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Introduction: Chronic stress is the main environmental factor in the aetiology of depression and it is known that this type of stress may cause alterations in brain regions such as the hippocampus. Nevertheless, changes in a cellular basis are still a subject of study. Objective: The analysis of microglial cells and immature neurons in the dentate gyrus (DG) of stressed mice. Methods: C57BL/6J mice were subjected to Social Defeat Stress model (SDS), consisting of 6 days of social isolation prior to 10 days of stressor. The DG was analysed using immunohistochemistry techniques against Iba1 (microglia) and DCX (immature neurons) following image analysis (ImageJ) to obtain morphological and distribution data of microglial somas. Furthermore, hippocampal neurogenesis was assessed through stereological quantification of DCX+ cells (Visiopharm). Results: An increase in soma size under chronic stress conditions was shown, as well as a less circular and more ameboid soma. These changes were observed mainly in the infrapyramidal blade of the DG. According to microglial cells distribution parameters, the granular cell layer (GCL) was the region which presented the highest microglial density under SDS. Regarding hippocampal neurogenesis, a decrease in the number of DCX+ Type 2-3 cells was observed in the whole DG. Conclusion: All these results o!er a more profound insight of stress changes at a cellular level and could contribute to a better understanding of neurobiological basis in pathologies such as depression. Projects: PSI2017-83408-P (MINECO) and P20 00460 (Consejería de Conocimiento, Investigación y Universidades, Junta de Andalucía). University of Málaga and the projects PID2020-117464RB-I00 (Ministerio de Ciencia e Innovación, Spain) to Pedraza C. and Pérez-Martin M., PSI2017-83408-P (FEDER/Ministerio de Ciencia, Innovación y Universidades, Spain) to Pedraza C., UMA20- FEDERJA-112 (FEDER/Junta de Andalucía) to Pedraza C. and Pérez-Martin M. and P20-00460 (Consejería de Conocimiento, Investigación y Universidades, Junta de Andalucía) to Pedraza C. Predoctoral Fellowship: FPU16/05308 to Nieto-Quero A. and FPU19/03629 to Infantes-López MI., Ayuda A.2 para Contrato Predoctoral Del I Plan Propio de Investigación, Transferencia y Divulgación Científica de la Universidad de Málaga, Convocatoria 2021 to Munoz-Martin J. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

Stress is the main environmental cause for depression, known to cause brain immune alterations. As major brain immune cells, microglia undergo transcriptional and, consequently, morphological changes that result in tissue damage, including new cell generation impairment. Even so, few brain regions have been thoroughly studied, excluding key regulators as the hypothalamus, in which this process remains partially unknown. Moreover, there is a poor understanding in physiology related to behavioral outcome. Therefore, it would be interesting to study the relationship between microglia and cell proliferation in stressed mice while controlling for behavior. Here, we used the social defeat stress (SDS) paradigm as a depression-inducing protocol in 8-week-old male C57BL/6J mice for 10 consecutive days. Intruder mice behavior was analyzed to assess depression using behavioral tests and K-means clustering. By immunohistochemical and imaging procedures, microglial morphology, and distribution, as well as cell survival, were analyzed in the hypothalamic paraventricular, ventromedial and arcuate nucleus. Finally, statistical mediation analysis was conducted to evaluate the relationship among variables. Results show mice response to SDS was different, being half the mice resilient and half sensitive to depressive-like symptoms. Microglial morphological activation was enhanced in the ventromedial and arcuate nucleus, especially in stress sensitive animals. Similar results were observed in cell survival, which was particularly affected in sensitive mice. Strikingly, these cell survival changes were statistically mediated by microglial activation. As a conclusion, hypothalamic regions were found to respond differently to stress, accordingly to behavioral outcome, in terms of microglial activation and subsequent decrease in cell survival. This study was supported by FEDER/Ministerio de Ciencia, Innovación y Universidades – Agencia Estatal de Investigación from Spain (PSI2017-83408-P to Pedraza C.), FEDER/Junta de Andalucía from Spain (UMA20-FEDERJA-112 to Pedraza C. and Pérez- Martín M), and Ministerio de Educación, Cultura y Deporte from Spain (FPU19/03629 to Infantes-López MI and FPU16/05308 to Nieto-Quero A). Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

Among all the factors that can contribute to the onset of psychopathological disorders, stress is the main environmental factor. The hippocampus is one of the most sensitive regions to the harmful effects of stress, in which the neurogenic process is impaired. On the other hand, under stress situations, microglia are also affected and can trigger a proinflammatory response, acting as anti-neurogenic cells and releasing cytokines and other proinflammatory molecules. Knowing what happens in the early stages of stress may be relevant to investigate the temporal aspects of the development of stressassociated psychopathological disorders, and even their possible treatment. Therefore, after subjecting C57BL/6J mice for 2 hours to an acute and intense stress procedure called WIRS (water immersion restraint stress), data were analyzed to study microglia, cell proliferation and neuronal maturation. In addition, a mediation analysis study was conducted for data integration. The results revealed that the applied acute stress is sufficiently intense to induce an increase in the number of microglia, accompanied by morphometric changes, as well as negatively affecting the neuronal maturational process. Furthermore, these data suggest that effects on the neurogenic process mediate the microglial response to an intense acute stressor. This leads to the conclusion that this may be the initial mechanism for any intense stress response, or may even be the first steps in the development of the response to a chronic stressor. Ministerio de Ciencia e Innovación – Plan Nacional I+D+i from Spain: PID2020- 117464RB-I00 to C. Pedraza and M. Pérez-Martín - FEDER/Ministerio de Ciencia e Innovación – Agencia Estatal de Investigación from Spain: PSI2017-83408-P to C. Pedraza -- FEDER/Junta de Andalucía – Proyectos I+D+I en el marco del Programa Operativo FEDER Andalucía 2014-2020: UMA20-FEDERJA-112 to C. Pedraza and M. Pérez- Martín - Consejería de Conocimiento, Investigación y Universidades, Junta de Andalucía: P20_00460 to C. Pedraza - Contract in charge of the project P20_00460 to P. Chaves-Peña - Ministerio de Universidades from Spain: FPU16/05308 to A. Nieto-Quero and FPU19/03629 to M.I. Infantes-López - I Plan Propio de Investigación, Transferencia y Divulgación Científica (convocatoria 2021) from University of Malaga: predoctoral fellowship to J. Munoz-Martin. II Plan Propio de Investigación, Transferencia y Divulgación Científica; Universidad de Málaga. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

Funding: This study was supported by FEDER/Ministerio de Ciencia, Innovación y Universidades – Agencia Estatal de Investigación from Spain (PSI2017-83408-P to C. Pedraza), and Ministerio de Universidades from Spain (FPU16/05308 to A. Nieto-Quero and FPU19/03629 to M.I. Infantes-López). Stressful life events may have a negative impact on mental health compromising people's well-being, so knowing the neurobiological changes that occur after psychosocial stressors can have an impact on overall health. However, the neurobiological mechanisms responsible for the negative effects are not known in detail, and the initial changes that take place after the initiation of a stress protocol are much less well understood. Hippocampus constitutes a target structure of the adverse effects of stress. Among the possible mechanisms involved, the response of microglia to stress is receiving increasing interest. For this reason, after 1 and 24 hours of submitted C57BL/6J mice to acute and intense stress procedure denominated WIRS (water immersion restraint stress), the microglial response were analysed using a set of morphofunctional parameters. Then, the levels of the cytokines: IL-6, IFN-gamma and TNF-alpha cytokine were measured. Furthermore, a complementary proteomic analysis based on the principle of mass spectrometry was carried out. Results reveal that acute stress increased the number of microglia and induced microglial morphofunctional changes. Regarding cytokines, acute stress only increased IL-6 levels, which remained elevated at 24 h. Proteomic analysis, over time (in 24 h post-stress), showed an increase in proteins associated with the intracellular calcium metabolism. These findings suggest a neuroinflammatory response after acute stress observed at one hour after the application of the WIRS protocol and maintained at least 24 hours after the end of the stressor. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

This study was supported by FEDER/Ministerio de Ciencia, Innovación y Universidades – Agencia Estatal de Investigación from Spain (PSI2017-83408-P to Pedraza C.), and Ministerio de Educación, Cultura y Deporte from Spain (FPU16/05308 to Nieto-Quero A). Microglial cells are an important glial population known to be involved in several biological processes such as stress response. These cells engage an activated state following a stress insult that may lead to nervous tissue damage, including new cell generation impairment. This has been widely studied in regions with notable neurogenesis such as de hippocampus, however, the effect in other regions with fewer yet relevant neurogenesis remains partially unknown. One of them is the hypothalamus, a key vegetative control center playing an important role in stress response. Moreover, most of the stress models studied concern neuroinflammatory and neurogenic changes due to a chronic stressor but not a single stress event. Given the repercussion of these processes alone, it would be interesting to elucidate the relationship between microglial response, hypothalamic neurogenesis, and acute stress. This project focuses on studying acute stressed C57BL/6J mice, both at the histological and molecular level. An intense stressor combining water immersion and movement restriction was performed. Using immunohistochemical and molecular analysis with Luminex, we could analyze microglial distribution and morphology, neurogenesis, and inflammatory environment in the hypothalamic parenchyma (paraventromedial, ventromedial and arcuate nucleus). Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

LPA1 receptor is one of the six characterized G protein-coupled receptors (LPA1-6) through which lysophosphatidic acid acts as an intercellular signalling molecule. It has been recently proposed that this receptor has a key role in controlling depression-like behaviours and in the detrimental consequences of stress. Here, we sought to establish the involvement of the LPA1 receptor in brain activity after an acute stressor. To this end, we examined behavioural despair in mice with a constitutive depletion of the LPA1 receptor (maLPA1-null mice), wild-type mice and mice receiving one single icv dose of the LPA1 receptor antagonist Ki16425 or vehicle. Furthermore, the expression of c-Fos protein in stress-related brain areas and the corticosterone response following acute stress were examined. Our data indicated that, contrary to the knockout model, the antagonism of the LPA1 receptor significantly increased immobility in the Forced Swim Test. However, latency to first immobility was reduced in both experimental conditions. Immunohistochemistry studies revealed an increased in activity in key limbic structures such as medial prefrontal cortex in both the LPA1 antagonist-treated mice and maLPA1-null mice, with an interesting opposed effect on hippocampal activity. Following acute stress, the sole infusion of Ki16425 in the cerebral ventricle increased corticosterone levels. In conclusion, the alteration of LPA1 receptor function, through both genetic deletion or pharmacological antagonism, is involved in behavioural despair and hyperactivity of brain stress systems, thus contributing to explore specific susceptibility mechanisms of stress as targets for therapeutic recovery. Funding by the Andalusian Ministry of Economy, Innovation, Science and Employment (SEJ1863) and the Spanish Ministry of Education, Culture and Sports ( PSI2017 - 83408 - P). Authors RD. M-F and A. N-Q hold a Grant of the Spanish Ministry of Education, Culture and Sports (FPU14/01610 and FPU16/05308, respectively). Author S.T. holds a Grant of the Andalusian Ministry of Economy, Innovation, Science and Employment C. R. (FPDI 2016); Andalucía Tech. I Plan Propio de Investiga ción y Transferencia de la Universidad de Málaga. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

LPA1 receptor is one of the six characterized G protein-coupled receptors (LPA1-6) through which lysophosphatidic acid acts as an intercellular signaling molecule. It has been shown that the LPA1 receptor is involved in emotional regulation and, when depleted, has a key role in vulnerability to stress. In this sense, maLPA1-null mice, a knockout model for LPA1 receptor has been recently proposed as a model of anxious depression. Here, we sought to elucidate the effect of the genetic depletion of this receptor of LPA1 receptor in both lipidome and Neuropeptide-Y (NPY) signaling, two factors associated with adaptive stress regulation. For that purpose, we measured the lipidomic profile of wild-type mice and maLPA1-null mice in both hippocampus and serum. In addition, through immunohistochemical procedures we quantified NPY+ cells in hippocampus, basolateral amygdala (BLA) and central amygdala (CeA). Interestingly, the comparative lipidomics analysis revealed differences in certain subspecies which are related to LPA1 receptor functionality. Regarding NPY, we found a reduction in BLA, but not in hippocampus. Overall, both lipid abnormalities and amygdalar dysfunction of NPY can be related to lower resources in stress coping and, in turn, higher vulnerability to the noxious effect of stress that might lead to anxiety and depressive-like states. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

Prevalence of stress-related disorders, such as depression, is raising in modern societies. Indeed, current neurobiological research aims to elucidate the link between deregulation of the hypothalamic-pituitary-adrenal (HPA) axis among vulnerable individuals and the onset of depressive symptoms, such as social withdrawal. Herein, we seek to determine the role of LPA1 receptor in social behaviour and the performance of maLPA1-null mice, a model of anxious depression, in the dexamethasone (DEX) suppression test. For that purpose, we used the three-chamber test for social preference. Also, we administered vehicle or DEX 0.1mg/kg to wild-type (WT) mice and maLPA1-null mice, analysed corticosterone (CORT) response by ELISA method and determine glucocorticoid receptor (GR) expression and serum/glucocorticoid regulated kinase 1 (SGK1) in the hippocampus by Western-Blot analysis. We found that maLPA1-null mice lack preference for the social chamber as compared to WT animals. Additionally, mice lacking the LPA1 receptor did not suppress CORT after DEX treatment and increased significantly hippocampal SGK1 expression despite unaltered GR protein levels. These results provide further insight on the role of LPA1 receptors in depressive-like behavior and the pathological intracellular signals involved in stress regulation. Andalusian Regional Ministries of Economy, Innovation, Science and Employment (SEJ1863 to CP and CTS-643 to GE-T) and of Health (Nicolas Monardes Programme to GE-T). Spanish Ministry of Economy and Competitiveness (PSI2013-44901-P to LJS and CP; and co-financed with Funds of the European Commission “FEDER” PSI2017-83408-P to CP). Author AN-Q and RDM-F hold Grants of the Spanish Ministry of Education, Culture and Sports (FPU 16/05308; FPU14/01610, respectively). Author FJG-S held a Grant of the First Research and Transfer Plan of the University of Malaga. University of Malaga, Campus de Excelencia Internacional Andalucía Tech, and I Plan Propio de Investigación y Transferencia of the University of Malaga.

Adverse events can impact brain structure and function and are considered primary sources of risk for depression, anxiety, and other psychiatric disorders. In this sense, the neurobiological circuitry in charge of dealing with stressors has been widely studied in animal models. Our group has demonstrated a role for lysophosphatidic acid (LPA) through the LPA1-receptor in controlling anxious and depressive states, owing to aggravation of the detrimental consequences of stress in the brain. Indeed, our group has recently proposed the variant maLPA1-null mice, i.e. mice lacking the LPA1 receptor, as an endophenotype for anxious depression. In addition, we have previously reported hyperactivation of key stress-related brain areas after stress, such as basolateral amygdala. Here, we seek to further examine the engagement of the LPA1 receptor in the regulation of the limbic circuit following an acute stressor, tail suspension test, in wildtype and knockout animals. To that end, c-Fos expression was evaluated as a measure of functional activity in both basal and stress conditions, followed by interregional correlation matrices to establish the brain map of functional activation. Additionally, we observed whether one single dose of the antidepressant treatment with desipramine is able to normalize the functional brain map. Results revealed that the absence of the LPA1 receptor induce an anomalous pattern of brain functional activity after TST, which was reverted by desipramine administration.These results provide further insight to the involvement of the LPA1 receptor in stress regulation and shed light on divergent brain pathways under normal and vulnerability conditions that can be implicated in depressive symptoms. Finally, how this pattern might be reverted by antidepressant treatment can be useful for developing new pharmaceutical targets regarding the LPA1 receptor. Funding: Andalusian Ministry of Economy, Innovation, Science and Employment (SEJ1863 to C.P) and of Health (Nicolas Monardes programme, to G.E-T); the Spanish Ministry of Economy and Competitiveness (PSI2013-44901-P to L.J.S. and C.P.). Author R.D. M-F holds a Grant of the Spanish Ministry of Education, Culture and Sports (FPU14/01610). Author S.T. holds a Grant of the Andalusian Ministry of Economy, Innovation, Science and Employment (FPDI 2014). I Plan Propio de Investigación y Transferencia, Universidad de Málaga. Campus de Excelencia. Andalucía Tech.

Stress serves as an adaptive mechanism and helps organisms to cope with life-threatening situations. However, individual vulnerability to stress and dysregulation of this system may precipitate stress-related disorders such as depression. The neurobiological circuitry in charge of dealing with stressors has been widely studied in animal models. Recently our group has demonstrated a role for lysophosphatidic acid (LPA) through the LPA1 receptor in vulnerability to stress, in particular the lack of this receptor relates to robust decrease of adult hippocampal neurogenesis and induction of anxious and depressive states. Nevertheless, the specific abnormalities in the limbic circuit in reaction to stress remains unclear. The aim of this study is to examine the differences in the brain activation pattern in the presence or absence of LPA1 receptor after acute stress. For this purpose, we have studied the response of maLPA1-null male mice and normal wild type mice to an intense stressor: Tail Suspension Test. Activation induced by behaviour of brain regions involved in mood regulation was analysed by stereological quantification of c-Fos immunoreactive positive cells. We also conducted multidimensional scaling analysis in order to unravel coativation between structures. Our results revealed hyperactivity of stress-related structures such as amygdala and paraventricular nucleus of the hypothalamus in the knockout model and different patterns of coactivation in both genotypes using a multidimensional map. This data provides further evidence to the engagement of the LPA1 receptors in stress regulation and sheds light on different neural pathways under normal and vulnerability conditions that can lead to mood disorders. Universidad de Malaga, Campus de Excelencia internacional Andalucía Tech. Andalusian Ministry of Economy, Innovation, Science and Employment (SEJ1863); Postdoctoral Fellowship ‘Sara Borrell’ of the National Institute of Health Carlos III E. C.; Grant of the Andalusian Ministry of Economy, Innovation , Science and Employment C. R. (FPDI 2010). Grant of the Spanish Ministry of Education, Culture and Sport s (FPU14/01610).

Neurogenesis in the adult rat hippocampal subgranular zone and the subventricular zone of the lateral ventricles has been well documented. Increasing evidence suggests that neurogenesis also occurs in the adult hypothalamus. We report that, after intracerebroventricular treatment with insulin-like growth factor I (IGF-I), cell proliferation significantly increased in both the periventricular and the parenchymal zones of the whole hypothalamus. Proliferation was particularly abundant in a distinct periventricular zone of the caudal hypothalamus. This is an overlapping zone of transition, between the cubic ciliated ependymal, dorsally located, and the tanycytic ependyma, ventrally located, where three cell layers can be found: ciliated ependyma, subependyma and underlying tanycytes. After IGF-I treatment, proliferating cells were seen in the subependyma and in the layer of tanycytes. Neurons, astrocytes, tanycytes, microglia and endothelial cells of the local vessels were stained with the proliferative marker 5-bromo-2'-deoxyuridine (BrdU) in response to IGF-I. However, we never observed BrdU-positive ciliated cubic ependymal cells. In the subependyma, proliferating glial fibrillary acidic protein-positive astrocytes contacted the ventricle by an apical process bearing a single cilium and there were many labyrinthine extensions of the periventricular basement membranes. Both features are typical of neurogenic niches in other brain zones, suggesting that the central overlapping zone of the rat hypothalamic wall could be considered a neurogenic niche in response to IGF-I. These effects will be compared with those obtained for other factors. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

Depression is a debilitating psychiatric condition characterized by anhedonia and behavioural despair among others symptoms. Despite the high prevalence and devastating impact of depression, underlying neurobiological mechanisms of mood disorders are still not well known. Regardless its complexity, central features of this disease can be modelled in rodents in order to better understand the potential mechanisms underlying. On the other hand, the lack of LPA1 receptor compromises the morphological and functional integrity of the limbic circuit and the neurogenesis in hippocampus, induces cognitive alterations on hippocampal-dependent tasks and dysfunctional coping of chronic stress, provokes exaggerated endocrine responses to emotional stimuli and impairs adaptation of the hypothalamic-pituitary-adrenal axis after chronic stress. Factors, which all have been related with depression. Here, we sought to establish the involvement of the LPA1 receptor in regulation of mood and emotion. To this end, in wild-type and maLPA1-null mice active coping responses to stress were examined using the forced swimming test (FST). To assess hedonic behaviour saccharine preference test and female urine sniffing test were used. Our data indicated that the absence of the LPA1 receptor significantly affected to coping strategies. Thus, while null mice displayed less immobility than wt in FST, exhibited more climbing and less swimming behaviour, responses that could be interpreted as an emotional over-reaction (i.e., a panic-like response) to stress situations. Concerning hedonic behaviour, the lack of the LPA1 receptor diminished saccharin preference and female urine sniffing time. Overall, these data supports the role of LPA1 receptor in mood and emotional regulation. Specially, the lack of this receptor induced emotional dysregulation and anhedonic behaviour, a core symptom of depression. Universidad de Málaga, Campus de Excelencia Andalucía Tech. Andalusian Regional Ministries of Economy, Innovation, Science and Employment (SEJ-1863; CTS643) and of Health (PI-0234-2013; Nicolas Monardes Programme), MINECO (PSI2013-44901-P) and National Institute of Health Carlos III (Sara Borrel).

Background: In many cases there seems to exist a tight relationship between the integrity of the ependymal barrier and the onset of hydrocephalus (see 1). We wanted to investigate this by means of a repetitive model that could be easily raised in the laboratory from normal rats. Material and methods: We observed that the, easily available, enzyme neuraminidase from Clostridum perfringens destroys the ependyma (2). So we proved different amounts of the drug at different times and explored by means of morphological techniques, at structural and ultra-structural levels, the events occurring after the intracerebroventricular administration of the drug into the normal rat brain Results: The administration provoked the detachment of a great part of the ciliated cubic ependyma but not other types of ependyma, particularly those attached by tight junctions, as is the notable case of the choroid plexus. The effect is dose-dependent and led to hydrocephalus when the detachment is massive and affects the brain aqueduct. The absence of ependyma marks a zone of great permeability where the immuno-responsible cells proceeding from the vessels, mainly from those venules located in the choroid plexus, easily penetrated the brain parenchyma. With time, these zones are covered by impermeable astrocytic glial scars (3, 4). We think that this could represent a good model for study the relationships between the ependymal detach and the onset of hydrocephalus. Conclusions: The microbial neuraminidase broke the intercellular junctions of the ependymal line, non sealed by tight junctions. The dissapearance of this barrier led to an increased permeability or/and a stenosis of the cerebral acueduct that in turn provokes hydrocephalus. References: 1. Jiménez AJ, et al. Structure and function of the ependymal barrier and diseases associated with ependyma disruption. Tissue Barriers 2014 Mar 19;2:e28426. 2. Grondona JM et al. Ependymal denudation, aqueductal obliteration and hydrocephalus after a single injection of neuraminidase into the lateral ventricle of adult rats. J Neuropathol Exp Neurol. 1996 55:999-1008.

Comunicación en forma de poster al congreso Neuraminidase from Clostridium perfringens, which cleaves terminal sialic acid from carbohydrate chains, was injected in the lateral ventricle of rats. It diffused in the ipsilateral ventricle, the third ventricle, and also towards the periventricular brain parenchyma. Soon after, the complement system activated, and some ependymal cells detached and died. In the affected zones, there was an increased expression of GFAP in astrocytes, IBA1 in microglia, and ICAM1 in the endothelial cells of blood vessels. Cytokines, such as IL1β secreted by activated macrophages and microglia, provoked the extravasation of leucocytes from about 4 h post-injection. The main sources of cells were large venules located in the choroid plexus, the meninges and the subependyma around the foramen interventricularis. Invading cells arrived orderly: first neutrophils, then macrophage-monocytes, and last lymphocytes (mainly CD8α-positive T-lymphocytes). Leucocytes invaded the ventricle and the meninges, and also penetrated the brain parenchyma, sometimes passing through the ependyma and the glia limitans. As a result, some myelinated tracts suffered vacuolar degeneration, being the stria medullaris consistently affected. Oligodendrocytes in the damaged tracts were not affected. Vacuolated myelin recovered with time. Thus, the intracerebroventricular injection of neuraminidase may represent a novel reversible animal model to study experimental neuroinflammation and myelin vacuolization. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech. Ministerio de Ciencia e Innovación, SAF2010-19087; Junta de Andalucía, Consejería de Sanidad, SAS 08-0029; Junta de Andalucía, Proyecto de excelencia P-11-CVI-07637.

La formación del profesorado para las tareas de evaluación y tutorización de los Trabajos Fin de Grado (TFG) constituye uno de los factores importantes a tener en cuenta para su exitosa implantación. Así, el objetivo de este trabajo es presentar las experiencias de formación que se están desarrollando en la Universidad de Málaga para apoyar al profesorado en estas tareas, mostrando su diseño y los resultados obtenidos. Se han impartido tres ediciones de un curso sobre evaluación y tutorización de los TFG, con la participación de 127 profesores de dieciséis Facultades diferentes, que imparten TFG en más de 20 Titulaciones, habiéndose realizado 23 trabajos diferentes relacionados con la temática de los cursos. Abstract Teacher training for the tasks of assessment and tutoring is one of the key factors to consider for a successful implementation of the Final Year Proyect (FYP). The aim of this paper is to present the Universidad de Málaga teacher training experiences to support the teachers for these tasks, showing its design and results obtained with them. Three courses have been held on evaluation and tutoring of FYP. One hundred and twenty seven teachers from 16 different Faculties, who teach FYP in more than 20 official Degrees, have participated. Twenty-three reports, related with the aim of the course, have been developed by the participants. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

Fecha de lectura de Tesis Doctoral 31-1-2020 El LPA es un lípido bioactivo que está involucrado en la señalización intracelular a través de los seis receptores acoplados a proteínas G (LPA1-6). Entre estos receptores, LPA1 es un fuerte candidato para mediar los efectos centrales de LPA en la emoción y puede participar en la regulación de conductas emocionales normales. De hecho, los ratones que carecen del receptor LPA1 exhiben desregulación emocional y una aumentada vulnerabilidad a los efectos negativos del estrés (Pedraza et al., 2014; Castilla-Ortega et al., 2011). Por otro lado, la administración continuada de LPA induce diferentes efectos neurobiológicos y conductuales en animales de investigación. Con el objetivo de estudiar el efecto del estrés en el sistema de LPA hipocampal en esta tesis doctoral se ha puesto apunto la técnica MALDI-TOF para la determinación de las concentraciones de las diferentes especies de LPA en el hipocampo. Con ello, se han llegando a las siguientes conclusiones:1) En condiciones fisiológicas, la especie de LPA más abundante en el hipocampo de ratón es la 18:0, seguida de la 18:1, tanto en WT como en maLPA1-nulos. 2)La ausencia del receptor LPA1 no causa cambio en las concentraciones de LPA, aunque sí modificó ligeramente el perfil de LPA hipocampal.3) El estrés por inmovilización, fundamentalmente si no es aplicado junto a EPM, produjo cambios significativos en las concentraciones de LPA en hipocampo, en cambio el estrés inducido por EPM afectó las proporciones relativas de este sistema lipídico. 4) El efecto del estrés agudo fue mayor en los animales WT que en ausencia del receptor LPA1. 5)El estrés crónico aumentó la concentración de la especie LPA 18:0 sin alterar el resto de especies de LPA en el hipocampo. Y por último, 6) La administración continuada de LPA 18:1 provocó un aumento en los niveles relativos de la especie 18:1 en el hipocampo.