ArticleBiological psychiatry2008
Augmented D1 dopamine receptor signaling and immediate-early gene induction in adult striatum after prenatal cocaine.
Article in Biological psychiatry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Pharmacologic neuroimaging of the ontogeny of dopamine receptor function.Developmental neuroscience · 2010Pooled it
- Article
- Serotonin-dopamine interactions in psychostimulant-induced gene regulation: SSRI antidepressants potentiate gene regulation by methylphenidate (Ritalin) in the striatum and enhance behavioral profile indicative of addiction liability in rodents.Neuroscience and biobehavioral reviews · 2025Review
- Prenatal cocaine exposure: Direct and indirect associations with 21-year-old offspring substance use and behavior problems.Drug and alcohol dependence · 2019Article
- Molecular Mechanism: ERK Signaling, Drug Addiction, and Behavioral Effects.Progress in molecular biology and translational science · 2016Review
- Structural brain imaging in children and adolescents following prenatal cocaine exposure: preliminary longitudinal findings.Developmental neuroscience · 2014Article
- Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants.Progress in neurobiology · 2013Review
- Enhanced dopamine D1 and BDNF signaling in the adult dorsal striatum but not nucleus accumbens of prenatal cocaine treated mice.Frontiers in psychiatry · 2011Article
- Prenatal cocaine exposure increases anxiety, impairs cognitive function and increases dendritic spine density in adult rats: influence of sex.Neuroscience · 2010Article
- The effects of prenatal cocaine exposure and gender on inhibitory control and attention.Neurotoxicology and teratologyArticle
- Pathways from prenatal cocaine exposure to adult substance use and behavior.Neurotoxicology and teratologyArticle
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7 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundPrenatal exposure to cocaine can impede normal brain development, triggering a range of neuroanatomical and behavioral anomalies that are evident throughout life. Mouse models have been especially helpful in delineating neuro-teratogenic consequences after prenatal exposure to cocaine. The present study employed a mouse model to investigate alterations in D(1) dopamine receptor signaling and downstream immediate-early gene induction in the striatum of mice exposed to cocaine in utero.
methodsBasal, forskolin-, and D(1) receptor agonist-induced cyclic adenosine monophosphate (cAMP) levels were measured ex vivo in the adult male striatum in mice exposed to cocaine in utero. Further studies assessed cocaine-induced zif 268 and homer 1 expression in the striatum of juvenile (P15), adolescent (P36), and adult (P60) male mice.
resultsThe D(1) dopamine receptor agonist SKF82958 induced significantly higher levels of cAMP in adult male mice treated with cocaine in utero compared with saline control subjects. No effects of the prenatal treatment were found for cAMP formation induced by forskolin. After an acute cocaine challenge (15 mg/kg, IP), these mice showed greater induction of zif 268 and homer 1, an effect that was most robust in the medial part of the mid-level striatum and became more pronounced with increasing age.
conclusionsTogether these findings indicate abnormally enhanced D(1) receptor signal transduction in adult mice after prenatal cocaine exposure. Such changes in dopamine receptor signaling might underlie aspects of long-lasting neuro-teratogenic effects evident in some humans after in utero exposure to cocaine and identify the striatum as one target potentially vulnerable to gestational cocaine exposure.
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