ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Prenatal exposure to cocaine produces unique developmental and long-term adaptive changes in dopamine D1 receptor activity and subcellular distribution.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 61 citations in OpenAlex.
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- Dopamine-induced pruning in monocyte-derived-neuronal-like cells (MDNCs) from patients with schizophrenia.Molecular psychiatry · 2022Article
- Behavioral and Neuroanatomical Consequences of Cell-Type Specific Loss of Dopamine D2 Receptors in the Mouse Cerebral Cortex.Frontiers in behavioral neuroscience · 2021Article
- Prenatal smoke exposure, DNA methylation and a link between DRD1 and lung cancer.International journal of epidemiology · 2019Article
- Cocaine-induced neurodevelopmental deficits and underlying mechanisms.Birth defects research. Part C, Embryo today : reviews · 2016Review
- Prenatal cocaine effects on brain structure in early infancy.NeuroImage · 2014Article
- Developmental origins of brain disorders: roles for dopamine.Frontiers in cellular neuroscience · 2013Review
- Subtle biobehavioral effects produced by paternal cocaine exposure.Synapse (New York, N.Y.) · 2012Article
- Adolescents with prenatal cocaine exposure show subtle alterations in striatal surface morphology and frontal cortical volumes.Journal of neurodevelopmental disorders · 2012Article
- The role of central nervous system development in late-onset neurodegenerative disorders.Developmental neuroscience · 2012Review
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- Effects of exogenous agents on brain development: stress, abuse and therapeutic compounds.CNS neuroscience & therapeutics · 2011Review
- Cocaine alters BDNF expression and neuronal migration in the embryonic mouse forebrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Differential subcellular distribution of rat brain dopamine receptors and subtype-specific redistribution induced by cocaine.Molecular and cellular neurosciences · 2011Article
- Prenatal IV Cocaine: Alterations in Auditory Information Processing.Frontiers in psychiatry · 2011Article
- Enhanced dopamine D1 and BDNF signaling in the adult dorsal striatum but not nucleus accumbens of prenatal cocaine treated mice.Frontiers in psychiatry · 2011Article
- Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.PloS one · 2010Article
- A transgenic mouse model of neuroepithelial cell specific inducible overexpression of dopamine D1-receptor.Neuroscience · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Low-dose intravenous cocaine administration to pregnant rabbits causes permanent structural alterations in dopamine-rich cerebral cortical areas, substantially reduced dopamine D1 receptor coupling to G(s)-protein, and deficits in cognitive function. The developmental influences of reduced D1-G(s) coupling and the underlying cellular basis are unknown. Using primary neuronal cultures derived from the medial frontal cortex and striatum of in utero saline- and cocaine-exposed embryos, spontaneous neurite outgrowth of in utero-exposed cortical neurons was greater than in control neurons. In contrast, striatal neurons exposed to cocaine in utero exhibited an entirely opposite adaptive response, with diminished spontaneous neurite outgrowth compared with saline-exposed controls. Control neurons isolated from the two structures also exhibited opposite regulatory responses to the D1 receptor agonist SKF38393 (1-phenyl-2,3,4-5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrochloride), inhibiting outgrowth in cortical cultures and stimulating outgrowth in striatal cultures. The agonist was ineffective in modulating neurite outgrowth of neurons from either structure isolated from cocaine-exposed fetuses, reflecting the reduced D1-Gs coupling. Total D1 receptor number was indistinguishable in neurons from the cocaine- and saline-exposed animals, but cell imaging and receptor binding of differentially isolated membranes showed that the lack of responsiveness was because of greatly reduced cell-surface localization of D1 receptors. These data suggest that prenatal exposure to cocaine causes a novel, long-lasting adaptive response in the subcellular distribution of D1 receptors, resulting in alterations in signaling capacity that have developmental and behavioral consequences.
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Registered trials
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.