Transient nicotine exposure in early adolescent male mice freezes their dopamine circuits in an immature state

Lauren M. Reynolds (), Aylin Gulmez, Sophie L. Fayad, Renan Costa Campos, Daiana Rigoni, Claire Nguyen, Tinaïg Le Borgne, Thomas Topilko, Domitille Rajot, Clara Franco, Sebastian P. Fernandez, Fabio Marti, Nicolas Heck, Alexandre Mourot, Nicolas Renier, Jacques Barik and Philippe Faure ()
Additional contact information
Lauren M. Reynolds: École supérieure de physique et de chimie industrielles de la Ville de Paris (ESPCI Paris)
Aylin Gulmez: École supérieure de physique et de chimie industrielles de la Ville de Paris (ESPCI Paris)
Sophie L. Fayad: École supérieure de physique et de chimie industrielles de la Ville de Paris (ESPCI Paris)
Renan Costa Campos: CNRS
Daiana Rigoni: CNRS
Claire Nguyen: Sorbonne Université
Tinaïg Le Borgne: École supérieure de physique et de chimie industrielles de la Ville de Paris (ESPCI Paris)
Thomas Topilko: ICM Institut du Cerveau et de la Moelle Epinière
Domitille Rajot: ICM Institut du Cerveau et de la Moelle Epinière
Clara Franco: Sorbonne Université
Sebastian P. Fernandez: CNRS
Fabio Marti: École supérieure de physique et de chimie industrielles de la Ville de Paris (ESPCI Paris)
Nicolas Heck: Sorbonne Université
Alexandre Mourot: École supérieure de physique et de chimie industrielles de la Ville de Paris (ESPCI Paris)
Nicolas Renier: ICM Institut du Cerveau et de la Moelle Epinière
Jacques Barik: CNRS
Philippe Faure: École supérieure de physique et de chimie industrielles de la Ville de Paris (ESPCI Paris)

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: Abstract How nicotine acts on developing neurocircuitry in adolescence to promote later addiction vulnerability remains largely unknown, but may hold the key for informing more effective intervention efforts. We found transient nicotine exposure in early adolescent (PND 21-28) male mice was sufficient to produce a marked vulnerability to nicotine in adulthood (PND 60 + ), associated with disrupted functional connectivity in dopaminergic circuits. These mice showed persistent adolescent-like behavioral and physiological responses to nicotine, suggesting that nicotine exposure in adolescence prolongs an immature, imbalanced state in the function of these circuits. Chemogenetically resetting the balance between the underlying dopamine circuits unmasked the mature behavioral response to acute nicotine in adolescent-exposed mice. Together, our results suggest that the perseverance of a developmental imbalance between dopamine pathways may alter vulnerability profiles for later dopamine-dependent psychopathologies.

Date: 2024
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DOI: 10.1038/s41467-024-53327-w

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