ArticleThe European journal of neuroscience2010
Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal.
Article in The European journal of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- DRD1 and DRD2 dopamine-sensitive neurons in the central amygdala respond differently to rewarding and aversive stimuli.Translational psychiatry · 2026Article
- Synaptic Plasticity of D1 and D2 Types of Neurons in the Central Amygdala After Sucrose and Cocaine Exposure.The European journal of neuroscience · 2025Article
- A Novel CaMKII Inhibitory Peptide Blocks Relapse to Morphine Seeking by Influencing Synaptic Plasticity in the Nucleus Accumbens Shell.Brain sciences · 2022Article
- Brain systems in cocaine abstinence-induced anxiety-like behavior in rodents: A review.Addiction neuroscience · 2022Article
- P/Q-type voltage-gated calcium channels mediate the ethanol and CRF sensitivity of central amygdala GABAergic synapses.Neuropharmacology · 2017Article
- Don't stress about CRF: assessing the translational failures of CRFPsychopharmacology · 2017Review
- PARP-1 is required for retrieval of cocaine-associated memory by binding to the promoter of a novel gene encoding a putative transposase inhibitor.Molecular psychiatry · 2017Article
- Dissociable Role of Corticotropin Releasing Hormone Receptor Subtype 1 on Dopaminergic and D1 Dopaminoceptive Neurons in Cocaine Seeking Behavior.Frontiers in behavioral neuroscience · 2017Article
- Early Antipsychotic Treatment in Juvenile Rats Elicits Long-Term Alterations to the Dopamine Neurotransmitter System.International journal of molecular sciences · 2016Article
- Neurogenetic and epigenetic correlates of adolescent predisposition to and risk for addictive behaviors as a function of prefrontal cortex dysregulation.Journal of child and adolescent psychopharmacology · 2015Review
- Corticotropin releasing factor and catecholamines enhance glutamatergic neurotransmission in the lateral subdivision of the central amygdala.Neuropharmacology · 2013Article
- Dampened dopamine-mediated neuromodulation in prefrontal cortex of fragile X mice.The Journal of physiology · 2013Article
- Allostasis and addiction: role of the dopamine and corticotropin-releasing factor systems.Physiology & behavior · 2012Review
- Dissociation of corticotropin-releasing factor receptor subtype involvement in sensitivity to locomotor effects of methamphetamine and cocaine.Psychopharmacology · 2012Article
- Cue-induced reinstatement of cocaine seeking in the rat "conflict model": effect of prolonged home-cage confinement.Psychopharmacology · 2012Article
- Role of corticotropin-releasing factor in drug addiction: potential for pharmacological intervention.CNS drugs · 2011Review
- Dissection of corticotropin-releasing factor system involvement in locomotor sensitivity to methamphetamine.Genes, brain, and behavior · 2011Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Corticotropin-releasing factor (CRF) in the amygdala is involved in stress responses. Moreover, dopaminergic neurotransmission in the brain reward system including the amygdala plays a significant role in the pathology of cocaine addiction. The present study analysed CRF-induced synaptic plasticity, its pharmacological sensitivity and interactions with the dopamine (DA) system in the basolateral to lateral capsula central amygdala (lcCeA) pathway after a 2-week withdrawal from repeated cocaine administration. A physiologically relevant CRF concentration (25 nm) induced long-term potentiation (LTP) that was enhanced after cocaine withdrawal. In saline-treated rats, CRF-induced LTP was mediated through N-methyl-d-aspartate (NMDA) receptors, L-type voltage-gated calcium channels (L-VGCCs) and CRF(1) receptors. However, in cocaine-withdrawn animals, activation of CRF(1) and CRF(2) receptors was found to enhance LTP. This enhanced CRF-induced LTP after cocaine withdrawal was mediated through endogenous activation of both D1- and D2-like receptors. Furthermore, expression of the D1 receptor (D1R) but not the D2R, D3R, D4R or D5R was significantly increased after cocaine withdrawal. CRF(1) but not CRF(2) protein expression was increased, suggesting that elevated levels of these proteins contributed to the enhancement of CRF-induced LTP during cocaine withdrawal. CRF interactions with the DA system in the amygdala may represent a fundamental neurochemical and cellular mechanism linking stress to cocaine-induced neuronal plasticity.
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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.