Selemon LD. A role for synaptic plasticity in the adolescent development of executive function. Transl Psychiatry 3: e238

Department of Neurobiology, Yale University School of Medicine, New Haven, CT, USA.
Translational Psychiatry (Impact Factor: 5.62). 03/2013; 3(3):e238. DOI: 10.1038/tp.2013.7
Source: PubMed


Adolescent brain maturation is characterized by the emergence of executive function mediated by the prefrontal cortex, e.g., goal planning, inhibition of impulsive behavior and set shifting. Synaptic pruning of excitatory contacts is the signature morphologic event of late brain maturation during adolescence. Mounting evidence suggests that glutamate receptor-mediated synaptic plasticity, in particular long term depression (LTD), is important for elimination of synaptic contacts in brain development. This review examines the possibility (1) that LTD mechanisms are enhanced in the prefrontal cortex during adolescence due to ongoing synaptic pruning in this late developing cortex and (2) that enhanced synaptic plasticity in the prefrontal cortex represents a key molecular substrate underlying the critical period for maturation of executive function. Molecular sites of interaction between environmental factors, such as alcohol and stress, and glutamate receptor mediated plasticity are considered. The accentuated negative impact of these factors during adolescence may be due in part to interference with LTD mechanisms that refine prefrontal cortical circuitry and when disrupted derail normal maturation of executive function. Diminished prefrontal cortical control over risk-taking behavior could further exacerbate negative outcomes associated with these behaviors, as for example addiction and depression. Greater insight into the neurobiology of the adolescent brain is needed to fully understand the molecular basis for heightened vulnerability during adolescence to the injurious effects of substance abuse and stress.

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Available from: Lynn Selemon, Jul 24, 2014
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    • "Thus, overall changes in synaptic density are limited during middle to late childhood. However, synaptic reorganization and turnover continues throughout this period (Rakic et al. 1994; Selemon 2013), and could play a role in the changes in functional connectivity observed here. "
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    ABSTRACT: The goal of this fMRI study was to examine how well developmental improvements in reasoning ability can be explained by changes in functional connectivity between specific nodes in prefrontal and parietal cortices. To this end, we examined connectivity within the lateral fronto-parietal network (LFPN) and its relation to reasoning ability in 132 children and adolescents aged 6-18 years, 56 of whom were scanned twice over the course of 1.5 years. Developmental changes in strength of connections within the LFPN were most prominent in late childhood and early adolescence. Reasoning ability was related to functional connectivity between left rostrolateral prefrontal cortex (RLPFC) and inferior parietal lobule (IPL), but only among 12-18-year olds. For 9-11-year olds, reasoning ability was most strongly related to connectivity between left and right RLPFC; this relationship was mediated by working memory. For 6-8-year olds, significant relationships between connectivity and performance were not observed; in this group, processing speed was the primary mediator of improvement in reasoning ability. We conclude that different connections best support reasoning at different points in development and that RLPFC-IPL connectivity becomes an important predictor of reasoning during adolescence. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail:
    Cerebral Cortex 10/2014; DOI:10.1093/cercor/bhv050 · 8.67 Impact Factor
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    • "Evidence suggests that experience during development changes the brain in order to prepare an organism to respond optimally during adulthood (Nederhof and Schmidt, 2012). Brain circuitry underlying emotional behavior, including in the prefrontal cortex, hippocampus and amygdala, undergoes plasticity and functions differently in adolescence compared to adulthood and may be vulnerable to environmental influence (Pattwell et al., 2011; Selemon, 2013). For instance the expression of fear in a contextual fear-conditioning paradigm is strikingly suppressed during adolescence from P29-P33 in mice, reflecting a transient alteration of hippocampal and amygdalar function (Pattwell et al., 2011). "
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    Frontiers in Behavioral Neuroscience 08/2014; 8:289. DOI:10.3389/fnbeh.2014.00289 · 3.27 Impact Factor
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    • "Previous studies have shown that in the adolescence occurs structural and functional maturation of the brain. In this period, there are significant modifications in brain organization and cortical circuitry [35]. Alcohol inhibits brain maturation and neurogenesis, becoming adolescent brain more susceptible to the neurotoxic effects of alcohol abuse [36]. "
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