Please use this identifier to cite or link to this item: https://doi.org/10.1186/s13041-019-0452-5
Title: Prenatal selective serotonin reuptake inhibitor (SSRI) exposure induces working memory and social recognition deficits by disrupting inhibitory synaptic networks in male mice
Authors: Yu, Weonjin 
Yen, Yi-Chun 
Lee, Young-Hwan
Tan, Shawn 
Xiao, Yixin 
Lokman, Hidayat 
Ting, Audrey Khoo Tze
Ganegala, Hasini
Kwon, Taejoon
Ho, Won-Kyung
Je, H Shawn 
Keywords: Science & Technology
Life Sciences & Biomedicine
Neurosciences
Neurosciences & Neurology
Prenatal
Serotonin (5-HT)
Selective serotonin reuptake inhibitor (SSRI)
Fluoxetine
Working memory
Social recognition
Serotonin 2A receptor (5-HT2AR)
AUTISM SPECTRUM DISORDER
MOUSE MODEL
COGNITIVE DYSFUNCTION
ANTIDEPRESSANT EXPOSURE
BEHAVIOR
RECEPTORS
ABNORMALITIES
ANTAGONIST
LACKING
HYPERACTIVITY
Issue Date: 1-Apr-2019
Publisher: BMC
Citation: Yu, Weonjin, Yen, Yi-Chun, Lee, Young-Hwan, Tan, Shawn, Xiao, Yixin, Lokman, Hidayat, Ting, Audrey Khoo Tze, Ganegala, Hasini, Kwon, Taejoon, Ho, Won-Kyung, Je, H Shawn (2019-04-01). Prenatal selective serotonin reuptake inhibitor (SSRI) exposure induces working memory and social recognition deficits by disrupting inhibitory synaptic networks in male mice. MOLECULAR BRAIN 12 (1). ScholarBank@NUS Repository. https://doi.org/10.1186/s13041-019-0452-5
Abstract: © 2019 The Author(s). Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed antidepressant drugs in pregnant women. Infants born following prenatal exposure to SSRIs have a higher risk for behavioral abnormalities, however, the underlying mechanisms remains unknown. Therefore, we examined the effects of prenatal fluoxetine, the most commonly prescribed SSRI, in mice. Intriguingly, chronic in utero fluoxetine treatment impaired working memory and social novelty recognition in adult males. In the medial prefrontal cortex (mPFC), a key region regulating these behaviors, we found augmented spontaneous inhibitory synaptic transmission onto the layer 5 pyramidal neurons. Fast-spiking interneurons in mPFC exhibited enhanced intrinsic excitability and serotonin-induced excitability due to upregulated serotonin (5-HT) 2A receptor (5-HT 2A R) signaling. More importantly, the behavioral deficits in prenatal fluoxetine treated mice were reversed by the application of a 5-HT 2A R antagonist. Taken together, our findings suggest that alterations in inhibitory neuronal modulation are responsible for the behavioral alterations following prenatal exposure to SSRIs.
Source Title: MOLECULAR BRAIN
URI: https://scholarbank.nus.edu.sg/handle/10635/155063
ISSN: 17566606
DOI: 10.1186/s13041-019-0452-5
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