ArticleAddiction biology2014
Relapse to cocaine-seeking after abstinence is regulated by cAMP-dependent protein kinase A in the prefrontal cortex.
Article in Addiction biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Physiological neuroadaptations in prefrontal cortical regulation of abstinence and cue-induced relapse to cocaine seeking.Addiction neuroscience · 2025Article
- EcoHIV infection effects on cocaine seeking and neuroimmune responses in male mice depend on cocaine exposure pattern.Addiction neuroscience · 2025Article
- Restraint stress effects on glutamate signaling protein levels in the rats' frontal cortex: Does β1 adrenoceptor activity matter?Frontiers in pharmacology · 2024Article
- The activity-regulated cytoskeleton-associated protein, Arc, functions in the nucleus accumbens shell to limit multiple triggers of cocaine-seeking behaviour.Addiction biology · 2023Article
- Increased Excitability and Synaptic Plasticity of Drd1- and Drd2-Expressing Prelimbic Neurons Projecting to Nucleus Accumbens after Heroin Abstinence Are Reversed by Cue-Induced Relapse and Protein Kinase A Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- BDNF as a therapeutic candidate for cocaine use disorders.Addiction neuroscience · 2022Article
- Increased Cocaine Motivation Is Associated with Degraded Spatial and Temporal Representations in IL-NAc Neurons.Neuron · 2019Article
- Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration.International journal of molecular sciences · 2019Review
- Biphasic effect of abstinence duration following cocaine self-administration on spine morphology and plasticity-related proteins in prelimbic cortical neurons projecting to the nucleus accumbens core.Brain structure & function · 2019Article
- Morphine Reward Promotes Cue-Sensitive Learning: Implication of Dorsal Striatal CREB Activity.Frontiers in psychiatry · 2017Article
- Glutamatergic neurotransmission in the prefrontal cortex mediates the suppressive effect of intra-prelimbic cortical infusion of BDNF on cocaine-seeking.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2016Article
- Synaptic mechanisms underlying persistent cocaine craving.Nature reviews. Neuroscience · 2016Review
- Molecular Mechanism: ERK Signaling, Drug Addiction, and Behavioral Effects.Progress in molecular biology and translational science · 2016Review
- Cocaine self-administration causes signaling deficits in corticostriatal circuitry that are reversed by BDNF in early withdrawal.Brain research · 2015Review
- Chronic cocaine disrupts mesocortical learning mechanisms.Brain research · 2015Review
- Dorsal medial prefrontal cortex (MPFC) circuitry in rodent models of cocaine use: implications for drug addiction therapies.Addiction biology · 2015Review
- Oxytocin reduces cocaine seeking and reverses chronic cocaine-induced changes in glutamate receptor function.The international journal of neuropsychopharmacology · 2014Article
- Assessment of a proposed "three-criteria" cocaine addiction model for use in reinstatement studies with rats.Psychopharmacology · 2014Article
- Short and long access to cocaine self-administration activates tyrosine phosphatase STEP and attenuates GluN expression but differentially regulates GluA expression in the prefrontal cortex.Psychopharmacology · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Abstinence from cocaine self-administration (SA) is associated with neuroadaptations in the prefrontal cortex (PFC) and nucleus accumbens (NAc) that are implicated in cocaine-induced neuronal plasticity and relapse to drug-seeking. Alterations in cAMP-dependent protein kinase A (PKA) signaling are prominent in medium spiny neurons in the NAc after repeated cocaine exposure but it is unknown whether similar changes occur in the PFC. Because cocaine SA induces disturbances in glutamatergic transmission in the PFC-NAc pathway, we examined whether dysregulation of PKA-mediated molecular targets in PFC-NAc neurons occurs during abstinence and, if so, whether it contributes to cocaine-seeking. We measured the phosphorylation of cAMP response element binding protein (Ser133) and GluA1 (Ser845) in the dorsomedial (dm) PFC and the presynaptic marker, synapsin I (Ser9, Ser62/67, Ser603), in the NAc after 7 days of abstinence from cocaine SA with or without cue-induced cocaine-seeking. We also evaluated whether infusion of the PKA inhibitor, 8-bromo-Rp-cyclic adenosine 3', 5'-monophosphorothioate (Rp-cAMPs), into the dmPFC after abstinence would affect cue-induced cocaine-seeking and PKA-regulated phosphoprotein levels. Seven days of forced abstinence increased the phosphorylation of cAMP response element binding protein and GluA1 in the dmPFC and synapsin I (Ser9) in the NAc. Induction of these phosphoproteins was reversed by a cue-induced relapse test of cocaine-seeking. Bilateral intra-dmPFC Rp-cAMPs rescued abstinence-elevated PKA-mediated phosphoprotein levels in the dmPFC and NAc and suppressed cue-induced relapse. Thus, by inhibiting abstinence-induced PKA molecular targets, relapse reverses abstinence-induced neuroadaptations in the dmPFC that are responsible, in part, for the expression of cue-induced cocaine-seeking.
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