Early Adolescence is a Critical Period for the Maturation of Inhibitory Behavior
Open accessAbstract
Psychiatric conditions marked by impairments in cognitive control often emerge during adolescence, when the prefrontal cortex (PFC) and its inputs undergo structural and functional maturation and are vulnerable to disruption by external events. It is not known, however, whether there exists a specific temporal window within the broad range of adolescence when the development of PFC circuitry and its related behaviors are sensitive to disruption. Here we show, in male mice, that repeated exposure to amphetamine during early adolescence leads to impaired behavioral inhibition, aberrant PFC dopamine connectivity, and reduced PFC dopamine function in adulthood. Remarkably, these deficits are not observed following exposure to the exact same amphetamine regimen at later times. These findings demonstrate that there is a critical period for the disruption of the adolescent maturation of cognitive control and PFC dopamine function and suggest that early adolescence is particularly relevant to the emergence of psychopathology in humans.
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Functional studies in adult rodent models link genetic or experimentally induced alterations in DA neuron activity, DA release, and receptor binding to transdiagnostic changes in motivation and cognitive control.
“Functional studies in adult rodent models have linked genetic or experimentally induced alterations in DA neuron activity, DA release, and receptor binding to transdiagnostic changes in motivation and cognitive control [49, 132–135].”
From Adolescent nicotine exposure and persistent neurocircuitry changes: unveiling lifelong psychiatric risks (2025) · cites this paper as [49]
The Discussion (page unavailable) reports that amphetamine exposure in early-adolescent male mice was followed by impaired behavioral inhibition and reduced prefrontal dopamine turnover in adulthood, supporting a link between an experimental alteration in dopamine function and cognitive control. The Results (page unavailable) report no comparable inhibition deficit after exposure in adulthood. This paper does not establish the broader claim about genetic alterations, dopamine neuron activity or release, receptor binding, and transdiagnostic changes in motivation. (LLM, conf=0.88)
Experimental — accuracy not yet measuredStriking, age-dependent differences can be reported in the enduring effects of the same experience on neural circuitry depending on the adolescent period in which this experience occurred.
“striking, age-dependent differences can be reported in the enduring effects of the same experience on neural circuitry depending on the adolescent period in which this experience occurred [48–51].”
From Adolescent nicotine exposure and persistent neurocircuitry changes: unveiling lifelong psychiatric risks (2025) · cites this paper as [49]
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- Authors
- Reynolds, L. M., Yetnikoff, L., Pokinko, M., Wodzinski, M., Epelbaum, J. G., Lambert, L. C., Cossette, M.-P., Arvanitogiannis, A., & Flores, C.
- Affiliations
- Douglas Mental Health University Institute (CA)
- The Graduate Center, CUNY (US)
- Concordia University (CA)
- Corresponding author
- Arvanitogiannis, Andreas
- Flores, Cecilia
- Venue
- Cerebral Cortex
- Publisher
- Oxford University Press (OUP)
- Published
- 2018-10-06
- Volume
- 29
- Issue
- 9
- Pages
- 3676-3686
- ISSN
- 1047-3211 (ISSN-L)
- 1460-2199
- PMC
- PMC6686753
- OpenAlex
- W2895745924
- Cited by
- 75
- References
- 81
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 16 · 2023: 19 · 2022: 2 · 2021: 6 · 2020: 9 · 2019: 3 · 2018: 1
- FWCI
- 2.83
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Cerebral Cortex (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (R01DA037911, F31DA041188)
- Natural Sciences and Engineering Research Council of Canada (2982226, 249848)
- Canadian Institutes of Health Research (MOP-74709)
- Fonds de Recherche du Québec - Santé
- Fulbright Canada
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Keywords
- early adolescence, cognitive control, prefrontal cortex, dopamine, amphetamine, critical period, behavioral inhibition, adolescent drug exposure, psychopathology, mouse model
- MeSH terms
- Animals, Critical Period, Psychological, Dextroamphetamine, Dopamine, Inhibition, Psychological, Male, Prefrontal Cortex, Presynaptic Terminals, Mice, Executive Function, Dopaminergic Neurons
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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