Maternal deprivation during early infancy in rats increases oxytocin immunoreactivity in females and corticosterone reactivity to a social test in both sexes without changing emotional behaviour.

Impairment of social behaviour is a hallmark of emotional disorders, with increased avoidance of social contact. In rats, the 24 h maternal deprivation (DEP) paradigm is used to understand the impact of extreme neglect on neurodevelopment. Due to the distinct immediate effects of DEP on postnatal days (PND) 3 (DEP3) or 11 (DEP11), in the present study we investigated the long-term effects of DEP at these ages on anxiety-like behaviour, by recording the visits and time spent in the centre part of the open-field, social investigation of a confined, same-sex, unfamiliar animal, basal and post-social test corticosterone plasma levels and the immunoreactivity to oxytocin in the paraventricular (PVN) and supraoptic nuclei of the hypothalamus (SON). Whole litters were distributed into control (CTL), DEP3 or DEP11 groups and behavioural tests and biological samples were collected between PNDs 40 and 45 in males and females. There were no differences in the exploration of the central part of the open field or on the time investigating the unfamiliar rat. However, the percent increase in post-test corticosterone secretion from baseline was greater for both DEP3 male and female subgroups than their CTL and DEP11 counterparts. DEP3 females showed more oxytocin staining than DEP11 counterparts in magnocellular neurons of the SON and PVN. These results suggest that DEP at the ages chosen does not alter social investigation, although it results in distinct neurobiological outcomes, depending on the developmental phase when it is imposed.

Bone marrow-derived mesenchymal stem cells repaired but did not prevent gentamicin-induced acute kidney injury through paracrine effects in rats.

This study evaluated the effects of bone marrow-derived mesenchymal stem cells (BMSCs) or their conditioned medium (CM) on the repair and prevention of Acute Kidney Injury (AKI) induced by gentamicin (G). Animals received daily injections of G up to 20 days. On the 10(th) day, injections of BMSCs, CM, CM+trypsin, CM+RNase or exosome-like microvesicles extracted from the CM were administered. In the prevention groups, the animals received the BMSCs 24 h before or on the 5(th) day of G treatment. Creatinine (Cr), urea (U), FENa and cytokines were quantified. The kidneys were evaluated using hematoxylin/eosin staining and immunohystochemistry. The levels of Cr, U and FENa increased during all the periods of G treatment. The BMSC transplantation, its CM or exosome injections inhibited the increase in Cr, U, FENa, necrosis, apoptosis and also increased cell proliferation. The pro-inflammatory cytokines decreased while the anti-inflammatory cytokines increased compared to G. When the CM or its exosomes were incubated with RNase (but not trypsin), these effects were blunted. The Y chromosome was not observed in the 24-h prevention group, but it persisted in the kidney for all of the periods analyzed, suggesting that the injury is necessary for the docking and maintenance of BMSCs in the kidney. In conclusion, the BMSCs and CM minimized the G-induced renal damage through paracrine effects, most likely through the RNA carried by the exosome-like microvesicles. The use of the CM from BMSCs can be a potential therapeutic tool for this type of nephrotoxicity, allowing for the avoidance of cell transplantations.