Presence of Mother Reduces Early-Life Social Stress: Linking the Alteration in Hypothalamic-Pituitary-Adrenal Axis and Serotonergic System.

In this study, we examined whether the presence of mother suppresses early-life stressful social experience (SSE)-induced anxiety-like behavior and impairment of short-term memory later in life. On postnatal day (PND)-5, mothers with pups were grouped as follows: (i) control; (ii) maternal separation (MS); (iii) pups with mother experience the presence of a stranger (M+P-ST); and (iv) maternal separated pups experience the presence of a stranger (MSP-ST). Individuals were subjected to light-dark box and spontaneous alternation from PND-29 to 32. We observed that the MSP-ST group exhibits anxiety-like behavior and impairment in short-term memory. Further, SSE significantly elevated the adrenocorticotropic hormone, corticosterone and expression of glucocorticoid receptor (GR) in MSP-ST pups. Similarly, serotonin (5-hydroxytryptamine; 5-HT), dopamine, noradrenaline and expression of serotonin transporter levels were significantly elevated in MSP-ST pups. These observations suggest that during early postnatal days, the pups may recognize strangers by the sense of smell, and the presence of mother reduces the SSE-induced stress.

Alterations in MicroRNA-132/212 Expression Impairs Fear Memory in Goldfish Carassius auratus.

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.