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Alterations in MicroRNA-132/212 Expression Impairs Fear Memory in Goldfish Carassius auratus
Subramanian Thangaleela1, Vasudevan Shanmugapriya1, Murugan Mukilan1
1Behavioural Neuroscience Laboratory, Department of Animal Science, School of Life Sciences, Bharathidasan University, Tiruchirappalli, India.
Background:
Earlier, we showed that nicotinamide (NAM) treatment impairs spatial memory through the downregulation of CREB-Sirt 1-brain-derived neurotrophic factor (Bdnf) signaling cascade.
Purpose:
In this study, we examine whether NAM treatment alters CREB-regulated genes through -microRNAs.
Method:
To test this hypothesis, goldfish (Carassius auratus) were divided into 2 groups: (i) vehicle group (VEH; double distilled water intra-peritoneally [i.p.]) (ii) nicotinamide group (NAM, 1,000 mg/kg, i.p.) and again divided into VEH untrained/trained, NAM untrained/trained. One hour after receiving VEH or NAM, individuals were subject to contextual fear conditioning (CFC) training. After 24 h, both the groups were tested for contextual fear memory. Subsequently, miR-132/212 levels, regulated immediate-early genes (IEGs: C-fos and EGR-1) and Bdnf but not its receptor. -TrkB1were examined following 0' and 60' min after training, and compared with the untrained group.
Results:
We observed that NAM treatment significantly impaired fear memory. Further, the analysis showed that miR-132 level was not altered, but miR-212 level was significantly upregulated after CFC training only in NAM-treated fish. We also found that NAM treatment downregulated IEGs and Bdnf but not its receptor TrkB1.
Conclusions:
Present study suggests that NAM-treatment impaired fear memory and control IEGs, Bdnf and TrkB1 expression by differentially regulating miR-132 and 212.
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