3,898 research outputs found

    Enriched Environment Experience Overcomes Learning Deficits and Depressive-Like Behavior Induced by Juvenile Stress

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    Mood disorders affect the lives and functioning of millions each year. Epidemiological studies indicate that childhood trauma is predominantly associated with higher rates of both mood and anxiety disorders. Exposure of rats to stress during juvenility (JS) (27–29 days of age) has comparable effects and was suggested as a model of induced predisposition for these disorders. The importance of the environment in the regulation of brain, behavior and physiology has long been recognized in biological, social and medical sciences. Here, we studied the effects of JS on emotional and cognitive aspects of depressive-like behavior in adulthood, on Hypothalamic-Pituitary-Adrenal (HPA) axis reactivity and on the expression of cell adhesion molecule L1 (L1-CAM). Furthermore, we combined it with the examination of potential reversibility by enriched environment (EE) of JS – induced disturbances of emotional and cognitive aspects of behavior in adulthood. Three groups were tested: Juvenile Stress –subjected to Juvenile stress; Enriched Environment – subjected to Juvenile stress and then, from day 30 on to EE; and Naïves. In adulthood, coping and stress responses were examined using the elevated plus-maze, open field, novel setting exploration and two way shuttle avoidance learning. We found that, JS rats showed anxiety- and depressive-like behaviors in adulthood, altered HPA axis activity and altered L1-CAM expression. Increased expression of L1-CAM was evident among JS rats in the basolateral amygdala (BLA) and Thalamus (TL). Furthermore, we found that EE could reverse most of the effects of Juvenile stress, both at the behavioral, endocrine and at the biochemical levels. The interaction between JS and EE resulted in an increased expression of L1-CAM in dorsal cornu ammonis (CA) area 1 (dCA1)

    Stimulus intensity-dependent modulations of hippocampal long-term potentiation by basolateral amygdala priming

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    There is growing realization that the relationship between memory and stress/emotionality is complicated, and may include both memory enhancing and memory impairing aspects. It has been suggested that the underlying mechanisms involve amygdala modulation of hippocampal synaptic plasticity, such as long-term potentiation (LTP). We recently reported that while in CA1 basolateral amygdala (BLA) priming impaired theta stimulation induced LTP, it enhanced LTP in the dentate gyrus (DG). However, emotional and stressfull experiences were found to activate synaptic plasticity within the BLA, raising the possibility that BLA modulation of other brain regions may be altered as well, as it may depend on the way the BLA is activated or is responding. In previous studies BLA priming stimulation was relatively weak (1 V, 50 μs pulse duration). In the present study we assessed the effects of two stronger levels of BLA priming stimulation (1 V or 2 V, 100 μs pulse duration) on LTP induction in hippocampal DG and CA1, in anesthetized rats. Results show that 1V-BLA priming stimulation enhanced but 2V-BLA priming stimulation impaired DG LTP; however, both levels of BLA priming stimulation impaired CA1 LTP, suggesting that modulation of hippocampal synaptic plasticity by amygdala is dependent on the degree of amygdala activation. These findings suggest that plasticity-induced within the amygdala, by stressful experiences induces a form of metaplasticity that would alter the way the amygdala may modulate memory-related processes in other brain areas, such as the hippocampus

    Exposure to Forced Swim Stress Alters Local Circuit Activity and Plasticity in the Dentate Gyrus of the Hippocampus

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    Studies have shown that, depending on its severity and context, stress can affect neural plasticity. Most related studies focused on synaptic plasticity and long-term potentiation (LTP) of principle cells. However, evidence suggests that following high-frequency stimulation, which induces LTP in principal cells, modifications also take place at the level of complex interactions with interneurons within the dentate gyrus, that is, at the local circuit level. So far, the possible effects of stress on local circuit activity and plasticity were not studied. Therefore, we set out to examine the possible alterations in local circuit activity and plasticity following exposure to stress. Local circuit activity and plasticity were measured by using frequency dependant inhibition (FDI) and commissural modulation protocols following exposure to a 15 minute-forced swim trial. Exposure to stress did not alter FDI. The application of theta-burst stimulation (TBS) reduced FDI in both control and stressed rats, but this type of plasticity was greater in stressed rats. Commissural-induced inhibition was significantly higher in stressed rats both before and after applying theta-burst stimulation. These findings indicate that the exposure to acute stress affects aspects of local circuit activity and plasticity in the dentate gyrus. It is possible that these alterations underlie some of the behavioral consequences of the stress experience

    Amygdala activation and GABAergic gene expression in hippocampal sub-regions at the interplay of stress and spatial learning

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    Molecular processes in GABAergic local circuit neurons critically contribute to information processing in the hippocampus and to stress-induced activation of the amygdala. In the current study, we determined expression changes in GABA-related factors induced in subregions of the dorsal hippocampus as well as in the BLA of rats 5 h after spatial learning in a Morris water maze (MWM), using laser microdissection and quantitative real-time PCR. Spatial learning resulted in highly selective pattern of changes in hippocampal subregions: gene expression levels of neuropeptide Y (NPY) were reduced in the hilus of the dentate gyrus (DG), whereas somatostatin (SST) was increased in the stratum oriens (SO) of CA3. The GABA-synthesizing enzymes GAD65 and GAD67 as well as the neuropeptide cholecystokinin (CCK) were reduced in SO of CA1. In the BLA, expression of GAD65 and GAD67 were reduced compared to a handled Control group. These expression patterns were further compared to alterations in a group of rats that have been exposed to the water maze but were not provided with an invisible escape platform. In this Water Exposure group, no expression changes were observed in any of the hippocampal subregions, but a differential regulation of all selected target genes was evident in the BLA. These findings suggest that expression changes of GABAergic factors in the hippocampus are associated with spatial learning, while additional stress effects modulate expression alterations in the BLA. Indeed, while in both experimental groups plasma corticosterone (CORT) levels were enhanced, only Water Exposure stress activated the basolateral amygdala (BLA), as indicated by increased levels of phosphorylated ERK 1/2. Altered GABAergic function in the BLA may thus contribute to memory consolidation in the hippocampus, in relation to levels of stress and emotionality associated with the experience

    From high anxiety trait to depression: a neurocognitive hypothesis

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    Although exposure to substantial stress has a major impact on the development of depression, there is considerable variability in the susceptibility of individuals to the adverse effects of stress. The personality trait of high anxiety has been identified as a vulnerability factor to develop depression. We propose here a new unifying model based on a series of neurocognitive mechanisms (and fed with crucial information provided by research on the fields of emotion, stress and cognition) whereby individuals presenting a high anxiety trait are particularly vulnerable to develop depression when facing stress and adversity. Our model highlights the importance of developing prevention programs addressed to restrain, in high anxious individuals, the triggering of a dysfunctional neurocognitive cascade while coping with stres

    Akutna primjena nikotina ne poboljšava kognitivne funkcije

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    Chronic smokers often claim that smoking improves their cognitive abilities, such as concentration. However, scientific evidence to support this claim is scarce. Previous studies gave inconclusive results, and some of them had significant methodological flaws. Therefore, the aim of this study was to test whether smoking a single cigarette affects performance across several cognitive domains. It included a group of 22 occasional smokers aged 19–29 years. Attention, working memory, and visuospatial reasoning were assessed using a within-subjects design with a control setting. There were two separate testing sessions two days apart. Half the group started with experimental and the other half with control setting. In the experimental setting, the participants completed the first block of tasks, smoked one cigarette (with a nicotine yield of 0.5 mg), and then completed the second block of tasks. In the control setting, the procedure was the same, except that the participants had a glass of water instead of a cigarette. Repeated measures ANOVA showed no significant effects of cigarette smoking on either reaction time rates or accuracy on any of the three cognitive domains. These results suggest that, at least among young, occasional smokers, smoking does not affect cognition and the claims of its improvement are probably a result of some sort of cognitive bias.Kronični pušači često tvrde da im pušenje, između ostaloga, pozitivno utječe na kognitivne sposobnosti (npr. pomaže im u održavanju koncentracije). Je li doista tako još uvijek nemamo jednoznačan odgovor, budući da su prethodne studije ne samo dale nekonzistentne rezultate nego su bile i metodološki manjkave. Stoga je cilj ovoga istraživanja bio utvrditi utječe li konzumacija jedne cigarete na izvedbu zadataka u nekoliko različitih kognitivnih domena. U istraživanju je sudjelovala skupina povremenih pušača u dobi od 19 do 29 godina. Pomoću računalnog programa E-Prime prezentirani su zadaci koji mjere pažnju, radno pamćenje i obradu vidno-prostornih informacija. Korišten je prije-poslije nacrt, uz kontrolni i eksperimentalni uvjet. Sudionici su iste zadatke rješavali četiri puta: prije i poslije tretmana u kontrolnom uvjetu te prije i poslije tretmana u eksperimentalnom uvjetu. U kontrolnom uvjetu tretman se sastojao od čaše vode koju su sudionici morali popiti, a u eksperimentalnom uvjetu od pušenja jedne cigarete koja otpušta 0,5 mg nikotina. Stanka između kontrolnoga i eksperimentalnoga testiranja bila je dva dana. Redoslijed uvjeta bio je rotiran. Niti u jednom zadatku nije utvrđen značajan utjecaj pušenja ni na vrijeme reakcije ni na točnost rješavanja. Ovi su nalazi u skladu s hipotezom da su samoiskazi o pozitivnom utjecaju pušenja na kognitivnu učinkovitost posljedica neutemeljenih subjektivnih dojmova

    Socioeconomic inequalities in health among Swedish adolescents - adding the subjective perspective

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    Abstract Background Socioeconomic inequalities in adolescent health predict future inequalities in adult health. Subjective measures of socioeconomic status (SES) may contribute with an increased understanding of these inequalities. The aim of this study was to investigate socioeconomic health inequalities using both a subjective and an objective measure of SES among Swedish adolescents. Method Cross-sectional HBSC-data from 2002 to 2014 was used with a total sample of 23,088 adolescents aged 11–15 years. Three measures of self-rated health (dependent variables) were assessed: multiple health complaints, life satisfaction and health perception. SES was measured objectively by the Family Affluence Scale (FAS) and subjectively by “perceived family wealth” (independent variables). The trend for health inequalities was investigated descriptively with independent t-tests and the relationship between independent and dependent variables was investigated with multiple logistic regression analysis. Gender, age and survey year was considered as possible confounders. Results Subjective SES was more strongly related to health outcomes than the objective measure (FAS). Also, the relation between FAS and health was weakened and even reversed (for multiple health complaints) when subjective SES was tested simultaneously in regression models (FAS OR: 1.03, CI: 1.00;1.06 and subjective SES OR: 0.66, CI: 0.63;0.68). Conclusions The level of socioeconomic inequalities in adolescent health varied depending on which measure that was used to define SES. When focusing on adolescents, the subjective appraisals of SES is important to consider because they seem to provide a stronger tool for identifying inequalities in health for this group. This finding is important for policy makers to consider given the persistence of health inequalities in Sweden and other high-income countries
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