and SERT protein was down-regulated. Furthermore, we show that C. sakazakii infection up-regulate microRNA-16 (miR-16) expression. The observed results highlight that C. sakazakii infections was responsible for improved fear memory retention and may have reduced the level of SERT protein, which is possibly associated with the interaction of up-regulated Hsp-90 with SERT protein or miR-16 with SERT mRNA. Taken together, observed results suggest that C. sakazakii infection alter the fear memory possibly through SERT. Hence, this model may be effective to test the C. sakazakii infection induced changes in synaptic plasticity through SERT and effect of other pharmacological agents against pathogen induced memory disorder.
Highlights
Serotonin (5-hydroxytryptamine, 5-HT) has been implicated as the modulator of learning and memory with special preference to consolidation of new information into long-term memory (Kandel, 2001). 5-HT play a key role in memory formation by interacting with other neurotransmitters/exerts its effect through their seven (5-HT1–5-HT7) subclass of receptors (Meneses, 1999, 2007, 2013; Meneses et al, 2011; Perez-Garcia and Meneses, 2009; Hoyer et al, 2002)
The observed data showed that C. sakazakii infection did not alter their learning during acquisition but IF group exhibited higher step-through latency during retention test, which showed the persistence of fear memory
Our analysis revealed that C. sakazakii infection significantly increased the expression level of toll-like receptors (TLRs)-3 (Figure 3), the Ct values of TLR-3 for each group followed by GAPDH (NC: 23.24 ± 0.038; 12.11 ± 0.041; medium control (MC): 23.24 ± 0.026; 11.77 ± 0.064; IF: 22.36 ± 0.122; 12.12 ± 0.054)
Summary
Serotonin (5-hydroxytryptamine, 5-HT) has been implicated as the modulator of learning and memory with special preference to consolidation of new information into long-term memory (Kandel, 2001). 5-HT play a key role in memory formation by interacting with other neurotransmitters/exerts its effect through their seven (5-HT1–5-HT7) subclass of receptors (Meneses, 1999, 2007, 2013; Meneses et al, 2011; Perez-Garcia and Meneses, 2009; Hoyer et al, 2002). Earlier studies reported that expression of SERT protein regulated by the interacting molecules such as ribonucleoprotein (RNP) and sequence specific microRNA (miR; Standart and Jackson, 1994; Wilkie et al, 2003; Bartel, 2009; Croce, 2009; Gyawali et al, 2010; Goldie and Cairns, 2012; Hartley et al, 2012) At this point, heterogeneous nuclear ribonucleoprotein K (hnRNPK) and miR-16 appears to negotiate for the binding site at 3′-untranslated region (UTR) of SERT and regulate the repression/depression of translation (Baudry et al, 2010; Yoon et al, 2013)
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