ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Cocaine alters BDNF expression and neuronal migration in the embryonic mouse forebrain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 65 citations in OpenAlex.
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- The Development of Neural Inhibition across Species: Insights from the Hurst Exponent.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Prenatal stress induces transient developmental alterations in distinct GABAergic populations and leads to long-lasting behavioral abnormalities.Neurobiology of stress · 2025Article
- Dopaminergic Perturbation in the Aetiology of Neurodevelopmental Disorders.Molecular neurobiology · 2025Review
- GABA system as the cause and effect in early development.Neuroscience and biobehavioral reviews · 2024Review
- Reactive Oxygen Species Mediate Transcriptional Responses to Dopamine and Cocaine in Human Cerebral Organoids.International journal of molecular sciences · 2023Article
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- A Progressive Loss of phosphoSer138-Profilin Aligns with Symptomatic Course in the R6/2 Mouse Model of Huntington's Disease: Possible Sex-Dependent Signaling.Cellular and molecular neurobiology · 2022Article
- Nicotine and the developing brain: Insights from preclinical models.Pharmacology, biochemistry, and behavior · 2022Article
- [G-protein coupled receptor Smo positively regulates proliferation and migration of adult neural stem cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Effects of Developmental Nicotine Exposure on Frontal Cortical GABA-to-Non-GABA Neuron Ratio and Novelty-Seeking Behavior.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Prenatal Environment That Affects Neuronal Migration.Frontiers in cell and developmental biology · 2019Review
- Article
- A Single Neonatal Exposure to BMAA in a Rat Model Produces Neuropathology Consistent with Neurodegenerative Diseases.Toxins · 2017Article
- Β-N-Methylamino-L-Alanine (BMAA) Toxicity Is Gender and Exposure-Age Dependent in Rats.Toxins · 2017Article
- In Vitro, Ex Vivo and In Vivo Techniques to Study Neuronal Migration in the Developing Cerebral Cortex.Brain sciences · 2017Review
- Hemispheric Asymmetry of Development Due to Drug Exposure.Journal of systems and integrative neuroscience · 2017Article
- Cocaine-induced neurodevelopmental deficits and underlying mechanisms.Birth defects research. Part C, Embryo today : reviews · 2016Review
- Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model.Developmental neuroscience · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Prenatal cocaine exposure impairs brain development and produces lasting alterations in cognitive function. In a prenatal cocaine exposure mouse model, we found that tangential migration of GABA neurons from the basal to the dorsal forebrain and radial neuron migration within the dorsal forebrain were significantly decreased during the embryonic period. The decrease in the tangential migration occurred early in gestation and normalized by late gestation, despite ongoing cocaine exposure. The decrease in radial migration was associated with altered laminar positioning of neurons in the medial prefrontal cortex. The cocaine exposure led to transient decreases in the expression of Tbr2 and Tbr1, transcription factors associated with intermediate progenitor cells and newborn neurons of the dorsal forebrain, respectively, although neurogenesis was not significantly altered. Since cocaine can modulate brain derived neurotrophic factor (BDNF) expression in the mature brain, we examined whether cocaine can alter BDNF expression in the embryonic brain. We found a transient decrease in BDNF protein expression in the cocaine-exposed embryonic forebrain early in gestation. By late gestation, the BDNF expression recovered to control levels, despite ongoing cocaine exposure. In basal forebrain explants from cocaine-exposed embryos, cell migration was significantly decreased, corroborating the in vivo data on tangential GABA neuron migration. Since BDNF can influence tangential neuronal migration, we added BDNF to the culture medium and observed increased cell migration. Our data suggest that cocaine can alter tangential and radial neuronal migration as well as BDNF expression in the embryonic brain and that decreased BDNF may mediate cocaine's effects on neuronal migration.
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