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Negative emotionality (NE) was evaluated as a candidate mechanism linking prenatal maternal affective symptoms and offspring internalizing problems during the preschool/early school age period. The participants were 335 mother–infant dyads from the Maternal Adversity, Vulnerability and Neurodevelopment project. A Confirmatory Bifactor Analysis (CFA) based on self-report measures of prenatal depression and pregnancy-specific anxiety generated a general factor representing overlapping symptoms of prenatal maternal psychopathology and four distinct symptom factors representing pregnancy-specific anxiety, negative affect, anhedonia and somatization. NE was rated by the mother at 18 and 36 months. CFA based on measures of father, mother, child-rated measures and a semistructured interview generated a general internalizing factor representing overlapping symptoms of child internalizing psychopathology accounting for the unique contribution of each informant. Path analyses revealed significant relationships among the general maternal affective psychopathology, the pregnancy- specific anxiety, and the child internalizing factors. Child NE mediated only the relationship between pregnancy-specific anxiety and the child internalizing factors. We highlighted the conditions in which prenatal maternal affective symptoms predicts child internalizing problems emerging early in development, including consideration of different mechanistic pathways for different maternal prenatal symptom presentations and child temperament.
Suicide is a multicausal phenomenon posing a great challenge to medicine and society, yet we still have limited knowledge concerning underlying biochemical, neuroanatomical and genetic factors. Research increasingly points to a role of the serotonergic system, both on the level of suicidal behavior, and such behavioural traits which may serve as important intermedier endophenotypes in suicide research. Although results are conflicting, several studies described an association between the 5-HTTLPR polymorphism and suicide, as well as this polymorphism and certain aggressive traits. Impulsive aggression is also thought to play a major contributory role in suicide. The aim of our research was to investigate the association between the 5-HTTLPR and aggressive traits in depressive patients carrying a higher risk for suicide and healthy controls.
Methods
137 major depressive and 164 healthy controls women were recruited. Participants completed the Buss-Durkee Hostility Inventory and were genotyped for 5-HTTLPR. Association of aggressive traits and indeces with 5-HTTLPR genotype in the two groups were analysed using ANCOVA.
Results
Diagnosis and 5-HTTLPR genotype showed a significant association with aggressive traits. The pattern of association was different in the depressed and control groups. The strongest interaction effect between genotype and diagnosis was observable in case of Resentment.
Conclusion
We found a significant association between 5-HTTLPR and several aggressive traits. In case of depressive patients the association was more marked. In depressed women the 5-HTTLPR shows a stronger association with aggressive traits related to aggression turned inward, which may play a role in the background of suicide.
Altered serum levels of vascular endothelial growth factor (VEGF) and tumor necrosis factor alpha (TNFalpha) have been implicated in therapy response of depression. We analyzed effects of 4 functional SNPs of VEGF and TNF alpha genes on MDD to test their possible role in pathomechanism of MDD.We recruited 293 inpatients diagnosed for major depressive disorder (MDD) and 443 healthy volunteers. MDD was diagnosed by DSM-IV criteria and measured by Montgomery-Asberg Depression Scale (MADRS). DNA was extracted from buccal mucosa samples given by all participants. Likelihood ratio tests for case-control and mutlivariate linear analysis for quantitative phenotype models were performed in SPSS 17.0 software. We identified a protective allele against MDD as the frequency of G allele of rs1800629 (previously associated with lower TNFa serum level) was 2.7 fold higher in the control group compared to MDD group (LRT = 4.197; p = 0.040). Higher frequency of the same allele was found among SSRI responders compared to non-responders (LRT = 6.281; p = 0.012). Significant GxG interactions were shown within MDD group: epistatic effect of allele variants and also genotypes of the four investigated SNPs were significant on MADRS score (for risk alleles: pmodell = 0.024; pinteraction = 0.005; Adj.R2 = 0.259; for genotypes: pmodell = 0.035; pinteraction = 0.007; Adj.R2 = 0.371). These findings suggest that TNFalpha and VEGF genes are associated with MDD and SSRI response. Our results support the molecular crosstalk between VEGF and TNFalpha pathway by a genetic interaction.This study was supported by the Hungarian Scientific Research Fund Grant (OTKA CK 80289/2009).
VEGF exerts diverse effects on the cardiovascular system. VEGF and its receptors are also expressed in the central nervous system. Moreover, accumulating data suggest that VEGF is involved in the etiopathogenesis of depression. to date, the association of the −2578 C/A SNP with depression has been investigated only by two research groups but their results are conflicting.
Aims:
In the present study we tried to assess the potential association of the −2578 C/A polymorphism with mood disorders (MDD and BD).
Methods:
220 patients (MDD: 140; BP: 80) with a current episode of major depression (MDE) were recruited at our department. HADS was used for the assessment of the severity of depressive symptoms. Control subjects without psychiatric history were also enrolled (n = 410). VEGF −2578 C/A SNP was analyzed with quantitative PCR.
Results:
We found no significant differences in allele frequencies between cases and controls (neither in the comparison of whole patient sample vs. controls nor in comparisons of patients with MDD or BP vs. controls). Nevertheless, depression scores of patients with MDD who carry the C allele were significantly higher (p = 0.012).
Conclusion:
Our preliminary results suggest that presence of the C allele might predispose to a more severe MDE in patients with MDD. This is in partial agreement with the results of Viiki et al. who found that the CC genotype was more frequent among patients with MDD than in control subjects and also associated with treatment resistant depression.
Acknowledgement:
The study was supported by OTKA 80289 national grant.
Despite growing evidence supporting the clinical interest of repetitive transcranial magnetic stimulation (rTMS) in treatment-resistant depression (TRD), little is known regarding the effects of clinical and sociodemographic factors on the clinical outcome in patients.
Methods
We retrospectively investigated the effects of clinical (using the 3-factor model of the Montgomery-Åsberg depression rating scale [MADRS] encompassing dysphoria, retardation and vegetative symptoms) and sociodemographic characteristics of participants on clinical outcome in a sample of 54 TRD patients receiving low frequency rTMS (1 Hz, 360 pulses) applied over the right dorsolateral prefrontal cortex combined with sham venlafaxine.
Results
Responders (n = 29) displayed lower retardation baseline scores (13.6 ± 2.9) than non-responders (15.6 ± 2.9; n = 25; P = 0.02). We also observed a significant difference between the numbers of ex-smokers in responders and non-responders groups; all ex-smokers (n = 8) were responders to rTMS (P = 0.005).
Conclusion
Low MADRS retardation factor and ex-smoker status is highly prevalent in responders to low frequency rTMS. Further studies are needed to investigate the predictive value of these factors.
A vast body of literature shows that maternal depression has long-term adverse consequences for children. However, only very few studies have documented the effect of maternal depression on children's ability to process emotional expressions and even fewer incorporated measures of observed maternal sensitivity to further tease apart whether it is the symptoms per se or the associated impact via maternal sensitivity that affects children's developing emotion-processing abilities. In a large community sample of Dutch preschoolers (N = 770), we examined independent and mediated effects of maternal depressive symptoms and sensitivity on children's ability to recognize emotional expressions using a nonverbal and a verbal task paradigm. Maternal depressive symptoms predicted less accurate emotion labeling in children, while maternal sensitivity was associated with more accurate emotion matching, especially for sadness and anger. Maternal sensitivity did not mediate the observed associations between mothers’ depressive symptoms and children's emotion recognition, and effects were similar for boys and girls. Given that maternal depressive symptoms and sensitivity affected nonoverlapping areas of young children's emotion recognition, prevention and intervention efforts should focus on both alleviating maternal depressive symptoms and improving maternal sensitivity at the same time in order to maximize benefit.
Understanding habitat selection and assessing habitat quality have an important role in habitat management and prioritisation of areas for protection. However, interpretations of habitat selection and habitat quality can be confounded by social effects such as conspecific attraction. Using 7 years’ data from a well monitored Great Bustard Otis tarda population in Central Europe, we investigated the roles of human disturbance and social cues in display site selection of male Great Bustards Otis tarda. The spatial distribution of displaying males was best predicted by human disturbance. In addition, the number of males attending display sites was strongly correlated to the number of females present and not with disturbance. This suggests that abundance could be a misleading metric for habitat quality in social species. Our results highlight the roles of disturbance and social cues in male habitat choice, and suggest that social factors need to be taken into consideration for management of endangered populations.
Humans live in large and extensive societies and spend much of their time interacting socially. Likewise, most other animals also interact socially. Social behaviour is of constant fascination to biologists and psychologists of many disciplines, from behavioural ecology to comparative biology and sociobiology. The two major approaches used to study social behaviour involve either the mechanism of behaviour - where it has come from and how it has evolved, or the function of the behaviour studied. With guest articles from leaders in the field, theoretical foundations along with recent advances are presented to give a truly multidisciplinary overview of social behaviour, for advanced undergraduate and graduate students. Topics include aggression, communication, group living, sexual behaviour and co-operative breeding. With examples ranging from bacteria to social mammals and humans, a variety of research tools are used, including candidate gene approaches, quantitative genetics, neuro-endocrine studies, cost-benefit and phylogenetic analyses and evolutionary game theory.
The great bustard Otis tarda became extinct in the UK during the 19th century due to a combination of factors, including hunting, egg collection and changes in agriculture. In 2003 a 10-year licence was granted to begin a trial to reintroduce the species back to the UK. Here we report on the first 5 years of the trial and assess the progress made towards establishing a founder population. From April 2004 to September 2009 a total of 102 great bustard chicks were imported from Russia and 86 released on Salisbury Plain. Monitoring showed that post-release survival was 18% in the first year following release, and that mortality of released bustards was mainly attributable to predation and collisions. Estimated adult survival was 74%, although the sample size was small. All known surviving great bustards are faithful to the surroundings of the release site, returning throughout the year. A lek has been established where males have been observed displaying to females. The first nesting attempt was in 2007, and in 2009 two females aged 3 and 4 years successfully nested, fledging one chick each. Models incorporating the new demographic estimates suggest that at the end of the 10-year trial period the project can expect to have 8–26 adults as a founder population.
This work reports a new type of actinospore, Unicapsulactinomyxon, which exhibits a unique morphological characteristic in that it has a single and large polar capsule (9·3×4·1 μm) (which possesses a longitudinally-folded polar filament) instead of the 3 polar capsules previously described for actinosporeans. The spore has a binucleated sporoplasm and 3 valves, each of which forms a long process. The spore has a total length of 241·3 μm. This parasite develops in groups of 8 inside pansporocysts in the coelomic cavity of the polychaete host. Molecular investigations on the SSU rDNA show that the new actinospore type is most closely related to Enteromyxum species (81–84% similarity). A survey of actinospore infections of the marine polychaete Diopatra neapolitana in 2007 and 2009, in the Aveiro Estuary (Portugal), showed an annual prevalence of 1·0% and 0·3%, respectively.
Social behaviour garners broad interest: biologists, social scientists, psychologists and economists all incorporate a consideration of social behaviour in their studies. This breadth of interest is unsurprising, as the vast majority of animals (and all that reproduce sexually) live partly (or fully) in social environments. As Robert Trivers (1985) succinctly put it, ‘Everybody has a social life.’ Some of this interest undoubtedly emerges because members of our own species (Homo sapiens) live in extensive societies and spend much time interacting with each other. Yet you do not have to be human for social behaviour to have a strong influence on biological processes. The significance of social behaviour is easy to see: if you isolate an ant, a fish or a bird from its peers in a sort of Kaspar Hauser setup, within a short time many of its ‘normal’ behaviours will change and be impaired. Social behaviour, heuristically defined as activities among members of the same species that have fitness consequences for both the focal individual and other individuals in the group, is thus ubiquitous.
The perplexing causes and far-reaching implications of social behaviour make it a rich subject to help understand evolution (Gardner & Foster 2008). The understanding of social evolution is challenging, given that social behaviour is often costly. Furthermore, unlike many traits that are passively selected by the environment, in the context of social behaviour the animals create selection for themselves by interacting with each other.
By
Lisa McGraw, University School of Medicine, Atlanta, Georgia, USA,
Tamás Székely, University of Bath, UK,
Larry J. Young, University School of Medicine, Atlanta, Georgia, USA
Pair bonds and parental behaviour are among the most variable social traits. To understand how and why these traits are so variable, we investigate three issues in this chapter. First, we present an overview of recent work on molecular and neural aspects of pair bonds and parental care using microtine rodents as model organisms. We focus on two neuropeptides, oxytocin and vasopressin, and show that although both molecules are found in both sexes, oxytocin plays a more prominent role in regulating parenting and pair bonding in females, whereas vasopressin serves this role in males. Variation in the expression of oxytocin and vasopressin receptors appears to contribute to species and individual differences in social behaviour. These studies also show that although oxytocin and vasopressin function in distinct brain regions, they act within the same neural circuit. Therefore, females and males appear to accomplish behavioural changes in pair bonding and parental care by altering the responsiveness of the same neural circuit. Second, studies of pair bonds and parental care in natural populations have revealed that these traits are often tied together. Cost–benefit analyses of both traits in a game-theoretic framework provide novel insights into how diverse pair bonding and parental care may have evolved. Recent work emphasises the role of social environment in influencing pair bonding and care. Finally, we point out that currently there is a schism between proximate and ultimate approaches to understanding pair bonding and parental care.
The study of social behaviour, often called sociobiology, is entering a new phase. A growing focus on mechanisms has enriched the older, evolutionary, perspective of sociobiology. The chapters in this book provide an overview of some of the most influential examples of research adopting the multifaceted approaches used to understand social evolution. There are top-down examinations of the way selection influences behaviour and, therefore, its neural and genetic structure, and bottom-up examinations of the genetic, hormonal or neurobiological substrates of behaviour. We therefore have a detailed understanding of the social, ecological, physiological, neurological, hormonal and genetic factors leading to complex social behaviour, but little integration. Picking apart the components and influences on behaviour is a reductionist approach, and although this has provided considerable insights we argue that it is now time for a synthetic perspective. We argue that a complementary perspective that unifies the particulate knowledge we have gained is now possible, and in keeping with current fashion we label this a systems biology approach to studying behavioural complexity. In reality, this is not new but a re-emphasis of the original synthetic view of sociobiology. Systems biology is simply a focus on interactions among components, and it works towards developing a predictive framework for resulting emergent properties of a system. Systems biology depends on a detailed understanding of the component parts to a system, and we believe this will be increasingly available for social behaviour, given the availability of new and less expensive approaches to gaining mechanistic information.