ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Cocaine exposure in utero alters synaptic plasticity in the medial prefrontal cortex of postnatal rats.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Prenatal Coca Paste Exposure Impairs Hippocampal Neuronal Development and Recognition Memory in Offspring.Neurotoxicity research · 2026Article
- Article
- Synaptic Interactions Between Serotonergic and Dopaminergic Systems in Parkinson's Disease.Current neuropharmacology · 2025Review
- Prenatal cocaine exposure and its influence on pediatric epigenetic clocks and epigenetic scores in humans.Scientific reports · 2024Article
- Paternal methamphetamine exposure induces higher sensitivity to methamphetamine in male offspring through driving ADRB1 on CaMKII-positive neurons in mPFC.Translational psychiatry · 2023Article
- Perturbed Developmental Serotonin Signaling Affects Prefrontal Catecholaminergic Innervation and Cortical Integrity.Molecular neurobiology · 2019Article
- Cocaine Promotes Coincidence Detection and Lowers Induction Threshold during Hebbian Associative Synaptic Potentiation in Prefrontal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Transgenerational Inheritance of Paternal Neurobehavioral Phenotypes: Stress, Addiction, Ageing and Metabolism.Molecular neurobiology · 2016Review
- Article
- Cocaine-induced neurodevelopmental deficits and underlying mechanisms.Birth defects research. Part C, Embryo today : reviews · 2016Review
- Prenatal Cocaine Exposure Upregulates BDNF-TrkB Signaling.PloS one · 2016Article
- Adolescent-onset GABAA α1 silencing regulates reward-related decision making.The European journal of neuroscience · 2015Article
- GABAAα1-mediated plasticity in the orbitofrontal cortex regulates context-dependent action selection.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Neurobehavioral and Developmental Traiectories Associated with Level of Prenatal Cocaine Exposure.Journal of neurology and psychology · 2014Article
- Spike-timing-dependent BDNF secretion and synaptic plasticity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Article
- Developmental origins of brain disorders: roles for dopamine.Frontiers in cellular neuroscience · 2013Review
- SHANK3 overexpression causes manic-like behaviour with unique pharmacogenetic properties.Nature · 2013Article
- Repeated cocaine exposure increases fast-spiking interneuron excitability in the rat medial prefrontal cortex.Journal of neurophysiology · 2013Article
- Repeated in vivo exposure of cocaine induces long-lasting synaptic plasticity in hypocretin/orexin-producing neurons in the lateral hypothalamus in mice.The Journal of physiology · 2013Article
- Overinhibition of corticostriatal activity following prenatal cocaine exposure.Annals of neurology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Cocaine exposure during pregnancy causes abnormality in fetal brain development, leading to cognitive dysfunction of the offspring, but the underlying cellular mechanism remains mostly unclear. In this study, we examined synaptic functions in the medial prefrontal cortex (mPFC) of postnatal rats that were exposed to cocaine in utero, using whole-cell recording from mPFC layer V pyramidal neurons in acute brain slices. Cocaine exposure in utero resulted in a facilitated activity-induced long-term potentiation (LTP) of excitatory synapses on these pyramidal neurons and an elevated neuronal excitability in postnatal rat pups after postnatal day 15 (P15). This facilitated LTP could be primarily attributed to the reduction of GABAergic inhibition. Biochemical assays of isolated mPFC tissue from postnatal rats further showed that cocaine exposure in utero caused a marked reduction in the surface expression of GABA(A) receptor subunits alpha1, beta2, and beta3, but had no effect on glutamate receptor subunit GluR1. Both facilitated LTP and reduced surface expression of GABA(A) receptors persisted in rats up to at least P42. Finally, the behavioral consequence of cocaine exposure in utero was reflected by the reduction in the sensitivity of locomotor activity in postnatal rats to cocaine and the dopamine receptor agonist apomorphine. Since the mPFC is an important part of the reward circuit in the rat brain and plays important roles in cognitive functions, these findings offer new insights into the cellular mechanism underlying the adverse effects of cocaine exposure in utero on brain development and cognitive functions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.