A habenula lateral (LHb) inibe neurônios dopaminérgicos no mesencéfalo através de um nodo GABAérgico no tegmento mesopontino, o núcleo tegmental rostromedial (RMTg). Ambos a LHb e o RMTg também projetam para o núcleo dorsal da rafe (DR). A organização das projeções da LHb e do RMTg para o DR foi investigada através de injeções de um traçador anterógrado na LHb ou no RMTg e confirmada com injeções de traçadores retrógrados. Para identificar o fenótipo neuroquímico das projeções RMTg-DR, combinamos a hibridização in situ para mRNA de GAD67 com a detecção imunoistoquímica de traçadores retrógrados injetados no DR. Caracterizamos as subdivisões-alvo das projeções RMTg-DR através de dupla-imunofluorescência para o traçador anterógrado injetado no RMTg e serotonina ou o transportador vesicular de glutamato do tipo 3. Detectamos uma projeção focal direta da divisão medial da LHb para a parte caudal do DR. Em contraste, projeções GABAérgicas robustas do RMTg foram direcionadas para uma subdivisão central do DR enriquecida em neurônios presumidamente glutamatérgicos. / The lateral habenula (LHb) inhibits mesencephalic dopamine neurons through a mesopontine GABAergic node, the rostromedial tegmental nucleus (RMTg). Both LHb and RMTg also project to the dorsal raphe nucleus (DR). The organization of LHb and RMTg projections to the DR was investigated using anterograde tracer injections into the LHb or RMTg and confirmed with retrograde tracer injections. To identify the neurochemical phenotype of RMTg-DR projections, we associated in situ hybridization for GAD67 mRNA with immunohistochemical detection of retrograde tracers deposited in the DR. DR target regions of RMTg projections were characterized using double-imunofluorescence techniques for the anterograde tracer deposited into the RMTg and either serotonin or the type 3 vesicular glutamate transporter. We detected a focal direct projection from the medial LHb division to the caudal DR. In contrast the RMTg emits robust GABAergic projections to a central DR subdivision rich in presumptive glutamatergic neurons.

Dadas a elevada prevalência e os grandes prejuízos sociais, familiares e pessoais que caracterizam o envolvimento patológico com jogos de azar, torna-se necessária a investigação sistemática de fatores de vulnerabilidade e de resistência que possam influir no desenvolvimento de tais condições. Uma das principais estratégias utilizadas para a profilaxia e tratamento dessas formas de envolvimento patológico tem sido a investigação dos componentes biológico-genéticos do Jogo Patológico (JP). O presente estudo objetivou investigar a associação de polimorfismos de genes candidatos do sistema serotonérgico e JP em pares de irmãos discordantes para este diagnóstico. Participaram do estudo 140 pares de irmãos discordantes para o diagnóstico de JP pelos critérios do Manual Diagnóstico e Estatístico da Associação Psiquiátrica Americana, DSM-IV. Foram genotipados os seguintes polimorfismos de genes que codificam: o transportador da serotonina (polimorfismo 5HTTLPR-l/s), o receptor serotoninérgico subtipo 1B (5HT1B G861C), e o receptor serotoninérgico subtipo 2A (polimorfismos 5HT2A T102C e C516T). Na análise estatística observou-se uma maior distribuição do alelo C do polimorfismo T102C do gene 5HT2A no grupo de irmãos com o diagnóstico de JP (p<0,01), sugerindo uma possível contribuição desse alelo na predisposição ao JP. Entretanto, faz-se necessária a investigação desses polimorfismos em amostras independentes envolvendo o fenótipo JP para a confirmação dos achados apresentados nesse trabalho. Uma análise preliminar dos haplótipos (102 e 516) apresentou resultados inconclusivos. É interessante notar que há associação entre esse polimorfismo e manifestações psiquiátricas outras que não o JP. / The high prevalence and the great social, familial and personal hazards that appear along with the occurrence of pathological involvement in gambling makes it necessary to systematically investigate vulnerability and resilience factors that may influence the development of such a condition. One of the main strategies in prevention and treatment of these pathological behaviors has been the investigation of the biological-genetic basis of pathological gambling (PG). The present study aimed to determine any association between candidate gene polymorphisms of the serotoninergic system and the occurrence of PG in sib-pairs discordant for this diagnosis. One hundred and forty (140) PG-discordant sib-pairs were evaluated by the Diagnostic and Statistical Manual from the American Psychiatric Association (DSM-IV), who had already been previously genotyped in other studies. We genotyped the polymorphisms which codified: the serotonin transporter (5HTTLPRl/ s polymorphism), the serotonergic receptor subtype 1B (5HT1B G861C polymorphism), and the serotonergic receptor subtype 2A (T102C and C516T polymorphisms). Statistical analysis revealed a greater distribution of the C allele of the T102C polymorphism of the 5HT2A gene in the gambling sib group (p<0,01), suggesting a possible contribution of this allele in the predisposition for PG. Nevertheless, it is necessary to further investigate these polymorphisms in independent samples involving PG phenotype for the adequate confirmation of such findings. A preliminary analysis of the haplotypes (102 and 516) show inconclusive results. It is noteworthy that there are previous associations between this polymorphism and psychiatric manifestations other than PG.

A atividade da serotonina (5-HT) pode estar envolvida no desenvolvimento do câncer colorretal, embora detalhes desse processo permaneçam desconhecidos. Camundongos knockout (KO) para triptofano hidroxilase 1 (Tph1) falham em sintetizar 5-HT e fornecem um sistema modelo apropriado para estudar o papel deste neuro-hormônio na carcinogênese colorretal. Animais Tph1KO apresentaram um desenvolvimento reduzido de tumores alográficos e tumores colorretais induzidos por colite. No entanto, o tratamento carcinogênico colorretal promoveu um aumento do número de tumores induzidos pela exposição à um carcinógeno. Também se observou uma alta intensidade de dano de DNA no nicho de células-tronco do cólon, bem como uma redução na populações de células enteroendócrinas e aumento daquelas unidades caliciformes. Antes da ativação da ataxia telangiectasia relacionada a Rad 3 (ATR) e proteína 53 relacionada à transformação (Trp53), a síntese de 5-HT promoveu a atividade da O-6-metilguanina-DNA metiltransferase (MGMT) em resposta à exposição carcinogênica. O resgata da síntese de 5-HT através do tratamento com 5-hidroxitriptofano reduziu o dano de DNA induzido pela radiação. O papel protetor da 5-HT foi confirmado em camundongos transgênicos com perda específica da expressão de Tph1 nos intestinos. Esta investigação demonstra um papel protetor da síntese de 5-HT contra o desenvolvimento da carcinogênese colorretal. / Serotonin (5-HT) activity may impact on the development of colorectal cancer. However, details of this process remain unknown. Tryptophan hydroxylase 1 knockout (Tph1KO) mice fail to synthesize 5-HT and provide an appropriate model system to study the role of this neurohormone in colorectal carcinogenesis. Tph1KO mice have a decreased development of allograft tumors and colitis-induced colorectal tumors. However, colorectal carcinogen treatment led to increased tumor numbers, with high DNA damage intensity in the colonic stem cell niche. It was related to decreased numbers of enteroendocrine cells but an increase in the goblet cell population. Indeed, 5-HT synthesis promoted O-6-methylguanine-DNA methyltransferase activity in response to azoxymethane before activating ataxia telangiectasia and Rad3 related (ATR) and transformation related protein 53 (Trp53) expression. Radiation-induced DNA damage could be rescued by 5-hydroxytryptophan. The protective role of 5-HT was confirmed in transgenic mice with intestine-specific loss of Tph1 expression. This investigation reveals a protective role of 5-HT synthesis against the development of colorectal carcinogenesis.

Serotonin syndrome (SS) is a drug-induced toxicity caused by an excess of serotonin (5-HT) in the central nervous system (CNS). The symptoms of the disorder range from mild to severe, with the severe state evoking life-threatening hyperthermia. Autonomic dysfunction is controlled in part by serotonin receptors, with the 5-HT2A receptor responsible for increasing core body temperature (Tcor). Our results show that the 5-HT2A receptors on the preoptic/anterior hypothalamus (PO/AH) and prefrontal cortex (PFC), in particular, are sensitive to changes in ambient temperature (Tamb). The toxic increase of 5-HT is postulated to occur due to the temperature-dependent activation of these receptors that promotes a positive feedback mechanism. Our results suggest that changes in Tamb can either exacerbate or alleviate the symptom and that this is mediated by the 5-HT2A receptors. Understanding the mechanism involved in elevating Tcor is imperative in treating and preventing the disorder. / by Swapna Krishnamoorthy. / Vita. / Thesis (M.S.)--Florida Atlantic University, 2008. / Includes bibliography. / Electronic reproduction. Boca Raton, Fla., 2008. Mode of access: World Wide Web.

Performance during prolonged exercise capacity diminishes with increasing temperatures. The onset of fatigue under these conditions is not adequately explained by peripheral mechanisms. Recently, drugs which inhibit the reuptake of dopamine and noradrenaline in the brain have been found to improve exercise performance in warm conditions. The aim of this thesis was to further explore and characterise the role of these neurotransmitters during prolonged exercise in warm conditions by manipulating their reuptake or synthesis. The first series of experiments were designed to further investigate the effects of bupropion, a dopamine and noradrenaline reuptake inhibitor, which has been found to improve performance in warm conditions. To explore gender differences in response to acute bupropion administration, the effects of bupropion on prolonged exercise performance in warm conditions in women was investigated in Chapter 3. The results of this study suggest that during the follicular phase of the menstrual cycle, acute administration of bupropion improves exercise performance. To determine whether there are any dose-dependent effects of bupropion, the experiment in Chapter 4 was designed to test three different doses of bupropion. Exercise performance was only improved for the maximal dose, suggesting a threshold for the performance effects of bupropion. Catecholamine precursors do not appear to improve exercise performance as consistently as reuptake inhibitors. In agreement with previous studies, the dopamine precursor L-DOPA did not affect exercise performance in warm conditions in Chapter 5. In Chapter 6 the effect of the atypical antidepressant nutritional supplement S-adenosylmethionine was investigated for its role in the synthesis of dopamine and noradrenaline. S-adenosylmethionine appeared to negatively influence cognitive function, increased skin temperature and circulating prolactin concentrations, but no effects on exercise performance were observed.

by Ng Ka On. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 100-122). / Abstract --- p.i / Acknowledgement --- p.vi / Chapter 1. --- Introduction / Chapter 1.1 --- Testicular vasculature --- p.1 / Chapter 1.1.1 --- Structural organization --- p.1 / Chapter 1.1.2 --- Peculiar structural organization pertinent to the Consideration of function --- p.3 / Chapter 1.2 --- Importance of the blood flow to testicular function --- p.6 / Chapter 1.3 --- Measurement of testicular blood flow --- p.8 / Chapter 1.4 --- Control of testicular blood flow --- p.16 / Chapter 1.5 --- Adrenergic control in the testis --- p.18 / Chapter 1.5.1 --- Adrenergic innervation and source of catecholamines --- p.18 / Chapter 1.5.2 --- Regulation of testicular function --- p.20 / Chapter 1.5.3 --- Effect on testicular blood flow --- p.22 / Chapter 1.6 --- Serotonergic control in the testis --- p.23 / Chapter 1.6.1 --- Serotonergic innervation and source of serotonin --- p.23 / Chapter 1.6.2 --- Regulation of testicular function --- p.24 / Chapter 1.6.3 --- Effect on testicular blood flow --- p.25 / Chapter 1.7 --- Cholinergic control in the testis --- p.26 / Chapter 1.7.1 --- Cholinergic innervation and source of acetylcholine --- p.26 / Chapter 1.7.2 --- Regulation of testicular function --- p.28 / Chapter 1.7.3 --- Effect on testicular blood flow --- p.29 / Chapter 1.8 --- Aims of the study --- p.30 / Chapter 2. --- Materials and methods / Chapter 2.1 --- Animals --- p.31 / Chapter 2.2 --- Drugs and chemicals --- p.32 / Chapter 2.3 --- In vivo videomicroscopy method --- p.33 / Chapter 2.4 --- Hydrogen gas clearance method --- p.37 / Chapter 2.5 --- Data and statistical analyses --- p.45 / Chapter 3. --- Results / Chapter 3.1 --- Adrenergic control --- p.46 / Chapter 3.1.1 --- Response of the testicular subcapsular artery to adrenergic agonists and antagonists --- p.46 / Chapter 3.1.2 --- Effect of adrenergic agonists on testicular capillary blood flow --- p.57 / Chapter 3.2 --- Serotonergic control --- p.60 / Chapter 3.2.1 --- Response of the testicular subcapsular artery to serotonergic agonists and antagonists --- p.60 / Chapter 3.2.2 --- Effect of serotonergic agonists on testicular capillary blood flow --- p.69 / Chapter 3.3 --- Cholinergic control --- p.76 / Chapter 3.3.1 --- Response of the testicular subcapsular artery to serotonergic agonists and antagonists --- p.76 / Chapter 3.3.2 --- Effect of serotonergic agonists on testicular capillary blood flow --- p.79 / Chapter 4. --- Discussion / Chapter 4.1 --- Adrenergic control --- p.86 / Chapter 4.2 --- Serotonergic control --- p.90 / Chapter 4.3 --- Cholinergic control --- p.96 / Chapter 4.4 --- General discussion --- p.98 / Chapter 5. --- References --- p.100

Action control arises from the interaction of two anatomically distinct decision-making systems, namely goal-directed and habitual behaviour. Goal-directed behaviour is characterized by the consideration of future choices and respective outcomes whereas habitual responding is driven by stimulus-response associations. Response inhibition is essential for goal-directed behaviour and deficits are shown in impulsivity. We administered an acute clinically relevant dosage of the commonly used serotonin reuptake inhibitor escitalopram to sixty-six healthy volunteers in a double-blind, randomized, placebo-controlled design. We administered a large task battery in order to study the effect of escitalopram in several cognitive functions including response inhibition, learning and affective processing. We found dissociate effects on cognitive aspects possibly mediated by distinct cortico-striatal loops. Acute escitalopram administration had a beneficial effect on action cancellation, one aspect of inhibitory control, without any effect on action restraint or waiting impulsivity. The treatment resulted in impaired performance in a probabilistic reversal-learning task and increased sensitivity to misleading feedback thus leading to maladaptive performance. An extra-dimensional set shift impairment during an attention set shift task and a tendency towards impaired instrumental learning discrimination were also observed in the escitalopram group. Our results are discussed in the context of well-documented effects of the dopaminergic system and suggestions of opponent interaction of serotonin and dopamine.

Vitamin A and its derivatives, known as retinoids, are involved in a number of functions in the developing and adult brain (Lane et al., 2005). Roaccutane (13-cis-retinoic acid, 13-cis-RA) is a synthetic retinoid used for the treatment of severe cystic acne, although its use has been controversially associated with adverse psychiatric events including depression. In this thesis, the presence of retinoid receptors in the rat hippocampus was verified and a similar profile of expression was observed in the rat raphe nuclei for the first time. The expression of retinoid receptors in brain regions that are implicitly associated with depression pathology provides proof of concept for retinoids to influence depressive behaviour. The ability of 13-cis-RA treatment to induce a pro-depressive profile in animal models of depression-related behaviour was tested. In the resident-intruder paradigm, adult rats treated for 7 or 14 days with 13-cis-RA (1mg/kg, i.p.) showed reduced aggressive behaviour, with a concomitant increase in flight submit and flight escape behaviours, compared with vehicle-treated controls. These findings are indicative of increased depression-related behaviour. However, chronic treatment did not alter depression-related behaviour in the forced swim test and sucrose consumption anhedonia paradigms The molecular mechanisms mediating 13-cis-RA-induced depression were investigated by examining monoaminergic gene expression, protein levels and neurotransmitter levels in rat brain tissue and plasma and an in vitro model. The majority of serotonergic components (SERT, 5-HT1AR, 5-HT1BR and MAOA) were not altered by chronic 13-cis-RA treatment, with the possible exception of TPH2 gene/protein expression and increased 5-HT levels in platelets. In fact, the expression of D2 dopamine receptor was significantly elevated in the RN46A-B14 cell line (10μM 13-cis-RA, 48 h) and was similarly elevated at the protein level in the juvenile rat hippocampus (1mg/kg/day, i.p., 6 weeks), suggesting dopaminergic pathways may be of importance. There was also a trend in the data to suggest that 13-cis-RA-treated juvenile rats may be more susceptible the molecular alterations than corresponding adult rats. xii

Diferentes estudos mostram o envolvimento da serotonina na modulação de respostas comportamentais e autonômicas relacionadas à ansiedade. Enquanto estudos com modelos experimentais de conflito indicam que a serotonina no complexo amigdalóide aumenta a ansiedade, resultados obtidos com a estimulação elétrica da matéria cinzenta periquedutal sugerem um papel ansiolítico para este neurotransmissor. Tais evidências levaram Deakin e Graeff (1991) a propor que as diferentes vias serotoninérgicas que inervam o complexo amigdalóide e a matéria cinzenta periaquedutal seriam responsáveis pela modulação de comportamentos defensivos associados a dois diferentes transtornos de ansiedade, à ansiedade generalizada e ao pânico, respectivamente. De acordo com esta proposição, diante de estímulos que representam ameaças potenciais estas vias serotoninérgicas seriam ativadas gerando o aumento da liberação de serotonina em ambas as estruturas. No complexo amigdalóide, a serotonina facilitaria o comportamento de esquiva inibitória, enquanto que na matéria cinzenta periaquedutal inibiria a resposta de fuga. Para testar esta teoria em laboratório foi desenvolvido o teste do labirinto em T elevado, no qual é possível se avaliar, em um mesmo animal, respostas de esquiva inibitória e de fuga. De maneira geral, estudos com este modelo corroboram a proposição de Deakin e Graeff de que a transmissão serotoninérgica na matéria cinzenta periaquedutal inibe a resposta de fuga. No entanto, resultados conflitantes têm sido observados quanto ao papel da serotonina no complexo amigdalóide. Neste sentido, o presente estudo tem como objetivo estender as investigações quanto ao envolvimento do complexo amigdalóide na modulação de respostas defensivas associadas à ansiedade e ao pânico. Assim, pretende-se avaliar o efeito da ativação de receptores serotoninérgicos dos tipos 5-HT1A e 5-HT2A/2C dos núcleos basolateral e medial do complexo amigdalóide sobre as respostas defensivas geradas nos testes do labirinto em T elevado e da transição claro-escuro. O comportamento de esquiva gerado neste último teste, assim como a esquiva inibitória medida no labirinto em T elevado, tem sido associado à ansiedade generalizada. Para tal, foram realizadas injeções bilaterais intra-núcleo basolateral ou intra-núcleo medial do agonista de receptores 5-HT1A 8-OH-DPAT ou do agonista preferencial de receptores 5-HT2A DOI. Os efeitos destes agonistas foram comparados aos causados pela administração nos mesmo núcleos do agonista benzodiazepínico midazolam. Quanto aos efeitos das drogas injetadas no núcleo basolateral, nossos resultados mostram que a injeção de midazolam, 8-OH-DPAT e DOI prejudicou a resposta de esquiva nos dois testes. Além disso, os agonistas serotoninérgicos produziram efeito do tipo panicolítico sobre a resposta de fuga. Já em relação aos efeitos da injeção das drogas no núcleo medial, somente o 8-OH-DPAT prejudicou a tarefa de esquiva. Nenhum dos agonistas serotoninérgicos alterarou a resposta de fuga, que foi inibida somente pela injeção de midazolam. Deste modo, nossos resultados indicam que núcleos amigdalóides distintos podem modular diferencialmente respostas defensivas associadas à ansiedade e ao pânico. Enquanto o sistema serotoninérgico do núcleo basolateral parece modular tanto a resposta de esquiva como a resposta de fuga, o sistema serotoninérgico do núcleo medial parece modular somente a resposta de esquiva. O conjunto dos nossos resultados não corrobora a proposição (Deakin e Graeff, 1991) quanto ao papel preponderante do complexo amigdalóide em modular comportamentos expressos em resposta aos perigos potenciais ou distais, como a esquiva inibitória, e quanto à proposição de que a serotonina nesta estrutura teria o papel de facilitar respostas de ansiedade. Desta forma, os resultados do presente estudo indicam que o papel da serotonina no complexo amigdalóide é mais complexo e abrangente do que o proposto na teoria original de Deakin e Graeff (1991). / Different studies have revealed the involvement of serotonin in modulation of behavioral and autonomic responses related to anxiety. Evidences obtained in conflict models led to the suggestion that serotonin enhances anxiety by acting in the amygdaloid complex. In contrast, results with intracerebral drug injection associated with aversive electrical stimulation indicate that serotonin inhibits aversion in the periaqueductal gray matter. To solve this contradiction, Deakin and Graeff (1991) proposed that different serotoninergic pathways innervating the amygdaloid complex and the periaqueductal gray matter would be responsible for regulating defensive behaviors associated to generalized anxiety and panic disorders, respectively. According to this proposition, aversive stimuli representing potential threats activate these serotoninergic pathways and increase serotonin release in both brain areas. In the amygdaloid complex, serotonin facilitates inhibitory avoidance, whereas in the periaqueductal gray matter it inhibits escape response. To test this hypothesis, the elevated T-maze has been designed. In this test it is possible to evaluate, in the same rat, inhibitory avoidance and escape responses. Overall, studies performed in this model corroborate the preposition of Deakin and Graeff (1991) that serotoninergic transmission in the dorsal periaqueductal gray matter inhibits escape response. However, conflicting results have been reported regarding to the role of serotonin in the amygdaloid complex. The objective of the present study was to extend the investigation about the involvement of the amygdaloid complex in the modulation of defensive responses related to anxiety and panic. Thus, we evaluated the effects of the activation of 5-HT1A and 5-HT2A/2C receptors in the basolateral and medial amygdaloid nuclei on defensive responses generated by the elevated T-maze and light-dark transition tests. In the latter test, inhibitory avoidance has also been associated with generalized anxiety disorder. To this end, either the 5-HT1A receptor agonist 8-OH-DPAT or the preferential 5-HT2A receptor agonist DOI was microinjected into basolateral or medial amygdaloid nuclei. The effects of these drugs were compared to those caused by the administration of the benzodiazepinic agonist midazolam. The results showed that all the agonists injected in the basolateral nucleus impaired inhibitory avoidance in both tests. Furthermore, the serotoninergic agonists had a panicolytic-like effect on escape response. Regarding to the effects of drugs injected in the medial nucleus, only 8-OH-DPAT impaired inhibitory avoidance, while none of the serotoninergic agonists changed the escape response. These results indicate that distinct amygdaloid nuclei may differentially modulate defensive responses associated with anxiety and panic. Whereas the serotoninergic system in the basolateral nucleus modulates inhibitory avoidance and escape responses, this neurotransmitter in the medial nucleus seems to modulate only inhibitory avoidance. Our results do not support the view (Deakin e Graeff, 1991) that the amygdaloid complex plays a preponderant role in modulating only response to potential or distal threats as inhibitory avoidance, and that serotonin in this structure enhances anxiety. The present results suggest that the role played by serotonin in this brain area is more complex and pervasive than that proposed by Deakin and Graeff (1991).

Foram estudados os efeitos de um estresse social, produzido pela introdução de um rato, na condição de \"intruso\", por uma hora, em uma comunidade formada por três elementos (macho dominante, macho submisso e fêmea), com relações sociais pré-estabelecidas, sobre o comportamento, a bioquímica e a atividade imune inata de neutrófilos. Os animais intrusos apresentaram, em relação ao grupo controle, tendência a serem mais ativos e menos ansiosos no Campo Aberto e no Labirinto em Cruz Elevado, níveis significantemente mais elevados de corticosterona sérica, burst oxidativo induzido por SAPI significantemente aumentado e, tanto no córtex frontal como no hipotálamo, sistemas serotonérgicos significantemente mais ativados. Os dados, foram interpretados como decorrentes de uma reação de estresse preparando o organismo dos animais intrusos para novo desafio: um eixo HPA mais ativado, com conseqüências favoráveis para uma ação rápida; uma resposta imune inata mais efetiva, para defesa contra possíveis injúrias e uma neuroquímica denotando um refreamento de comportamentos impulsivos, permitindo escolhas mais adequadas em contexto de confrontação social. Essa reação tornou os organismos mais ativos e eficazes, um exemplo do aspecto positivo do estresse. Demonstrou-se, também, a existência e importância das grandes diferenças individuais e necessidade de se tratar estatisticamente e interpretar com muito cuidado os efeitos de estímulos estressores mais sutis, onde essas diferenças despontam com menor clareza e podendo induzir a erro interpretativo. / The present works shows the effects of social stress, produced by introducing a rat, in the condition of \"intruder\", for one hour, in a community formed for three elements namely a dominant male , submissive male and a female, with preset social relations, concerning their behaviour, the biochemistry and the innate immune activity of neutrophils. The intruder animals displayed, in relationship to the control group, a tendency towards being more active and less anxious in the Open Field and the Plus Maze, as well as of serum corticosterone levels with higher values, as well as its oxidative burst being significantly increased. And, as in the frontal cortex as in hypothalamus is concerned, the author found significant activation of serotonergic systems. The data, had been indicative of the function of the reaction of stress in order to prepare the organism for a challenge: a activated HPA axis was increased, with favorable consequences for a fast action; an innate immune reply more effective and neurochemistry denoting cohibition of impulsive behaviours, allowing more adjusted choices in the context of social confrontation This reaction turned the organisms more active and efficient, in an example of the positive aspect of stress reaction. The data also demonstrated the existence and importance of the great individual differences and the need of keeping in mind the statistic approach and very careful interpretation of subtle stressors, whenever these differences appear clearly and may eventually induce to an interpretative error.