Adult animals submitted to a single prolonged episode of maternal deprivation [24 h, postnatal day 9–10] show behavioral alterations that resemble specific symptoms of schizophrenia. According to the neurodevelopmental theory, these behavioral deficits might be mediated by detrimental neurodevelopmental processes that might be associated, at least partially, with stress‐induced corticosterone responses. In order to address this hypothesis, we have focused on the hippocampus and cerebellar cortex, two brain regions that show high density of glucocorticoid receptors, and analyzed possible neuronal and glial alterations by immunohistochemical techniques. To evaluate the presence of degenerated neurons we used Fluoro‐Jade‐C (FJ‐C) staining and for the study of astrocytes we employed glial fibrillary acidic protein (GFAP). Within control animals, females showed significantly more GFAP positive cells than males and a trend towards more FJ‐C positive cells. Maternal deprivation induced neuronal degeneration and astroglial changes in the hippocampus and cerebellar cortex of neonatal rats that, in general, were more marked in males. This differential effect may be attributable to a greater vulnerability of males to this kind of early environmental insult and/or to sex‐dependent differences in the onset and/or progression of the effects. The present experimental procedure may be instrumental in elucidating sex‐dependent mechanisms of neurodevelopmental psychiatric disorders with a basis in early environmental insults.

Chronic kidney disease (CKD) is a silent and poorly known killer. The current concept of CKD is relatively young and uptake by the public, physicians and health authorities is not widespread. Physicians still mix up CKD with chronic kidney insufficiency or failure, For the wider public and health authorities, CKD evokes kidney replacement therapy (KRT). In Spain, the prevalence of KRT is 0.13%. Thus, health authorities may consider CKD a non-issue: very few persons eventually need KRT and, for those in whom kidneys fail, the problem is “solved” by dialysis or kidney transplantation. However, KRT is the tip of the iceberg in the burden of CKD. The main burden of CKD is accelerated aging and premature death. The cut-off points for kidney function and kidney damage indexes that define CKD also mark an increased risk for all-cause premature death. CKD is the most prevalent risk factor for lethal COVID-19 and the factor that most increases the risk of death in COVID-19, after old age. Men and women undergoing KRT still have an annual mortality which is 10- o 100-fold higher than similar age peers, and life expectancy is shortened by around 40 years for young persons on dialysis and by 15 years for young persons with a functioning kidney graft. CKD is expected to become the fifth global cause of death by 2040 and the second cause of death in Spain before the end of the century, a time when 1 in 4 Spaniards will have CKD. However, by 2022, CKD will become the only top-15 global predicted cause of death that is not supported by a dedicated well-funded CIBER network research structure in Spain. Realizing the underestimation of the CKD burden of disease by health authorities, the Decade of the Kidney initiative for 2020-2030 was launched by the American Association of Kidney Patients (AAKP) and the European Kidney Health Alliance (EKHA). Leading Spanish kidney researchers grouped in the kidney collaborative research network REDINREN have now applied for the RICORS call of collaborative research in Spain with the support of the Spanish Society of Nephrology, ALCER and ONT: RICORS2040 aims to prevent the dire predictions for the global 2040 burden of CKD from becoming true.

The experience of social stress during adolescence is associated with higher vulnerability to drug use. Increases in the acquisition of cocaine self-administration, in the escalation of cocaine-seeking behavior, and in the conditioned rewarding effects of cocaine have been observed in rodents exposed to repeated social defeat (RSD). In addition, prolonged or severe stress induces a proinflammatory state with microglial activation and increased cytokine production. The aim of the present work was to describe the long-term effects induced by RSD during adolescence on the neuroinflammatory response and synaptic structure by evaluating different glial and neuronal markers. In addition to an increase in the conditioned rewarding effects of cocaine, our results showed that RSD in adolescence produced inflammatory reactivity in microglia that is prolonged into adulthood, affecting astrocytes and neurons of two reward-processing areas of the brain (the prelimbic cortex, and the nucleus accumbens core). Considered as a whole these results suggest that social stress experience modulates vulnerability to suffer a loss of glia-supporting functions and neuronal functional synaptic density due to drug consumption in later life.

Sepsis is a multi‐organ dysfunction caused by the host uncontrolled inflammatory response to an infection, mediated by proinflammatory cytokines and oxygen free radicals. LPS is unable to trespass the Blood–Brain‐Barrier (BBB), but it can act on the TLR4 (Toll‐Like Receptor 4) receptor, found in the endothelium, causing the secretion of cytokines and chemokines that lead to the activation of glial cells. On the other hand, cisplatin (CISP), also called Cis‐dichlorodiammineplatinum [II], is a heavy metal antineoplastic agent widely employed in the treatment of different forms of cancer. Neurotoxicity has been reported as some of the adverse effects resulting from CISP administration. CISP alters intracellular signal transduction pathways that, in the end, provoke apoptosis through different mechanisms such as the generation of reactive oxygen species, DNA alterations, mitochondrial and/or endoplasmic reticulum dysfunction, and the production of proinflammatory cytokines and chemokines. Both sepsis and CISP cause a systemic damage that can result in brain impairments affecting different areas of the Central Nervous System (CNS), but to our knowledge, the effects of the systemic damage over the retinal cell populations, and specially on macroglial cells, have not been studied in detail. We employed two animal models using male Wistar rats: (1) a model of sepsis based on the systemic administration of bacterial lipopolysaccharide (LPS, 10 mg/kg, i.p.), or its vehicle; to induce a systemic inflammatory response; (2) a model of cisplatin based on the administration of a daily single dose of cisplatin (CISP, 5 mg/kg, i.p.) or its vehicle for 5 consecutive days until sacrifice in order to induce neurotoxicity. Animals were transcardiacally perfused, eyes were extracted, and retinal sections were used for immunohistochemical assays, where Brn3a and GFAP were employed to stain retinal ganglion cells and macroglial cells respectively. LPS induced a reduction in the number of Brn3a+ cells in the whole retina, neurodegenerative effects being more critical in the nasal inferior retina; and provoked a generalized increase in GFAP expression, specially in the nasal and central regions of the retina. Preliminary results indicate that the CISP administration leads to a reduction in the total number of Brn3a+ cells in the retina; and CISP may induce a generalized reduction of GFAP+ cells mainly within the nasal and temporal inferior retina. Taken together, we have provided evidence of retinal damage following the systemic inflammatory processes caused by LPS and CISP administration, which affects macroglial cells, with an increased or decreased GFAP expression depending on the activation pathway of the neuroinflammatory response. This dysregulation of the macroglial response could lead to a significant diminishment of the retinal ganglion cells of the retina, causing an irreversible loss of vision. Supported by Complutense University of Madrid, UCM Research Group: 951579. Keywords: LPS‐induced sepsis, cisplatin, ganglionar...