A developmental neurobiological model of motivated behavior: Anatomy, connectivity and ontogeny of the triadic nodes
ABSTRACT Adolescence is the transition period that prepares individuals for fulfilling their role as adults. Most conspicuous in this transition period is the peak level of risk-taking behaviors that characterize adolescent motivated behavior. Significant neural remodeling contributes to this change. This review focuses on the functional neuroanatomy underlying motivated behavior, and how ontogenic changes can explain the typical behavioral patterns in adolescence. To help model these changes and provide testable hypotheses, a neural systems-based theory is presented. In short, the Triadic Model proposes that motivated behavior is governed by a carefully orchestrated articulation among three systems, approach, avoidance and regulatory. These three systems map to distinct, but overlapping, neural circuits, whose representatives are the striatum, the amygdala and the medial prefrontal cortex. Each of these system-representatives will be described from a functional anatomy perspective that includes a review of their connectivity and what is known of their ontogenic changes.
SourceAvailable from: José María Ruiz Sánchez de LeónNeurociencias y adiciones, Edited by Eduardo Pedrero Pérez, José María Ruiz Sánchez de León, Antonio Verdejo García, Marcos Llanero Luque, Emilio Ambrosio Flores, 01/2011: chapter Factores de vulnerabilidad para desarrollar una adicción: elementos para su prevención: pages 99-110; Sociedad Española de Toxicomanías., ISBN: 978-84-615-0572-2
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ABSTRACT: There are two key alcohol use patterns among human adolescents that confer increased vulnerability for later alcohol abuse/dependence, along with neurocognitive alterations: (a) early initiation of use during adolescence, and (b) high rates of binge drinking that are particularly prevalent late in adolescence. The central thesis of this review is that lasting neurobehavioral outcomes of these two adolescent exposure patterns may differ. Although it is difficult to disentangle consequences of early use from later binge drinking in human studies given the substantial overlap between groups, these two types of problematic adolescent use are differentially heritable and hence separable to some extent. Although few studies using animal models have manipulated alcohol exposure age, those studies that have have typically observed timing-specific exposure effects, with more marked (or at least different patterns of) lasting consequences evident after exposures during early-mid adolescence than late-adolescence/emerging adulthood, and effects often restricted to male rats in those few instances where sex differences have been explored. As one example, adult male rats exposed to ethanol during early-mid adolescence (postnatal days [P] 25-45) were found to be socially anxious and to retain adolescent-typical ethanol-induced social facilitation into adulthood, effects that were not evident after exposure during late-adolescence/emerging adulthood (P45-65); exposure at the later interval, however, induced lasting tolerance to ethanol's social inhibitory effects that was not evident after exposure early in adolescence. Females, in contrast, were little influenced by ethanol exposure at either interval. Exposure timing effects have likewise been reported following social isolation as well as after repeated exposure to other drugs such as nicotine (and cannabinoids), with effects often, although not always, more pronounced in males where studied. Consistent with these timing-specific exposure effects, notable maturational changes in brain have been observed from early to late adolescence that could provide differential neural substrates for exposure timing-related consequences, with for instance exposure during early adolescence perhaps more likely to impact later self-administration and social/affective behaviors, whereas exposures later in adolescence may be more likely to influence cognitive tasks whose neural substrates (such as the prefrontal cortex [PFC]) are still undergoing maturation at that time. More substantial work is needed, however to characterize timing-specific effects of adolescent ethanol exposures and their sex dependency, determine their neural substrates, and assess their comparability to and interactions with adolescent exposure to other drugs and stressors. Such information could prove critical for informing intervention/prevention strategies regarding the potential efficacy of efforts directed toward delaying onset of alcohol use versus toward reducing high levels of use and risks associated with that use later in adolescence. Copyright © 2015. Published by Elsevier Inc.Physiology & Behavior 01/2015; DOI:10.1016/j.physbeh.2015.01.027 · 3.03 Impact Factor
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ABSTRACT: De puberteit is een belangrijke periode gedurende de ontwikkeling die wordt gekenmerkt door een sterke toename in geslachtshormonen. Studies die gebruikmaken van beeldvormingtechnieken, zoals MRI, rapporteren veelvuldig dat de hersenen van gezonde kinderen in de puberteit anatomische veranderingen ondergaan. Het proces van anatomische reorganisatie in de puberteit zou kunnen wijzen op het ‘fine-tunen’ van neuronale netwerken. Deze bewering wordt gesterkt door dierexperimenteel onderzoek, waaruit blijkt dat geslachtshormonen een directe invloed hebben op de vertakking van dendrieten (‘grijze stof’) en de vorming van myeline om axonen (‘witte stof’). Een belangrijke vraag die nu rijst is in hoeverre puberteitshormonen bijdragen aan hersenontwikkeling bij mensen. Dit artikel bespreekt de mogelijke evidentie voor de rol die geslachtshormonen spelen bij de ontwikkeling van grijze en witte stof. We kunnen concluderen dat individuele verschillen in de modulatie van geslachtshormonen op de organisatie van de hersenen aanknopingspunten geven om typisch gedrag in de puberteit te verklaren, zoals verhoogde gevoeligheid voor beloningen, risicogedrag en cognitieve flexibiliteit. Abstract Puberty is a critical period during development and is characterized by an increase in levels of sex steroid levels. Human neuroimaging studies have consistently reported that in typically developing pubertal children, the brain undergoes significant structural reorganization that is thought to reflect the fine-tuning of neuronal networks. This notion is supported by animal studies that have shown that sex steroids influence dendritic branching (gray matter) and myelination of axons (white matter). An important question that comes to mind is to what extent pubertal hormones play a role in human brain development during this critical period. In this paper, evidence is provided that sex steroids are involved in gray and white matter development. Individual differences in the modulation of sex steroids and brain restructuring might provide a neuroendocrinological basis for explaining enhanced reward sensitivity, risk taking behaviour and cognitive flexibility during puberty.12/2011; 15(6):178-183. DOI:10.1007/s12474-011-0032-7