Following interpersonal transgressions, victims? neuroticism and agreeableness have been previously associated with post-conflict anxiety and forgiveness. However, the perceptions that victims have about their transgressors? personalities have received little attention. The current investigation examined relationships between victims? neuroticism and agreeableness, their perceptions of their transgressors? agreeableness, and postconflict anxiety and affiliative motivation measured via plasma cortisol and oxytocin as well as self-reports of post-conflict anxiety and forgiveness in premenopausal women. Victims who perceived their transgressors as more agreeable reported lower post-conflict anxiety, experienced less plasma cortisol reactivity following a simulated speech to the transgressor, and more self-reported forgiveness. Exploratory analyses also revealed that forgiveness was negatively associated with oxytocin reactivity.

This paper presents an experimental study with 47 participants on the influence of lighting on performance and well-being in an office environment. Well-being, alertness and performance were evaluated and measured in two rooms with artificial lighting and one room with day lighting. The evaluations were correlated to cortisol/melatonin saliva samples, illuminance and spectral compo-sition of the lighting. The results show day lighting to have a sustained influence on alertness and performance and it is furthermore concluded that the level of cortisol in saliva was not influenced by the illuminance and did not have an influence on performance. The participants preferred a lighting with different kinds of light sources to a more neutral lightning and gave it higher ratings for well-being.The analysis shows that comfort did not influence alertness.

These studies present a series of novel roles for glucocorticoid signaling in the developing zebrafish embryo. The best-characterized roles of cortisol, the primary circulating corticosteroid in teleost fish, are known to occur by the activation of the glucocorticoid receptor (GR) in the post-hatch animal to mobilize energy reserves for response and recovery from stressful situations. For the first time, evidence is presented that GR and cortisol are key developmental regulators in the pre-hatch zebrafish embryo and that glucocorticoid signaling modulates multiple critical developmental pathways and affects embryogenesis in diverse ways. Prior to these experiments, very little was known regarding the developmental role of glucocorticoids in lower vertebrates. In mammalian models, there has been extensive study of the action of these steroids in late-stage organ maturation, and they have a variety of clinical and biomedical applications. However, in fish, there was a relative dearth of information regarding the basic dynamics and potential functional roles of cortisol and GR in embryogenesis. Zebrafish are a popular model for developmental study, with optically transparent embryos that allow for reliable observation. Additionally, the zebrafish genome is fully sequenced and extensively annotated, and a variety of molecular biology techniques are well-established in the existing literature. The zebrafish is also now recognized as an advantageous model for endocrine and stress axis studies, as it expresses a single GR gene, unique among teleosts but comparable to mammals. Preliminary studies published in the literature described cortisol and GR as deposited in the zebrafish embryo prior to fertilization, and showed their expression declining prior to hatch, then rising significantly as larvae approach the stage of first feeding. This dynamic expression of both ligand and receptor during embryogenesis, combined with knowledge from mammalian models, led to the hypothesis that glucocorticoid signaling may be functionally relevant in zebrafish development. A variety of techniques were used to examine the roles of cortisol and GR in the zebrafish embryo. Morpholino oligonucleotides were injected into one-cell embryos to block GR protein translation, allowing for the identification of GR-responsive developmental events and putative GR target genes. High-density microarray analysis of GR morphants presented numerous novel genes and pathways that are modulated by glucocorticoid signaling in the embryo. The ability to microinject molecules into a newly-fertilized zygote also allowed for other manipulations, including the addition of exogenous cortisol or the use of a cortisol-specific antibody to sequester maternally deposited cortisol. These studies provided the first evidence regarding the functional importance of the maternal cortisol deposition in the zebrafish oocyte prior to fertilization. The detailed temporal and spatial expression of GR mRNA and protein in the developing embryo has been characterized for the first time. GR expression is widespread, especially in developing mesoderm, and de novo GR transcription in the zebrafish embryo begins within 12 hours post fertilization. Lack of GR protein expression in the developing zebrafish embryo causes reduced growth, delayed somitogenesis, altered myogenesis, and severely reduces post-hatch survival. Additionally, GR modulates the expression of bone morphogenetic proteins, a family of morphogens that are involved in major developmental events including dorsoventral patterning, somitogenesis, myogenesis, and organogenesis. Reduction in GR protein content in the developing embryo is also linked to other major developmental processes including neurogenesis, eye formation, cellular adhesion, and development and function of the hypothalamic-pituitary-interrenal (HPI) axis. Cortisol in the early embryo, which is contributed entirely by maternal deposition prior to fertilization, is an important regulator of cardiogenesis and development of the HPI axis. Modulation of cortisol content in the early embryo causes an impairment of the post-hatch response to a physical stressor, as larvae exposed to increased cortisol during embryogenesis displayed an inability to increase heart rate in response to an acute physical stress, and did not display the classical increase in cortisol that follows a stressor challenge. Embryos that experience lowered glucocorticoid signaling in development tend to have a heightened post-hatch response to stress, further supporting the conclusion that HPI axis development is regulated by glucocorticoid signaling. These studies have identified key cardiogenic and HPI axis genes that are GR-responsive, providing mechanistic explanations for these phenotypic changes. Together these findings indicate that maternal deposition of cortisol in the embryo can pattern the post-hatch larva and has definitive impacts on performance as the offspring begin locomotion and approach feeding stages. In total, these studies demonstrate that glucocorticoid signaling is critically important to zebrafish embryogenesis, defining novel roles that are completely independent of the classical vertebrate stress response. These functions have significant effects on diverse developmental pathways and processes, and with the potential applicability of the zebrafish model to studies in higher vertebrates, may have important biomedical applications.

El cortisol és el principal glucocorticoide en peixos teleostis, assumint també funcions com a mineralocorticoide. És el principal indicador de la resposta a l'estrès, però també participa en diverses vies metabòliques, és immunosupresor amb funcions antiinflamatòries i és la principal hormona osmorreguladora en peixos. Al fetge, els glucocorticoides augmenten la transcripció de gens implicats en la gluconeogènesi, en el catabolisme dels aminoàcids i en la resposta de fase aguda. La secreció de cortisol en peixos està regulada per l'eix hipotalàmico-pituitàrio-interrenal (HPI), equivalent a l'eix hipotalàmico-pituitàrio-adrenal (HPA) en mamífers. Les hormones corticosteroidees, en mamífers, actuen a través de receptors intracel·lulars específics: el receptor mineralocorticoide (MR) i el receptor glucocorticoide (GR). Ambdós actuen com a factors de transcripció depenents del lligand. Darrerament s'ha demostrat que algunes espècies de peixos expressen un MR i/o més d'un GR. En aquest treball hem clonat, per primera vegada, el GR de l'orada (Sparus aurata). La regió codificant es tradueix en una proteïna putativa de 784 aa i mostra elevada homologia amb els principals dominis funcionals, domini d'unió a DNA i domini d'unió a l'hormona, d'altres GR, inclosos els de mamífers. L'expressió del GR de l'orada és ubiqua en els teixits i s'ha detectat a tots els teixits estudiats: cor, fetge, melsa, ronyó anterior i posterior, intestí, gònada, teixit adipós, brànquia, cervell i múscul.La resposta global a l'estrès requereix la interacció neuro-immuno-endocrina mitjançant comunicacions paracrines bidireccionals. Aquesta comunicació és important per a mantenir la homeostasi en diferents condicions estressants, inclosa l'endotoxèmia. L'endotoxina dels bacteris gramnegatius o LPS, en els vertebrats, desencadena una reacció immunitària complexa que implica la producció de citoquines proinflamatòries per part dels macròfags, principalment el TNF? (factor de necrosi tumoral ?) i la IL-1? (interleuquina 1 beta). Les citoquines produïdes en resposta al LPS estan implicades també en l'activació de l'eix HPA i activen, per tant, l'alliberació de cortisol. Els nostres resultats mostren que l'administració in vivo de LPS estimula l'eix HPI en l'orada desencadenant l'alliberació de cortisol, seguint un patró de resposta aguda. Aquesta hormona modula la resposta inflamatòria inhibint la producció de citoquines induïdes per LPS. El nostre estudi mostra que aquesta regulació es podria donar a través del GR perquè interfereix amb els factors de transcripció encarregats d'induir la transcripció de gens implicats en la resposta inflamatòria. L'expressió del GR en l'orada després d'una injecció de LPS ve regulada de manera específica segons el temps i el teixit. En general, veiem que existeix una correlació inversa entre els nivells de cortisol plasmàtic i els nivells d'expressió del GR en els teixits. La injecció intraperitoneal de LPS també augmenta l'expressió d'altres gens immunes (TNF?, IL1?, proteïna Mx, catepsina D, receptor activat proliferador de peroxisoma gamma (PPAR?)) en els principals teixits immunològics de l'orada, concretament a ronyó anterior, melsa, intestí anterior i brànquies. Els canvis en l'expressió d'aquests gens són diferents en funció del teixit i el temps.En el cultiu primari d'hepatòcits d'orada, dosis baixes d'un estímul immune (rTNF?) o endocrí (cortisol) alteren l'expressió de gens immunes (TNF?, IL1? i PPAR?) i endocrins (GR, catD), respectivament. Aplicant dosis més elevades es disminueix l'expressió de TNF? i GR, 12 hores després del tractament endocrí però no es detecten canvis amb el tractament immune. Els canvis en l'expressió d'aquests dos gens, després del tractament endocrí amb dosis altes, segueix una seqüència temporal, ja que 3 hores després augmenta l'expressió del GR i disminueix l'expressió del TNF?. Aquesta resposta demostra que, en peixos, la resposta inflamatòria pot estar regulada per les interaccions entre el cortisol i el seu receptor (GR).Finalment, la perca europea (Perca fluviatilis) sotmesa a factors estressants típics de les pràctiques aqüícoles (transport i manipulació) mostra la resposta fisiològica primària d'alliberació de cortisol però baix nivell d'activitat en les respostes secundàries, com la glucosa i el lactat. / Cortisol is the main glucocorticoid in teleosts, playing a rule also as mineralocorticoid. It is the main stress response indicator, but also participates in different metabolic pathways, as an immune-supressor with antiinflamatory actions and is the main osmorregulatory hormone in fishes. In the liver, glucocorticoids increase the gene transcription involved in gluconeogenesis, in the catabolism of amino acids and in the acute phase response. Cortisol secretion in fishes is regulated by the hypothalamic-pituitary-interrenal axis (HPI), equivalent to the hypothalamic-pituitary-adrenal axis (HPA) in mammals. In mammals, corticosteroids hormones act by specific intracellular receptors: mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) that act as ligand-dependant transcription factors. Recently, it has been demonstrated that some fish species can express one MR and/or more than one GR. In this work we have cloned, for the first time, GR of gilthead sea bream (Sparus aurata). The coding region translate to a putative protein of 784 aa and shows high homology with other species, including mammals, within the most important functional domains; DNA binding domain and hormone binding domain. Sea bream GR expression is ubiquitous in tissues and has been detected in all tissues studied: heart, liver, spleen, anterior and posterior kidney, intestine, gonads, adipose tissue, gill, brain and muscle.General response to stress, demands neuro-immune-endocrine interaction through bidireccional paracrine communication. This communication is important to maintain homeostasis under different stress conditions, including endotoxin stress. Gram-negative bacterial endotoxin or LPS, in vertebrates, induces a complex immune reaction that involves pro-inflammatory cytokine production by macrophages, mainly TNF? (tumor necrosis factor ?) and IL-1? (interleukin 1 beta). LPS-induced cytokines are involved in HPA activation and therefore activate cortisol release. Our results show that LPS in vivo administration stimulates the HPI axis in sea bream resulting in cortisol release, in an acute fashion. This hormone modulates the inflammatory response by inhibiting LPS-produced cytokines. Our study show that this regulation could be produced by GR as it is interfering with transcription factors involved in inducing inflammatory gene transcription. Sea bream GR expression after an LPS injection is specifically regulated in both time and tissue context. In general, we have observed that there is a reverse correlation between plasma cortisol levels and tissue GR expression levels. LPS intraperitoneal injection also increases immune gene expression (TNF?, IL1?, Mx protein, cathepsin D, peroxisome proliferator activated gamma (PPAR?)) in immunological tissues in sea bream, specifically head kidney, spleen, anterior intestine and gills. Changes in gene expression is both time and tissue dependant.In primary cultured hepatocytes of sea bream, low doses of an immune stimulation (rTNF?) or endocrine stimulation (cortisol) modifies expression of immune gene (TNF? IL1? i PPAR?) and endocrine genes (GR, catD), respectively. The highest doses applied decrease TNF? and GR expression 12 hours after endocrine treatment but there are no changes after immune treatment. Observed changes in gene expression follow a temporal response; 3 hours after a high dose of cortisol, GR expression increases and TNF? expression decreases. This response shows that, in fishes, inflammatory responses may be mediated by GR-cortisol interaction.Finally, European perch (Perca fluviatilis) subjected to typical stressor factors in aquaculture (transport and handling) have shown primary physiological response of cortisol release but a slow level in secondary responses such as glucose and lactate.

Over the recent years, venlafaxine has become the predominant antidepressant drug detected in municipal wastewater effluents (MWWE) and aquatic systems. However, very little is known about the effect of this drug in the aquatic environment on non-target organisms, including fish. Venlafaxine is a pharmaceutical compound designed to inhibit serotonin and norepinephrine reuptake, thereby increasing the synaptic availability of these neurotransmitters. In teleosts, the key aspect of stress adaptation involves the activation of the hypothalamus-pituitary-interrenal (HPI) axis, leading to the production of cortisol. Given that monoamine neurotransmitters (serotonin, norepinephrine, and dopamine) are involved in the regulation of a wide range of neuroendocrine responses, including stress axis function, my primary hypothesis was that venlafaxine acts as a neuroendocrine disruptor impacting the functioning of the corticosteroid stress axis in rainbow trout (Oncorhynchus mykiss). This hypothesis was tested through a series of in vivo exposure studies, as well as in vitro experiments, using environmentally relevant levels of venlafaxine, in order to tease out potential mode of action of this drug on target tissues involved in HPI axis functioning. The results suggest that venlafaxine alters monoamine neurotransmitter levels and their turnover rates in a region-specific manner in trout brain, and that the midbrain is the prime target. The monoamine changes may be responsible for the downstream effects on neuroendocrine responses coordinated in the hypothalamus, as this region receives monoaminergic inputs from the midbrain. The functional relevance of the above finding was confirmed by showing that venlafaxine exposure disrupted the neuroendocrine responses associated with social stress and appetite regulation. Functional downstream effects of HPI axis dysfunction were further confirmed by subjecting the fish to a handling disturbance, which revealed that the highly conserved cortisol and glucose responses to stressors were disrupted by venlafaxine. Also, there were tissue-specific effects of venlafaxine exposure on metabolic capacities, including enhanced gluconeogenesis and amino acid catabolism in the liver (a key glucose producing tissue), and alterations in the glycolytic capacity and sodium potassium ATPase activity in the gill (a key glucose utilizing tissue). The results suggest that the mode of action of venlafaxine may involve disruption of each target tissue involved in the HPI axis functioning. In vitro mechanistic studies indicated that hypothalamus functioning is disrupted by venlafaxine and this may involve effects mediated by serotonergic pathways. The reduced phosphorylation of cAMP response element binding protein (CREB) suggests that venlafaxine may impact downstream signalling cascades that are CREB-dependent. The transcript changes observed with venlafaxine in the hypothalamus include changes in mRNA levels of key genes involved in appetite regulation and stress response, including corticotropin releasing factor (CRF) and neuropeptide Y (NPY). At the pituitary level, venlafaxine impaired adrenocorticotropic hormone (ACTH) production, and this involved disruption of corticotropin releasing factor-receptor type 1 (CRF-R1), which is a key sensor for CRF stimulation. At the interrenal tissue level, the responsiveness of steroidogenic cells to ACTH stimulation was altered by venlafaxine and the mode of action appears to involve pathways upstream of the intracellular cAMP production. Also, cortisol biosynthetic capacity was disrupted by venlafaxine and this was accompanied by changes in transcript abundances of steroidogenic acute regulatory protein and cytochrome P450 side chain cleavage in the interrenal tissue. Taken together, the results demonstrate for the first time that the antidepressant venlafaxine, a human pharmaceutical contaminating aquatic systems, disrupts neuroendocrine responses and affects stress, feeding and metabolic responses in rainbow trout. The mode of action may include disruptions in brain monoamine levels and pathways involved in CREB signalling, while the exact mechanism of action remains to be elucidated. Exposure of fish to this pharmaceutical drug adversely affects the highly conserved adaptive responses that are essential to cope with subsequent stressors, and may translate into reduced fitness over the long-term. The findings underscore the necessity to understand the mechanisms of action of chemicals present in MWWE, and develop and utilize effective risk management strategies aimed at minimizing discharge of pharmaceuticals into the aquatic environment.

The current study compared infant cortisol responses during the still-face procedure with those shown during other parent-infant interactions. It also examined how stress hormones can affect memory retention. Six-month-old infants (n = 38) were exposed to either a repeated still-face procedure, normal face-to-face interaction, or a divided-attention task. Salivary cortisol was collected at multiple time points. Infants were assigned to a memory demonstration (n = 30) or a no-demonstration (n = 8) group. Infants in the demonstration group were shown 3 target actions with a puppet, and subsequently given a chance to repeat the target actions. Infants in the no demonstration group were not shown the target actions. Only the infants who experienced the still-face procedure showed a significant change in salivary cortisol throughout the procedure. Cortisol values did not significantly predict memory performance. There are still many questions regarding how stress induction during memory consolidation affects memory performance.

The current study compared infant cortisol responses during the still-face procedure with those shown during other parent-infant interactions. It also examined how stress hormones can affect memory retention. Six-month-old infants (n = 38) were exposed to either a repeated still-face procedure, normal face-to-face interaction, or a divided-attention task. Salivary cortisol was collected at multiple time points. Infants were assigned to a memory demonstration (n = 30) or a no-demonstration (n = 8) group. Infants in the demonstration group were shown 3 target actions with a puppet, and subsequently given a chance to repeat the target actions. Infants in the no demonstration group were not shown the target actions. Only the infants who experienced the still-face procedure showed a significant change in salivary cortisol throughout the procedure. Cortisol values did not significantly predict memory performance. There are still many questions regarding how stress induction during memory consolidation affects memory performance.

These studies present a series of novel roles for glucocorticoid signaling in the developing zebrafish embryo. The best-characterized roles of cortisol, the primary circulating corticosteroid in teleost fish, are known to occur by the activation of the glucocorticoid receptor (GR) in the post-hatch animal to mobilize energy reserves for response and recovery from stressful situations. For the first time, evidence is presented that GR and cortisol are key developmental regulators in the pre-hatch zebrafish embryo and that glucocorticoid signaling modulates multiple critical developmental pathways and affects embryogenesis in diverse ways. Prior to these experiments, very little was known regarding the developmental role of glucocorticoids in lower vertebrates. In mammalian models, there has been extensive study of the action of these steroids in late-stage organ maturation, and they have a variety of clinical and biomedical applications. However, in fish, there was a relative dearth of information regarding the basic dynamics and potential functional roles of cortisol and GR in embryogenesis. Zebrafish are a popular model for developmental study, with optically transparent embryos that allow for reliable observation. Additionally, the zebrafish genome is fully sequenced and extensively annotated, and a variety of molecular biology techniques are well-established in the existing literature. The zebrafish is also now recognized as an advantageous model for endocrine and stress axis studies, as it expresses a single GR gene, unique among teleosts but comparable to mammals. Preliminary studies published in the literature described cortisol and GR as deposited in the zebrafish embryo prior to fertilization, and showed their expression declining prior to hatch, then rising significantly as larvae approach the stage of first feeding. This dynamic expression of both ligand and receptor during embryogenesis, combined with knowledge from mammalian models, led to the hypothesis that glucocorticoid signaling may be functionally relevant in zebrafish development. A variety of techniques were used to examine the roles of cortisol and GR in the zebrafish embryo. Morpholino oligonucleotides were injected into one-cell embryos to block GR protein translation, allowing for the identification of GR-responsive developmental events and putative GR target genes. High-density microarray analysis of GR morphants presented numerous novel genes and pathways that are modulated by glucocorticoid signaling in the embryo. The ability to microinject molecules into a newly-fertilized zygote also allowed for other manipulations, including the addition of exogenous cortisol or the use of a cortisol-specific antibody to sequester maternally deposited cortisol. These studies provided the first evidence regarding the functional importance of the maternal cortisol deposition in the zebrafish oocyte prior to fertilization. The detailed temporal and spatial expression of GR mRNA and protein in the developing embryo has been characterized for the first time. GR expression is widespread, especially in developing mesoderm, and de novo GR transcription in the zebrafish embryo begins within 12 hours post fertilization. Lack of GR protein expression in the developing zebrafish embryo causes reduced growth, delayed somitogenesis, altered myogenesis, and severely reduces post-hatch survival. Additionally, GR modulates the expression of bone morphogenetic proteins, a family of morphogens that are involved in major developmental events including dorsoventral patterning, somitogenesis, myogenesis, and organogenesis. Reduction in GR protein content in the developing embryo is also linked to other major developmental processes including neurogenesis, eye formation, cellular adhesion, and development and function of the hypothalamic-pituitary-interrenal (HPI) axis. Cortisol in the early embryo, which is contributed entirely by maternal deposition prior to fertilization, is an important regulator of cardiogenesis and development of the HPI axis. Modulation of cortisol content in the early embryo causes an impairment of the post-hatch response to a physical stressor, as larvae exposed to increased cortisol during embryogenesis displayed an inability to increase heart rate in response to an acute physical stress, and did not display the classical increase in cortisol that follows a stressor challenge. Embryos that experience lowered glucocorticoid signaling in development tend to have a heightened post-hatch response to stress, further supporting the conclusion that HPI axis development is regulated by glucocorticoid signaling. These studies have identified key cardiogenic and HPI axis genes that are GR-responsive, providing mechanistic explanations for these phenotypic changes. Together these findings indicate that maternal deposition of cortisol in the embryo can pattern the post-hatch larva and has definitive impacts on performance as the offspring begin locomotion and approach feeding stages. In total, these studies demonstrate that glucocorticoid signaling is critically important to zebrafish embryogenesis, defining novel roles that are completely independent of the classical vertebrate stress response. These functions have significant effects on diverse developmental pathways and processes, and with the potential applicability of the zebrafish model to studies in higher vertebrates, may have important biomedical applications.

Incluir como ag?ncias financiadoras: Companhia Energ?tica de Minas Gerais S.A.(CEMIG), Companhia de Desenvolvimento dos Vales do S?o Francisco e do Parna?ba (CODEVASF). / Submitted by Jos? Henrique Henrique (jose.neves@ufvjm.edu.br) on 2018-09-21T20:50:29Z No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) stella_indira_rocha_lobato.pdf: 953253 bytes, checksum: 1b554bfb96e88b3984474bb4d25d0d9c (MD5) / Approved for entry into archive by Rodrigo Martins Cruz (rodrigo.cruz@ufvjm.edu.br) on 2018-10-04T19:12:25Z (GMT) No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) stella_indira_rocha_lobato.pdf: 953253 bytes, checksum: 1b554bfb96e88b3984474bb4d25d0d9c (MD5) / Made available in DSpace on 2018-10-04T19:12:25Z (GMT). No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) stella_indira_rocha_lobato.pdf: 953253 bytes, checksum: 1b554bfb96e88b3984474bb4d25d0d9c (MD5) Previous issue date: 2017 / Banco do Nordeste do Brasil (BNB) / Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico (CNPq) / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior (CAPES) / Funda??o de Amparo ? Pesquisa do estado de Minas Gerais (FAPEMIG) / Foram realizados dois experimentos, o primeiro para avaliar a influ?ncia do simbi?tico, do antibi?tico florfenicol e o cons?rcio de ambos, e o segundo avaliou o efeito do simbi?tico, antibi?tico e do probi?tico no cultivo de juvenis de matrinx? criados em baixa temperatura, sobre as vari?veis de desempenho produtivo, composi??o qu?mica corporal dos peixes, qualidade da ?gua e an?lise de cortisol. No primeiro experimento foram selecionados 250 juvenis, com peso e comprimento de 0,38 ? 0,07 g e 3,24 ? 0,19 cm, respectivamente, sob os seguintes tratamentos: controle ? ?gua e ra??o sem aditivo; SIMR - 2 g.kg - 1 de simbi?tico na ra??o; ANTAG - 0,002 g.L - 1 de antibi?tico na ?gua; ANTAG + SIMR - 0,002 g.L - 1 de antibi?tico na ?gua e 2 g.kg - 1 de simbi?tico na ra??o; ANTR - 0,01 g.kg - 1 de antibi?tico na ra??o, dispostos em delineamento inteiramente casualizado, com cinco tratamentos e cinco repeti??es de 10 peixes por aqu?rio. No segundo experimento 200 animais foram utilizados, com peso e comprimento de 2,38 ? 0,51 g e 6,32 ? 0,52 cm, respectivamente, sob os seguintes tratamentos: Controle - ra??o sem inclus?o de aditivo; PROBR - 10 g.kg - 1 de Saccharomyces cerevisiae na ra??o; SIMBR - 2 g.kg - 1 de simbi?tico na ra??o; ANTR - 0,01 g.kg - 1 de antibi?tico na ra??o, dispostos em delineamento inteiramente casualizado com cinco tratamentos e cinco repeti??es de 10 peixes por aqu?rio. Os dois experimentos tiveram dura??o de 60 dias em sistema fechado de recircula??o de ?gua no Setor de Aquicultura e Ecologia Aqu?tica da UFVJM. Para o primeiro experimento os juvenis de matrinx? n?o apresentaram diferen?a para os par?metros de desempenho produtivo e sobreviv?ncia em nenhum dos tratamentos avaliados. J? para a composi??o qu?mica dos peixes verificou-se uma maior concentra??o de mat?ria seca com o tratamento contendo antibi?tico na ra??o quando comparado ao grupo controle. O cultivo de juvenis de Brycon amazonicus suplementadas com simbi?tico, antibi?tico e/ou cons?rcio de ambos em baixas temperatura n?o melhora o desempenho dos peixes. Os aditivos estudados n?o interferem nos par?metros de qualidade da ?gua, observado pelas altas taxas de sobreviv?ncia. As condi??es adequadas dispensam o uso de antibi?tico e simbi?tico. Para o segundo experimento, os par?metros de consumo de ra??o, convers?o alimentar e o fator de condi??o de Fulton apresentaram melhores resultados com a inclus?o de antibi?tico na dieta. Os tratamentos com o probi?tico na ra??o, simbi?tico na ra??o e antibi?tico na ra??o, apresentaram menor teor de cortisol plasm?tico quando comparado com o grupo controle. Portanto, indica-se o uso de antibi?tico para melhorar o rendimento de cultivo de matrinx?, e antibi?tico, simbi?tico e probi?tico como fator antiestressante. / Disserta??o (Mestrado) ? Programa de P?s-Gradua??o em Zootecnia, Universidade Federal dos Vales do Jequitinhonha e Mucuri, 2017. / Two experiments were carried out, the first one to evaluate the influence of the symbiotic antibiotic florfenicol and the consortium of both, and the second one evaluated the symbiotic, antibiotic and probiotic effects in the cultivation of juveniles of matrinx? raised in low temperature, on the variables of productive performance, che mical composition of fish, water quality and cortisol analysis. In the first experiment, 250 juveniles were selected, with weight and length of 0,38 ? 0,07 g and 3,24 ? 0,19 cm, respectively, under the following treatments: control - water and feed without additive; SIMR - 2 g.kg - 1 of symbiotic in ration; ANTAG - 0.002 g.L - 1 of antibiotic in water; ANTAG + SIMR - 0.002 g.L - 1 of antibiotic in water and 2 g.kg - 1 of symbiotic in ration; ANTR - 0.01 g.kg - 1 of antibiotic in the diet, arranged in a completely ran domized design, with five treatments and five replicates of 10 fish per aquarium. In the second experiment 200 animals were used, with weight and length of 2.38 ? 0.51 g and 6.32 ? 0.52 cm, respectively, under the following treatments: Control - ration wit hout inclusion of additive; PROBR - 10 g.kg - 1 of Saccharomyces cerevisiae in the diet; SIMBR - 2 g.kg - 1 of symbiotic in ration; ANTR - 0.01 g.kg - 1 of antibiotic in the diet, arranged in a completely randomized design with five treatments and five of 10 fis h per aquarium. The two experiments had a duration of 60 days in a closed water recirculation system in the Aquaculture and Aquatic Ecology Sector of the UFVJM. For the first experiment the juveniles of matrinx? presented no difference to the parameters of productive performance and survival in any of the evaluated treatments. For the chemical composition of the fish, a higher concentration of dry matter was observed with the treatment containing antibiotic in the diet when compared to the control group. Th e cultivation of juveniles of Brycon amazonicus supplemented with symbiotic, antibiotic and/or consortium of both at low temperature does not improve fish performance. The additives studied did not interfere in the parameters of water quality, observed by the high survival rates. Adequate conditions do not require antibiotic and symbiotic use. For the second experiment, the parameters of feed intake, feed conversion and Fulton condition factor presented better results with the inclusion of antibiotic in the diet. Treatments with probiotic in the diet, symbiotic in ration and antibiotic in ration, had lower levels of plasma cortisol when compared to the control group. Therefore, the use of antibiotic to improve the yield of matrinx?, and antibiotic, symbiotic and probiotic culture as an anti - stressing factor is indicated.

A well-developed body of literature has established the deleterious effects of chronic stress on children’s cognitive development. However, there has been almost no research examining the impact of acutely stressful experiences on children’s cognitive performance. This is surprising given evidence in adults that acute stress alters cognition and plausible links between stress system reactivity and cognitive function. Extending such temporally precise acute stress research to the childhood age range may be valuable for identifying new ways to support children’s function across contexts and elucidating how repetitive stress leads to pervasive alterations in cognitive development. The first chapter reviews the theorized links between acute stress and subsequent cognitive vulnerability as well as the possible role of biological stress systems (i.e. autonomic nervous system, ANS; Hypothalamic Pituitary Adrenal Axis, HPA) in supporting cognitive function. The second chapter serves to validate an in-laboratory stressor paradigm (modified from previous research) as effective at inducing biological reactivity across HPA and ANS systems. Validating this ‘matching task’ was important given the challenges of eliciting stress system reactivity in the early childhood age range. In the third chapter, the relevance of stress system reactivity to children’s concurrent performance on a cognitively challenging matching task was examined. This study was conducted to establish profiles of HPA and ANS (parasympathetic, PNS, and sympathetic, SNS, branches) associated with adaptive cognitive function, under stress. Results indicated that indices of both HPA and PNS reactivity were predictive of cognitive performance, with different results by gender. Finally, we examined the extent to which acute stress (versus control) altered children’s subsequent selective attention and inhibitory control performance. Largely consistent with the adult literature employing Go/No-Go tasks, stress-exposed children experienced selective attention impairment, but no inhibitory control change. Amongst stress-exposed children, higher maternal stress predicted selective attention impairment, which highlights the relevance of early caregiving to children’s stress regulatory ability. In contrary to hypotheses, this effect was not mediated by HPA or ANS reactivity. The final chapter concludes with a discussion of broad implications, limitations, and future directions for acute stress research in early childhood. / 10000-01-01