Open AccessPerinatal antidepressant exposure alters cortical network function in rodents
Author(s) -
Kate Simpson,
Kristin J. Weaver,
Étienne de Villers-Sidani,
Jordan Y.-F. Lu,
Zhengwei Cai,
Yi Pang,
Federico RodríguezPorcel,
Ian A. Paul,
Michael M. Merzenich,
Rick C.S. Lin
Publication year - 2011
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1109353108
Subject(s) - neuroscience , antidepressant , serotonin , citalopram , serotonergic , raphe , autism , psychology , biology , medicine , hippocampus , developmental psychology , receptor
Serotonin (5-HT) plays a key role in early brain development, and manipulation of 5-HT levels during this period can have lasting neurobiological and behavioral consequences. It is unclear how perinatal exposure to drugs, such as selective serotonin reuptake inhibitors (SSRIs), impacts cortical neural network function and what mechanism(s) may elicit the disruption of normal neuronal connections/interactions. In this article, we report on cortical wiring organization after pre- and postnatal exposure to the SSRI citalopram. We show that manipulation of 5-HT during early development in both in vitro and in vivo models disturbs characteristic chemoarchitectural and electrophysiological brain features, including changes in raphe and callosal connections, sensory processing, and myelin sheath formation. Also, drug-exposed rat pups exhibit neophobia and disrupted juvenile play behavior. These findings indicate that 5-HT homeostasis is required for proper brain maturation and that fetal/infant exposure to SSRIs should be examined in humans, particularly those with developmental dysfunction, such as autism.