ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Prenatal exposure to cocaine disrupts D1A dopamine receptor function via selective inhibition of protein phosphatase 1 pathway in rabbit frontal cortex.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 68 citations in OpenAlex.
- GSK-3β Interacts with Dopamine D1 Receptor to Regulate Receptor Function: Implication for Prefrontal Cortical D1 Receptor Dysfunction in Schizophrenia.CNS neuroscience & therapeutics · 2017Article
- 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
- Developmental consequences of fetal exposure to drugs: what we know and what we still must learn.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Review
- Article
- Moderate Alcohol Exposure during the Rat Equivalent to the Third Trimester of Human Pregnancy Alters Regulation of GABAA Receptor-Mediated Synaptic Transmission by Dopamine in the Basolateral Amygdala.Frontiers in pediatrics · 2014Article
- Enhanced dopamine D1 and BDNF signaling in the adult dorsal striatum but not nucleus accumbens of prenatal cocaine treated mice.Frontiers in psychiatry · 2011Article
- Pharmacology of signaling induced by dopamine D(1)-like receptor activation.Pharmacology & therapeutics · 2010Review
- Prenatal cocaine exposure increases anxiety, impairs cognitive function and increases dendritic spine density in adult rats: influence of sex.Neuroscience · 2010Article
- Specificity of prenatal cocaine exposure effects on cortical interneurons is independent from dopamine D1 receptor co-localization.Journal of chemical neuroanatomy · 2010Article
- Sex differences in the effects of cocaine abuse across the life span.Physiology & behavior · 2010Article
- Cocaine exposure modulates dopamine and adenosine signaling in the fetal brain.Neuropharmacology · 2010Article
- Cocaine exposure in utero alters synaptic plasticity in the medial prefrontal cortex of postnatal rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Prenatal cocaine reduces AMPA receptor synaptic expression through hyperphosphorylation of the synaptic anchoring protein GRIP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Modes and mishaps of neuronal migration in the mammalian brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Review
- Oxycodone plus ultra-low-dose naltrexone attenuates neuropathic pain and associated mu-opioid receptor-Gs coupling.The journal of pain · 2008Article
- Cocaine exposure during the early postnatal period diminishes medial frontal cortex Gs coupling to dopamine D1-like receptors in adult rat.Neuroscience letters · 2008Article
- Augmented D1 dopamine receptor signaling and immediate-early gene induction in adult striatum after prenatal cocaine.Biological psychiatry · 2008Article
- Prenatal exposure to cocaine produces unique developmental and long-term adaptive changes in dopamine D1 receptor activity and subcellular distribution.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Differential localization of protein phosphatase-1alpha, beta and gamma1 isoforms in primate prefrontal cortex.Cerebral cortex (New York, N.Y. : 1991) · 2005Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previous work has demonstrated that in utero cocaine exposure induces an uncoupling of brain D(1A) dopamine receptors (D(1A)DARs) from G(s)-protein. The present work is an attempt to define the mechanism underlying the uncoupling. We detected a significant elevation of phosphoserine in frontal cortical D(1A)DARs of rabbits that were exposed prenatally to cocaine compared with saline controls. This increase in phosphorylation is observed at gestational day 22 and persists to postnatal day 20. The hyperphosphorylation of the D(1A)DAR is accompanied by a 45% inhibition in frontal cortex (FCX) protein phsphatase-1 (PP1) activity that appears to be mediated via DARPP-32 (dopamine and cAMP-regulated phosphoprotein) as indicated by elevated FCX phospho-DARPP-32 (Thr(34)). Furthermore, we demonstrated in both FCX and in PC2 cells that express D(1A)DARs that PP1 is physically associated with D(1A)DARs. We also observed a dramatic decrease in D(1A)DAR-associated PP1 activity in FCX of prenatal cocaine-exposed rabbits, indicating that the reduction in PP1 activity may be responsible for the hyperphosphorylation of the receptor. Furthermore, pretreatment of cortical membranes obtained from cocaine-exposed animals with exogenous PP1 dephosphorylated the phosphorylated D(1A)DAR and significantly reversed the impaired receptor-G(alphas) coupling. This work indicates (1) that D(1A)DAR dephosphorylation via PP1 is essential for receptor resensitization or reactivation and (2) an alteration in the DARPP-32/PP1 cascade appears to be a primary event responsible for D(1A)DAR dysfunction in in utero cocaine-exposed rabbit progeny. The present finding of an altered DARPP-32/PP1 cascade in association with a dysfunction in D(1A)DAR signal transmission in the prenatal cocaine-exposed rabbit brain may implicate novel strategies for the prevention and treatment for in utero cocaine-induced developmental and behavioral abnormalities.
Indexed as
Identifiers
11717349PMC6763896W2145592505What OpenQuestion holds
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.