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• W2566563717 abstract "Prenatal cocaine exposure remains a major public health concern because of its adverse impact on cognitive function in children and adults. We report that prenatal cocaine exposure produces significant deficits in reversal learning, a key component of cognitive flexibility, in a mouse model. We used an olfactory reversal learning paradigm and found that the prenatally cocaine-exposed mice showed a marked failure to learn the reversed paradigm. Because brain-derived neurotrophic factor (BDNF) is a key regulator of cognitive functions, and because prenatal cocaine exposure increases the expression of BDNF and the phosphorylated form of its receptor, tyrosine kinase B (TrkB), we examined whether BDNF-TrkB signaling is involved in mediating the reversal learning deficit in prenatally cocaine-exposed mice. Systemic administration of a selective TrkB receptor antagonist restored normal reversal learning in prenatally cocaine-exposed mice, suggesting that increased BDNF-TrkB signaling may be an underlying mechanism of reversal learning deficits. Our findings provide novel mechanistic insights into the reversal learning phenomenon and may have significant translational implications because impaired cognitive flexibility is a key symptom in psychiatric conditions of developmental onset." @default.
• W2566563717 created "2017-01-06" @default.
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• W2566563717 date "2016-01-01" @default.
• W2566563717 modified "2023-10-02" @default.
• W2566563717 title "Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model" @default.
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• W2566563717 doi "https://doi.org/10.1159/000452739" @default.
• W2566563717 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5360472" @default.
• W2566563717 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27951531" @default.
• W2566563717 hasPublicationYear "2016" @default.
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