ArticleAnnals of neurology2013
Overinhibition of corticostriatal activity following prenatal cocaine exposure.
Article in Annals of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Single Cocaine Exposure Inhibits GABA Uptake via Dopamine D1-Like Receptors in Adolescent Mice Frontal Cortex.Neurotoxicity research · 2020Article
- The Striatum's Role in Executing Rational and Irrational Economic Behaviors.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Review
- Calcium currents in striatal fast-spiking interneurons: dopaminergic modulation of CaBMC neuroscience · 2018Article
- Loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors.NPJ Parkinson's disease · 2018Article
- Altered functional connectivity to stressful stimuli in prenatally cocaine-exposed adolescents.Drug and alcohol dependence · 2017Article
- Models of Intergenerational and Transgenerational Transmission of Risk for Psychopathology in Mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Review
- Prenatal cocaine exposure, illicit-substance use and stress and craving processes during adolescence.Drug and alcohol dependence · 2016Article
- Identifying the role of pre-and postsynaptic GABA(B) receptors in behavior.Neuroscience and biobehavioral reviews · 2015Review
- Adolescent-onset GABAA α1 silencing regulates reward-related decision making.The European journal of neuroscience · 2015Article
- Neurobehavioral and Developmental Traiectories Associated with Level of Prenatal Cocaine Exposure.Journal of neurology and psychology · 2014Article
- Prenatal cocaine exposure and adolescent neural responses to appetitive and stressful stimuli.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Enduring effects of adolescent drug exposure.Biological psychiatry · 2013Article
- Acetylcholine encodes long-lasting presynaptic plasticity at glutamatergic synapses in the dorsal striatum after repeated amphetamine exposure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectivePrenatal cocaine exposure (PCE) can cause persistent neuropsychological and motor abnormalities in affected children, but the physiological consequences of PCE remain unclear. Conclusions drawn from clinical studies can sometimes be confounded by polysubstance abuse and nutritional deprivation. However, existing observations suggest that cocaine exposure in utero, as in adults, increases synaptic dopamine and promotes enduring dopamine-dependent plasticity at striatal synapses, altering behaviors and basal ganglia function.
methodsWe used a combination of behavioral measures, electrophysiology, optical imaging, and biochemical and electrochemical recordings to examine corticostriatal activity in adolescent mice exposed to cocaine in utero.
resultsWe show that PCE caused abnormal dopamine-dependent behaviors, including heightened excitation following stress and blunted locomotor augmentation after repeated treatment with amphetamine. These abnormal behaviors were consistent with abnormal γ-aminobutyric acid (GABA) interneuron function, which promoted a reversible depression in corticostriatal activity. PCE hyperpolarized and reduced tonic GABA currents in both fast-spiking and persistent low-threshold spiking type GABA interneurons to increase tonic inhibition at GABAB receptors on presynaptic corticostriatal terminals. Although D2 receptors paradoxically increased glutamate release following PCE, normal corticostriatal modulation by dopamine was reestablished with a GABAA receptor antagonist.
interpretationThe dynamic alterations at corticostriatal synapses that occur in response to PCE parallel the reported effects of repeated psychostimulants in mature animals, but differ in being specifically generated through GABAergic mechanisms. Our results indicate approaches that normalize GABA and D2 receptor-dependent synaptic plasticity may be useful for treating the behavioral effects of PCE and other developmental disorders that are generated through abnormal GABAergic signaling.
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