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BackgroundSubstance use (SU) typically increases from middle to late adolescence. Anxiety is one factor associated with greater SU, although variability in who uses substances remains. Some models suggest that brain-based susceptibility markers could reveal which adolescents are at a higher risk for psychopathology, but it is unknown whether these individual differences attenuate or accentuate the association between anxiety and elevated SU even if normative. This study addressed this gap by testing whether neural response to social exclusion moderates the association between anxiety symptoms and increased SU from middle to late adolescence.MethodsParticipants were 181 Mexican-origin adolescents (48% female; 16-17 years old) who completed a social exclusion task during a functional magnetic resonance imaging scan and filled out questionnaires about their SU and anxiety symptoms. Analyses focused on neural response to social exclusion versus inclusion within 3 regions of interest and change in SU across 2 years.ResultsDorsal anterior cingulate cortex response to social exclusion, but not subgenual anterior cingulate cortex or anterior insula, moderated the relation between anxiety symptoms and SU, such that higher anxiety symptoms predicted a greater relative increase in SU only for those youth with a lower dorsal anterior cingulate cortex response to exclusion.ConclusionsBlunted dorsal anterior cingulate cortex response to social exclusion may serve as a neural susceptibility marker of altered conflict monitoring or emotion regulation in middle adolescence that, in combination with high levels of anxious feelings, elevates the risk for onset of and/or increased SU by late adolescence. These findings have implications for designing targeted interventions to mitigate SU among adolescents.

Early adversities, including prenatal drug exposure (PDE) and a negative postnatal emotional caregiving environment, impact children's long-term development. The protracted developmental course of memory and its underlying neural systems offer a valuable framework for understanding the longitudinal associations of pre- and postnatal factors on children with PDE. This study longitudinally examines memory and hippocampal development in 69 parent-child dyads to investigate how the early caregiving emotional environment affects children with PDE's neural and cognitive systems. Measures of physical health, drug exposure, caregiver stress, depression, and distress were collected between 0 and 24 months At age 14 years, adolescents completed multiple measures of episodic memory, and at ages 14 and 18 years, adolescents underwent magnetic resonance imaging (MRI) scans. Latent constructs of episodic memory and the caregiving environment were created using Confirmatory Factor Analysis. Multiple regressions revealed a negative emotional caregiving environment during infancy was associated with poor memory performance and smaller left hippocampal volumes at 14 years. Better memory performance at 14 years predicted larger right hippocampal volume at 18 years. At 18 years, the association between the emotional caregiving environment and hippocampal volume was moderated by sex, such that a negative emotional caregiving environment was associated with larger left hippocampal volumes in males but not females. Findings suggest that the postnatal caregiving environment may modulate the effects of PDE across development, influencing neurocognitive development. [ABSTRACT FROM AUTHOR]

Early adversities, including prenatal drug exposure (PDE) and a negative postnatal emotional caregiving environment, impact children’s long-term development. The protracted developmental course of memory and its underlying neural systems offer a valuable framework for understanding the longitudinal associations of pre- and postnatal factors on children with PDE. This study longitudinally examines memory and hippocampal development in 69 parent–child dyads to investigate how the early caregiving emotional environment affects children with PDE’s neural and cognitive systems. Measures of physical health, drug exposure, caregiver stress, depression, and distress were collected between 0 and 24 months At age 14 years, adolescents completed multiple measures of episodic memory, and at ages 14 and 18 years, adolescents underwent magnetic resonance imaging (MRI) scans. Latent constructs of episodic memory and the caregiving environment were created using Confirmatory Factor Analysis. Multiple regressions revealed a negative emotional caregiving environment during infancy was associated with poor memory performance and smaller left hippocampal volumes at 14 years. Better memory performance at 14 years predicted larger right hippocampal volume at 18 years. At 18 years, the association between the emotional caregiving environment and hippocampal volume was moderated by sex, such that a negative emotional caregiving environment was associated with larger left hippocampal volumes in males but not females. Findings suggest that the postnatal caregiving environment may modulate the effects of PDE across development, influencing neurocognitive development.

Uncertainty permeates decisions from the trivial to the profound. Integrating brain and behavioral evidence, we discuss how probabilistic (varied outcomes) and temporal (delayed outcomes) uncertainty differ across age and individuals; how critical tests adjudicate between theories of uncertainty (prospect theory and fuzzy-trace theory); and how these mechanisms might be represented in the brain. The same categorical gist representations of gains and losses account for choices and eye-tracking data in both value-allocation (add money to gambles) and risky-choice tasks, disconfirming prospect theory and confirming predictions of fuzzy-trace theory. The analysis is extended to delay discounting and disambiguated choices, explaining hidden-zero effects that similarly turn on categorical distinctions between some gain and no gain, certain gain and uncertain gain, gain and loss, and now and later. Bold activation implicates dorsolateral prefrontal and posterior parietal cortices in gist strategies that are not just one tool in a grab-bag of cognitive options but rather are general strategies that systematically predict behaviors across many different tasks involving probabilistic and temporal uncertainty. High valuation (e.g., ventral striatum; ventromedial prefrontal cortex) and low executive control (e.g., lateral prefrontal cortex) contribute to risky and impatient choices, especially in youth. However, valuation in ventral striatum supports reward-maximizing and gist strategies in adulthood. Indeed, processing becomes less "rational" in the sense of maximizing gains and more noncompensatory (eye movements indicate fewer tradeoffs) as development progresses from adolescence to adulthood, as predicted. Implications for theoretically predicted "public-health paradoxes" are discussed, including gist versus verbatim thinking in drug experimentation and addiction. [ABSTRACT FROM AUTHOR]

Graph theory analysis of structural brain networks derived from diffusion tensor imaging (DTI) has become a popular analytical method in neuroscience, enabling advanced investigations of neurological and psychiatric disorders. The purpose of this study was to investigate (1) the effects of edge weighting schemes and (2) the effects of varying interscan periods on graph metrics within the adolescent brain. We compared a binary (B) network definition with three weighting schemes: fractional anisotropy (FA), streamline count, and streamline count with density and length correction (SDL). Two commonly used global and two local graph metrics were examined. The analysis was conducted with two groups of adolescent volunteers who received DTI scans either 12 weeks apart (16.62 ± 1.10 years) or within the same scanning session (30 min apart) (16.65 ± 1.14 years). The intraclass correlation coefficient was used to assess test-retest reliability and the coefficient of variation (CV) was used to assess precision. On average, each edge scheme produced reliable results at both time intervals. Weighted measures outperformed binary measures, with SDL weights producing the most reliable metrics. All edge schemes except FA displayed high CV values, leaving FA as the only edge scheme that consistently showed high precision while also producing reliable results. Overall findings suggest that FA weights are more suited for DTI connectome studies in adolescents.

Summary: Sleep spindles are developmentally relevant cortical oscillatory patterns; however, they have mostly been studied by considering the entire spindle frequency range (11–15 Hz) without a distinction between the functionally and topographically different slow and fast spindles, using relatively few electrodes and analysing wide age‐ranges. Here, we employ high‐density night sleep electroencephalography in three age‐groups between 12 and 20 years of age (30 females and 30 males) and analyse the adolescent developmental pattern of the four major parameters of slow and fast sleep spindles. Most of our findings corroborate those very few previous studies that also make a distinction between slow and fast spindles in their developmental analysis. We find spindle frequency increasing with age. A spindle density change is not obvious in our study. We confirm the declining tendencies for amplitude and duration, although within narrower, more specific age‐windows than previously determined. Spindle frequency seems to be higher in females in the oldest age‐group. Based on the pattern of our findings, we suggest that high‐density electroencephalography, specifically targeting slow and fast spindle ranges and relatively narrow age‐ranges would advance the understanding of both adolescent cortical maturation and development and the functional relevance of sleep spindles in general. [ABSTRACT FROM AUTHOR]

Introduction: Childhood trauma is known to have dramatic effects on the risks for developing psychiatric disorders and increased suicidality. We conducted a meta-analysis of whole brain voxel-based morphometry (VBM) correlates of childhood trauma in adolescents exposed to childhood maltreatment (N = 379) and unexposed controls (N = 348). Methods: Anisotropic effect size-signed differential mapping (AES-SDM) was utilized to synthesize the studies. Results: We observed increased volume amongst adolescents with a history of childhood trauma in regions that are involved in motor functions and language production: left precentral gyrus, including part of the left inferior frontal gyrus, left fibers of the body of corpus callosum, and left postcentral gyrus. We observed decreased volume amongst adolescents with a history of childhood trauma in regions that are involved in language processing and/or sensory processing: bilateral cerebellum, bilateral middle temporal gyrus, left rostrum of corpus callosum, and bilateral supramarginal gyrus. Discussion: We suggest that these morphometric differences may be reflective of impaired motor development and increased sensory sensitivity and hypervigilance in adolescents with experiences of childhood trauma. Our results differ from meta-analytical findings in adults with history of childhood trauma and may contribute to a better understanding of neural mechanisms of childhood trauma, prediction of neurodevelopmental outcomes, and development of more effective and personalized therapies. [ABSTRACT FROM AUTHOR]

IntroductionChildhood trauma is known to have dramatic effects on the risks for developing psychiatric disorders and increased suicidality. We conducted a meta-analysis of whole brain voxel-based morphometry (VBM) correlates of childhood trauma in adolescents exposed to childhood maltreatment (N = 379) and unexposed controls (N = 348).MethodsAnisotropic effect size-signed differential mapping (AES-SDM) was utilized to synthesize the studies.ResultsWe observed increased volume amongst adolescents with a history of childhood trauma in regions that are involved in motor functions and language production: left precentral gyrus, including part of the left inferior frontal gyrus, left fibers of the body of corpus callosum, and left postcentral gyrus. We observed decreased volume amongst adolescents with a history of childhood trauma in regions that are involved in language processing and/or sensory processing: bilateral cerebellum, bilateral middle temporal gyrus, left rostrum of corpus callosum, and bilateral supramarginal gyrus.DiscussionWe suggest that these morphometric differences may be reflective of impaired motor development and increased sensory sensitivity and hypervigilance in adolescents with experiences of childhood trauma. Our results differ from meta-analytical findings in adults with history of childhood trauma and may contribute to a better understanding of neural mechanisms of childhood trauma, prediction of neurodevelopmental outcomes, and development of more effective and personalized therapies.

In the last decades, a great development in both neurophysiologic and neuropsychological areas have been observed that offered new possibilities to support the main principles of psychoanalytic theory. Can psychoanalytic conceptions of the psychic apparatus remain consonant with what is currently documented to function in nature? Can the psychoanalytic theoretical model contemplate psychic function and biological structure together? The purpose of these notes is to briefly expose the recent advances in neuroscience regarding the adolescent mind and pursue the goal of interesting the reader in the possible "metaphorical" psychodynamic union of these biological facts. In this perspective the present study was firstly aimed at reviewing the most relevant characteristics of the adolescent brain, clarifying the development of the cerebral structures connected to emotions and impulse control. A particular focus was offered to the role of mirror neurons in the development of empathic reactions and, thus, of inter-subjectivity. A second aim of the study was to clarify the role of neuronal plasticity in the evolution of adolescent brain and in the process of change. The interpersonal contact during the psychotherapeutic process was particularly examined as an instrument that facilitate personality changes, with a particular focus on patient-therapist moments of meetings that permit to modify the implicit relational knowing. [ABSTRACT FROM AUTHOR]

Myelin development during adolescence is becoming an area of growing interest in view of its potential relationship to cognition, behavior, and learning. While recent investigations suggest that both white matter (WM) and gray matter (GM) undergo protracted myelination during adolescence, quantitative relations between myelin development in WM and GM have not been previously studied. We quantitatively characterized the dependence of cortical GM, WM, and subcortical myelin density across the brain on age, gender, and puberty status during adolescence with the use of a novel macromolecular proton fraction (MPF) mapping method. Whole-brain MPF maps from a cross-sectional sample of 146 adolescents (age range 9–17 years) were collected. Myelin density was calculated from MPF values in GM and WM of all brain lobes, as well as in subcortical structures. In general, myelination of cortical GM was widespread and more significantly correlated with age than that of WM. Myelination of GM in the parietal lobe was found to have a significantly stronger age dependence than that of GM in the frontal, occipital, temporal and insular lobes. Myelination of WM in the temporal lobe had the strongest association with age as compared to WM in other lobes. Myelin density was found to be higher in males as compared to females when averaged across all cortical lobes, as well as in a bilateral subcortical region. Puberty stage was significantly correlated with myelin density in several cortical areas and in the subcortical GM. These findings point to significant differences in the trajectories of myelination of GM and WM across brain regions and suggest that cortical GM myelination plays a dominant role during adolescent development.

Meditation has shown to benefit a wide range of conditions and symptoms, but the neural mechanisms underlying the practice remain unclear. Magnetic resonance imaging (MRI) studies have investigated the structural brain changes due to the practice by examining volume, density, or cortical thickness changes. However, these studies have focused on adults; meditation’s structural effects on the adolescent brain remain understudied. In this study, we investigated how meditation training affects the structure of the adolescent brain by scanning a group of 38 adolescents (16.48 ± 1.29 years) before and after participating in a 12-week meditation training. Subjects underwent Training for Awareness, Resilience, and Action (TARA), a program that mainly incorporates elements from mindfulness meditation and yoga-based practices. A subset of the adolescents also received an additional control scan 12 weeks before TARA. We conducted voxel-based morphometry (VBM) to assess gray matter volume changes pre- to post-training and during the control period. Subjects showed significant gray matter (GM) volume decreases in the left posterior insula and to a lesser extent in the left thalamus and left putamen after meditation training. There were no significant changes during the control period. Our results support previous findings that meditation affects regions associated with physical and emotional awareness. However, our results are different from previous morphometric studies in which meditation was associated with structural increases. We posit that this discrepancy may be due to the differences between the adolescent brain and the adult brain.

In this article, we analyze the contributions of neuroscience to the development of the adolescent brain and shed additional light on the minimum age of criminal responsibility in the context of Latin America. In neurobiology, maturity is perceived to be complex because the brain’s temporal development process is not uniform across all its regions. This has important consequences for adolescents’ behavior; in their search for the acceptance of their peers, they are more vulnerable to pressure and more sensitive to stress than adults. Their affectivity is more unstable, and they show signs of low tolerance to frustration and important emotional reactivity, with a decrease in the capacity to self-regulate. Consequently, risky behavior presents itself more frequently during adolescence, and behaviors that transgress norms and social conventions typically peak between the ages of 17 and 19 years. However, only a small percentage of young offenders escalate their behavior to committing crimes during adulthood. In comparative law, there are considerable differences in Latin American countries’ legal dispositions regarding the minimum age of criminal responsibility; Brazil, Costa Rica, and Ecuador regard the age of criminal responsibility to be 12 years, while Argentina accepts this to be 16 years. From a legal viewpoint, however, the debate about the minimum age of criminal responsibility is connected to other circumstances that, because they are still at a developmental stage, are attributed to adolescents’ rights in their decision-making and understanding of autonomy (e.g., the minimum ages for voting, alcohol consumption, and medical consent). We argue that research on the development of the adolescent brain does not provide definitive answers about the exact age required for different juridical purposes. Nonetheless, the current state of knowledge does allow for reflection on the development and maturation of adolescents and the implications for considering them criminally responsible. It also validates demands for a system that provides adolescents with greater protection and that favors their healthy integral development. In any case, although a specific minimum age is not evident, this study is disposed not to recommend lowering the age of criminal responsibility, but rather increasing it.

Meditation has shown to benefit a wide range of conditions and symptoms, but the neural mechanisms underlying the practice remain unclear. Magnetic resonance imaging (MRI) studies have investigated the structural brain changes due to the practice by examining volume, density, or cortical thickness changes. However, these studies have focused on adults; meditation's structural effects on the adolescent brain remain understudied. In this study, we investigated how meditation training affects the structure of the adolescent brain by scanning a group of 38 adolescents (16.48 ± 1.29 years) before and after participating in a 12-week meditation training. Subjects underwent Training for Awareness, Resilience, and Action (TARA), a program that mainly incorporates elements from mindfulness meditation and yoga-based practices. A subset of the adolescents also received an additional control scan 12 weeks before TARA. We conducted voxel-based morphometry (VBM) to assess gray matter volume changes pre- to post-training and during the control period. Subjects showed significant gray matter (GM) volume decreases in the left posterior insula and to a lesser extent in the left thalamus and left putamen after meditation training. There were no significant changes during the control period. Our results support previous findings that meditation affects regions associated with physical and emotional awareness. However, our results are different from previous morphometric studies in which meditation was associated with structural increases. We posit that this discrepancy may be due to the differences between the adolescent brain and the adult brain. [ABSTRACT FROM AUTHOR]

In this article, we analyze the contributions of neuroscience to the development of the adolescent brain and shed additional light on the minimum age of criminal responsibility in the context of Latin America. In neurobiology, maturity is perceived to be complex because the brain's temporal development process is not uniform across all its regions. This has important consequences for adolescents' behavior; in their search for the acceptance of their peers, they are more vulnerable to pressure and more sensitive to stress than adults. Their affectivity is more unstable, and they show signs of low tolerance to frustration and important emotional reactivity, with a decrease in the capacity to self-regulate. Consequently, risky behavior presents itself more frequently during adolescence, and behaviors that transgress norms and social conventions typically peak between the ages of 17 and 19 years. However, only a small percentage of young offenders escalate their behavior to committing crimes during adulthood. In comparative law, there are considerable differences in Latin American countries' legal dispositions regarding the minimum age of criminal responsibility; Brazil, Costa Rica, and Ecuador regard the age of criminal responsibility to be 12 years, while Argentina accepts this to be 16 years. From a legal viewpoint, however, the debate about the minimum age of criminal responsibility is connected to other circumstances that, because they are still at a developmental stage, are attributed to adolescents' rights in their decision-making and understanding of autonomy (e.g., the minimum ages for voting, alcohol consumption, and medical consent). We argue that research on the development of the adolescent brain does not provide definitive answers about the exact age required for different juridical purposes. Nonetheless, the current state of knowledge does allow for reflection on the development and maturation of adolescents and the implications for considering them criminally responsible. It also validates demands for a system that provides adolescents with greater protection and that favors their healthy integral development. In any case, although a specific minimum age is not evident, this study is disposed not to recommend lowering the age of criminal responsibility, but rather increasing it. [ABSTRACT FROM AUTHOR]

This article is part of a doctoral thesis and aims at analyzing changes that occur in adolescents' brain, and also debating the further role of school education on integral development at this stage of human development from the historical-cultural psychology. Therefore, this study was divided into two phases: we primarily present the first approaches to studies concerned to brain's physiology which have been denominated as phenomenology of adolescent brain; secondly, the comprehension of the adolescent brain far beyond its apparent aspect was established by analyzing social activity as well as the dialectical unity of psychical and physiological processes. We conclude that human psychism is only formed as an entire complex structure as a result of the social activity and, on the contrary, such structures may not be formed effectively if certain activities do not take part in one's life. [ABSTRACT FROM AUTHOR]

Adolescence is characterized both by the exacerbation of the experience of anxiety, fear or threat, on one hand, and by increased reward seeking (reward sensitivity) and risk taking on the other hand. The rise of these apparently opposite processes, i.e., threat-related anxiety and reward-related sensation seeking, seems to stem from a relatively decreased top-down inhibition of amygdala and striatal circuits by regulatory systems (e.g., prefrontal cortex, hippocampus) that mature later. The present commentary article aims to discuss recent related literature and focusses on two main issues: (i) the septo-hippocampal system (in particular the ventral hippocampus) might be a crucial region for the regulation of approach–avoidance conflict and also for the selection of the most appropriate responses during adolescence, and (ii) developmental studies involving early-life pleasurable-enriched experience (as opposed to early-life adversity) might be a useful study paradigm in order to decipher whether neuroplasticity induced by such experiences (for example, in the hippocampus and associated circuitry) may lead to better top-down inhibition and more “balanced” adolescent responses to environmental demands.

Exposing the adolescent brain to drugs of abuse is associated with increased risk for adult onset psychopathologies. Cannabis use peaks during adolescence, with largely unknown effects on the developing brain. Cannabis' major psychoactive component, Δ 9 -tetrahydrocannabinol (THC) alters neuronal, astrocytic, and microglial signaling. Therefore, multiple cellular and signaling pathways are affected with a single dose of THC. The endogenous cannabinoids (eCBs), N -arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG) are members of an interconnected lipidome that includes an emerging class of AEA structural analogs, the lipoamines, additional 2-acyl glycerols, free fatty acids, and prostaglandins (PGs). Lipids in this lipidome share many biosynthetic and metabolic pathways, yet have diverse signaling properties. Here, we show that acute THC drives age-dependent changes in this lipidome across 8 regions of the female mouse brain. Interestingly, most changes are observed in the adult, with eCBs and related lipids predominately decreasing. Analysis of THC and metabolites reveals an unequal distribution across these brain areas; however, the highest levels of THC were measured in the hippocampus (HIPP) in all age groups. Transcriptomic analysis of the HIPP after acute THC showed that like the lipidome, the adult transcriptome demonstrated significantly more changes than the adolescent. Importantly, the regulation of 31 genes overlapped between the adolescent and the adult, suggesting a conserved transcriptomic response in the HIPP to THC exposure independent of age. Taken together these data illustrate that the first exposure to a single dose of THC has profound effects on signaling in the CNS. [ABSTRACT FROM AUTHOR]

Abstract: Principles of adolescent development have accelerated positive changes to the juvenile justice system. These changes have been most pronounced in reducing reliance on incarceration and in approaches to sentencing of youth tried as adults. While juvenile probation has made some developmentally friendly adjustments, it remains an area that is fertile for reform. Many of the principles and goals in this paper have been endorsed by the National Council of Juvenile and Family Court Judges (NCJFCJ), which “supports and is committed to juvenile probation systems that conform to the latest knowledge of adolescent development and adolescent brain science,” and which “recommends that courts cease imposing ‘conditions of probation’ and instead support probation departments’ developing, with families and youth, individualized case plans that set expectations and goals.” NCJFCJ's July, 2017 resolution in support of developmentally appropriate juvenile probation services built on earlier NCJFCJ policies. From the time NCJFCJ adopted Juvenile Delinquency Guidelines in 2005, those policies have grown increasingly robust. [ABSTRACT FROM AUTHOR]

Aims The use of emotion regulation strategies can reduce the intensity of negative emotional experiences. Event related potentials (ERPs), specifically the late positive potential (LPP), are known to be sensitive to this modulation in adults. This is the first study to explore the neural correlates of expressive suppression in adolescents. We sought to replicate previous findings from emotion regulation studies with adult populations, show that the LPP can be modulated by expressive suppression in healthy adolescents, and examine the influence of age on LPP changes. Method ERPs of 53 healthy adolescents (12–17 years old) performing an emotion regulation task (expressive suppression) were recorded. Results Expressive suppression altered the LPP in adolescents with both increases and decreases noted depending on time window and recording site. The LPP during expressive suppression was decreased with increasing age. Conclusions The findings suggest that 1) the LPP is an effective tool to study processes associated with emotion regulation in adolescents, and 2) expressive suppression, in terms of its neural indicators, seems to become more effective with age. The nature and utility of expressive suppression as a specific form of emotion regulation in adolescents are discussed. [ABSTRACT FROM AUTHOR]

Current evidence emerging from genome-wide association studies indicates that the genetic underpinnings of complex traits are likely attributable to genetic variation that changes gene expression, rather than (or in combination with) variation that changes protein-coding sequences. This is particularly compelling with respect to psychiatric disorders, as genetic changes in regulatory regions may result in differential transcriptional responses to developmental cues and environmental/psychosocial stressors. Until recently, however, the link between transcriptional regulation and psychiatric genetic risk has been understudied. Multiple obstacles have contributed to the paucity of research in this area, including challenges in identifying the positions of remote (distal from the promoter) regulatory elements (e.g. enhancers) and their target genes and the underrepresentation of neural cell types and brain tissues in epigenome projects - the availability of high-quality brain tissues for epigenetic and transcriptome profiling, particularly for the adolescent and developing brain, has been limited. Further challenges have arisen in the prediction and testing of the functional impact of DNA variation with respect to multiple aspects of transcriptional control, including regulatory-element interaction (e.g. between enhancers and promoters), transcription factor binding and DNA methylation. Further, the brain has uncommon DNA-methylation marks with unique genomic distributions not found in other tissues - current evidence suggests the involvement of non- CG methylation and 5-hydroxymethylation in neurodevelopmental processes but much remains unknown. We review here knowledge gaps as well as both technological and resource obstacles that will need to be overcome in order to elucidate the involvement of brain-relevant gene-regulatory variants in genetic risk for psychiatric disorders. [ABSTRACT FROM AUTHOR]

This article presents a critique of neuroscientific claims regarding the adolescent brain and the suggestion that adolescent motherhood disrupts the healthy development of the mother and her child. It does so by presenting a genealogical investigation of the conceptualisation of ‘adolescence’ in Western psychology and the emergence of the problematization of ‘adolescent motherhood’. This examination reveals that antecedents to neuroscientific claims regarding adolescent immaturity, impulsivity and instability were articulated by psychologists throughout the first half of the 20th century. However, up until the 1960s there was no problematization of ‘adolescent motherhood’ per se and adolescent mothers were only discussed as part of the concern with ‘unwed mothers’. Exploring the continuities and shifts in assertions regarding adolescence, this article highlights the complex history of some of the notions currently found in neuroscience. In doing so it aims to contribute to a growing body of critical literature questioning the universality of neuroscientific findings. [ABSTRACT FROM AUTHOR]

In the Province of Quebec, an adolescent aged 14 years or older may, subject to a few exceptions, consent alone to medical treatment required for his or her condition. However, neuroscience research on the adolescent’s brain indicates that: 1) the acquisition of “brain maturity” is a continuing process, which can last until the mid-twenties and 2) certain decisional capacities such as assessment of short and long-term risks and benefits differ from those of adults, particularly in emotionally charged situations. I argue that, from the perspective of a child’s best interest, the neurophysiological capacity of the adolescent should be taken into consideration in the health care context. Thus, I question the adequacy of the presumption of ability to make autonomous judgments from the age of 14, and point out the paradox of allowing judicial review of such judgments in cases of refusal of treatment. I also question the relevance of age considerations in the context of the doctor-patient relationship, where assessment of decisional ability is of the essence in obtaining an informed consent. Finally, I question the exclusion of parents from the decision-making process in light of both their continuing responsibility to protect their child’s best interests and the benefits that parental guidance may provide to the adolescent. Consequently, I argue that a reconsideration of the case for giving decisional authority to the adolescent aged 14 or older is desirable and that a uniform standard, with a few possible exceptions, applicable throughout childhood would better reflect recent neuroscience findings.

Abstract: The objective of the present study was to examine the influence of prenatal drug exposure (PDE) on memory performance and supporting brain structures (i.e., hippocampus) during adolescence. To achieve this goal, declarative memory ability and hippocampal volume were examined in a well-characterized sample of 138 adolescents (76 with a history of PDE and 62 from a non-exposed comparison group recruited from the same community, mean age=14years). Analyses were adjusted for: age at time of the assessments, gender, IQ, prenatal exposure to alcohol and tobacco, and indices of early childhood environment (i.e., caregiver depression, potential for child abuse, and number of caregiver changes through 7years of age). Results revealed that adolescents with a history of PDE performed worse on the California Verbal Learning Test—Child Version (CVLT-C), and story recall from the Children''s Memory Scale (CMS), and had larger hippocampal volumes, even after covariate adjustment. Hippocampal volume was negatively correlated with memory performance on the CVLT-C, with lower memory scores associated with larger volumes. These findings provide support for long-term effects of PDE on memory function and point to neural mechanisms that may underlie these outcomes. [Copyright &y& Elsevier]

Abstract: Neurophysiological and behavioral development is particularly complex in adolescence. Youngsters experience strong emotions and impulsivity, reduced self-control, and preference for actions which offer immediate rewards, among other behavioral patterns. Given the growing interest in endocrine effects on adolescent central nervous system development and their implications on later stages of life, this article reviews the effects of gonadal steroid hormones on the adolescent brain. These effects are classified as organizational, the capacity of steroids to determine nervous system structure during development, and activational, the ability of steroids to modify nervous activity to promote certain behaviors. During transition from puberty to adolescence, steroid hormones trigger various organizational phenomena related to structural brain circuit remodelling, determining adult behavioral response to steroids or sensory stimuli. These changes account for most male-female sexual dimorphism. In this stage sex steroids are involved in the main functional mechanisms responsible for organizational changes, namely myelination, neural pruning, apoptosis, and dendritic spine remodelling, activated only during embryonic development and during the transition from puberty to adolescence. This stage becomes a critical organizational window when the appropriately and timely exerted functions of steroid hormones and their interaction with some neurotransmitters on adolescent brain development are fundamental. Thus, understanding the phenomena linking steroid hormones and adolescent brain organization is crucial in the study of teenage behavior and in later assessment and treatment of anxiety, mood disorders, and depression. Adolescent behavior clearly evidences a stage of brain development influenced for the most part by steroid hormones. [Copyright &y& Elsevier]

The brain is one of the major target organs of alcohol actions. Alcohol abuse can lead to alterations in brain structure and functions and, in some cases, to neurodegeneration. Cognitive deficits and alcohol dependence are highly damaging consequences of alcohol abuse. Clinical and experimental studies have demonstrated that the developing brain is particularly vulnerable to alcohol, and that drinking during gestation can lead to a range of physical, learning and behavioral defects (fetal alcohol spectrum disorders), with the most dramatic presentation corresponding to fetal alcohol syndrome. Recent findings also indicate that adolescence is a stage of brain maturation and that heavy drinking at this stage can have a negative impact on brain structure and functions causing important short- and long-term cognitive and behavioral consequences. The effects of alcohol on the brain are not uniform; some brain areas or cell populations are more vulnerable than others. The prefrontal cortex, the hippocampus, the cerebellum, the white matter and glial cells are particularly susceptible to the effects of ethanol. The molecular actions of alcohol on the brain are complex and involve numerous mechanisms and signaling pathways. Some of the mechanisms involved are common for the adult brain and for the developing brain, while others depend on the developmental stage. During brain ontogeny, alcohol causes irreversible alterations to the brain structure. It also impairs several molecular, neurochemical and cellular events taking place during normal brain development, including alterations in both gene expression regulation and the molecules involved in cell--cell interactions, interference with the mitogenic and growth factor response, enhancement of free radical formation and derangements of glial cell functions. However, in both adult and adolescent brains, alcohol damages specific brain areas through mechanisms involving excitotoxicity, free radical formation and neuroinflammatory damage resulting from activation of the innate immune system mediated by TLR4 receptors. Alcohol also acts on specific membrane proteins, such as neurotransmitter receptors ( e.g. NMDA, GABA-A), ion channels ( e.g. L-type Ca2++ channels, GIRKs), and signaling pathways ( e.g. PKA and PKC signaling). These effects might underlie the wide variety of behavioral effects induced by ethanol drinking. The neuroadaptive changes affecting neurotransmission systems which are more sensitive to the acute effects of alcohol occur after long-term alcohol consumption. Alcohol-induced maladaptations in the dopaminergic mesolimbic system, abnormal plastic changes in the reward-related brain areas and genetic and epigenetic factors may all contribute to alcohol reinforcement and alcohol addiction. This manuscript reviews the mechanisms by which ethanol impacts the adult and the developing brain, and causes both neural impairments and cognitive and behavioral dysfunctions. The identification and the understanding of the cellular and molecular mechanisms involved in ethanol toxicity might contribute to the development of treatments and/or therapeutic agents that could reduce or eliminate the deleterious effects of alcohol on the brain. [ABSTRACT FROM AUTHOR]

Advances in brain research are increasingly having an impact on clinical interventions in all fields of psychotherapy. For adolescent family therapists it is important not only to understand the developing adolescent brain, but also how brain research can influence interventions aimed at interrupting problematic familial interactions. Interpersonal neurobiology and the ideas of Dr Daniel Siegel synthesise the interpersonal with the scientific, offering practical clinical methods of incorporating the research into everyday practice. This article incorporates a verbatim interview with Dr Siegel about the adolescent brain, interpersonal neurobiology and attachment with an outline of key concepts from interpersonal neurobiology including the hand model of the brain, nine functions of the prefrontal cortex, the triangle of wellbeing and eight domains of integration. Clinical applications are suggested using a common presenting problem of escalating conflict between teenagers and their parents. [ABSTRACT FROM AUTHOR]

Abstract: A number of studies in various species including man indicated a greater risk of drug preference and addictive behavior in young as compared to adults. Such age dependent preference was also found with nicotine. To examine possible mechanisms for this difference in our continuing study of reward mechanisms, we compared nicotine-induced neurotransmitter changes in the brain regions of adult and young Sprague-Dawley rats, assaying the transmitters via microdialysis in conscious freely moving animals. In general, nicotine-induced changes were significantly less in the regions measured in the young. Nicotine-induced effects on dopamine in the dorsal and ventral hippocampus (VH), prefrontal and medial temporal cortex, and superior cerebral peduncle were lower in the young than in adult, the same in the ventral tegmental area (VTA) and lateral septal nucleus (LS), and somewhat higher in the nucleus accumbens shell (NAccS). Norepinephrine levels in the young were lower in all areas except in the VH where they were the same, and serotonin levels were lower except in the VTA and LS where they remained the same, and higher in the NAccS. Age-dependent differences in the metabolites measured were more mixed. We conclude that the greater nicotine preference in young is not paralleled by a greater effect of nicotine on the release of monoamines at least in most of the brain areas assayed. Thus, increases of nicotine reward are not likely due to increases of monoamines in reward and cognitive areas. The small increase of dopamine (DA) and more significant increase of serotonin (5-HT) only in the NAccS are of significance, and would indicate a more significant role of 5-HT than of DA at least in the age difference in nicotine preference. Developmental changes in receptor composition and distribution involving several transmitter systems and other components such as neuropeptides are also likely to play a role. [Copyright &y& Elsevier]

Adolescence is characterized both by the exacerbation of the experience of anxiety, fear or threat, on one hand, and by increased reward seeking (reward sensitivity) and risk taking on the other hand. The rise of these apparently opposite processes, i.e., threat-related anxiety and reward-related sensation seeking, seems to stem from a relatively decreased top-down inhibition of amygdala and striatal circuits by regulatory systems (e.g., prefrontal cortex, hippocampus) that mature later. The present commentary article aims to discuss recent related literature and focusses on two main issues: (i) the septo-hippocampal system (in particular the ventral hippocampus) might be a crucial region for the regulation of approach–avoidance conflict and also for the selection of the most appropriate responses during adolescence, and (ii) developmental studies involving early-life pleasurable-enriched experience (as opposed to early-life adversity) might be a useful study paradigm in order to decipher whether neuroplasticity induced by such experiences (for example, in the hippocampus and associated circuitry) may lead to better top-down inhibition and more "balanced" adolescent responses to environmental demands. [ABSTRACT FROM AUTHOR]