This study addressed how bilingual speakers switch between their first and second language when speaking. Event-related brain potentials (ERPs) and naming latencies were measured while unbalanced German (L1)-Dutch (L2) speakers performed a picture-naming task. Participants named pictures either in their L1 or in their L2 (blocked language conditions), or participants switched between their first and second language unpredictably (mixed language condition). Furthermore, form similarity between translation equivalents (cognate status) was manipulated. A cognate facilitation effect was found for L1 and L2 indicating phonological activation of the non-response language in blocked and mixed language conditions. The ERP data also revealed small but reliable effects of cognate status. IntroductionBilingual speakers show remarkable flexibility in their ability to control their language output. They can restrict their speech to one language only but also intentionally switch between languages in bilingual settings. The question arises how bilinguals select the intended language and what mechanisms they rely on when switching from one language to the other. Bilinguals vary in proficiency of their second language ranging from very high levels of proficiency (highly proficient bilinguals or balanced bilinguals) to low levels of proficiency (L2 learners and L2 attriters). Even highly proficient bilinguals usually have a dominant and a non-dominant language which is reflected, for instance, in faster picture-naming latencies for their first compared to their second language (e.g., Chen and Leung, 1989;Christoffels et al., 2006;Potter et al., 1984). However, under language switching conditions, this difference in naming latencies between L1 and L2 may disappear or even reverse, with shorter picture-naming latencies for the second than the first language (Costa and Santesteban, 2004;Costa et al., 2006;Meuter and Allport, 1999;Philipp et al., 2006; see also Kroll et al., 2006). Switching between languages may therefore profoundly affect production in the native tongue. In this study, we address intentional language switching and the impact of the bilingual switching context on distinguishing transient and sustained components of language control.
The high plasticity of the adolescent brain permits environmental influences to exert particularly strong effects on cortical circuitry. While this makes intellectual and emotional development possible, it also opens the door to potentially harmful influences.
The use of a tryptophan-rich hydrolyzed protein source may be more adequate to increase brain tryptophan and 5-HT function compared with intact alpha-lactalbumin protein or pure tryptophan.
A genetic predisposition to depression may be a potential risk factor in the development of depression. Although the neurobiological equivalent of the predisposition remains unclear, it seems as though the brain serotonin (5-HT) system plays an important mediating role. Therefore, individuals with a family history of depression (FH+) may be more likely to develop depression due to an innate vulnerability related to altered serotonergic neurotransmission in the brain. A major problem, however, is that the role of brain 5-HT in depression is complex and this serotonin-related innate vulnerability, by itself, is not sufficient enough to cause a depressive episode. In the search for additional factors, stress has received particular attention. Stressful life events influence and precede the onset of depression. Furthermore, depression is associated with stress hormone dysregulation and bidirectional interactions are thought to occur between stress-related changes in the neuroendocrine stress system and the 5-HT system. In the current review, we argue that healthy individuals with a positive family history of depression are more prone to develop depression due to a genetic 5-HT susceptibility, which deteriorates stress coping mechanisms and increases stress vulnerability.
Social‐Emotional competencies evolve early in life. For example, early emotion regulation is learned primarily in the context of mother–child interaction, which may allow for maternal influences to shape children's social‐emotional development. The aim of the current study was to longitudinally examine maternal determinants of children's early social‐emotional development in a community‐based sample of first‐time mothers (N = 61, aged 22–39 years). Specifically, we used structural equation modeling to examine how maternal emotion regulation difficulties and subclinical depression directly and indirectly, through sensitivity and postnatal bonding, assessed at 6 to 8 months predicted child outcomes at 12 to 16 months. We found that mothers’ sensitivity predicted fewer social‐emotional and behavioral problems and that stronger bonding predicted fewer problems and more social‐emotional competencies. Emotion regulation difficulties were significantly associated with depressive symptoms; yet, when accounting for shared variances, both factors differentially predicted less positive child outcomes such that more difficulties indirectly, through poorer bonding, predicted greater delay in competencies, and more symptoms indirectly, through less sensitivity, predicted more problems. Current findings underline the significance of maternal factors impacting the quality of mother–child interaction for children's positive development. Potential implications for early prevention programs to support children who are otherwise at risk for negative emotional outcomes due to mothers’ emotional state postpartum are discussed.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.