ArticleNeuropharmacology2017
Norepinephrine regulates cocaine-primed reinstatement via α1-adrenergic receptors in the medial prefrontal cortex.
Article in Neuropharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Cocaine facilitates CaMolecular psychiatry · 2026Article
- Cocaine Use Disorder: Neuropathology and Exploratory Treatments.Molecular neurobiology · 2026Review
- The role of the prefrontal cortex in cocaine-induced noradrenaline release in the nucleus accumbens: a computational study.Biological cybernetics · 2025Article
- Article
- Commentary: AlphaFrontiers in behavioral neuroscience · 2023Article
- The Therapeutic Potential of 2-{[4-(2-methoxyphenyl)piperazin-1-yl]alkyl}-1H-benzo[d]imidazoles as Ligands for Alpha1-Adrenergic Receptor - Comparative In Silico and In Vitro Study.Applied biochemistry and biotechnology · 2022Article
- Norepinephrine and dopamine contribute to distinct repetitive behaviors induced by novel odorant stress in male and female mice.Hormones and behavior · 2022Article
- Noradrenergic circuits and signaling in substance use disorders.Neuropharmacology · 2022Review
- The role of anterior insula-brainstem projections and alpha-1 noradrenergic receptors for compulsion-like and alcohol-only drinking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Neurochemical mechanisms and neurocircuitry underlying the contribution of stress to cocaine seeking.Journal of neurochemistry · 2021Review
- Effects of the Alpha-1 Antagonist Prazosin on KOR Agonist-Induced Reinstatement of Alcohol Seeking.The international journal of neuropsychopharmacology · 2019Article
- Transgenic increase in the β-endorphin concentration in cerebrospinal fluid alleviates morphine-primed relapse behavior through the μ opioid receptor in rats.Journal of medical virology · 2019Article
- Divergent effects of repeated cocaine and novel environment exposure on locus coeruleus c-fos expression and brain catecholamine concentrations in rats.Brain and behavior · 2019Article
- Common neurocircuitry mediating drug and fear relapse in preclinical models.Psychopharmacology · 2019Review
- Modeling cocaine relapse in rodents: Behavioral considerations and circuit mechanisms.Progress in neuro-psychopharmacology & biological psychiatry · 2018Review
- α1b-Adrenergic Receptor Localization and Relationship to the D1-Dopamine Receptor in the Rat Nucleus Accumbens.Neuroscience · 2018Article
- Single Prazosin Infusion in Prelimbic Cortex Fosters Extinction of Amphetamine-Induced Conditioned Place Preference.Frontiers in pharmacology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Drug-primed reinstatement of cocaine seeking in rats is thought to reflect relapse-like behavior and is mediated by the integration of signals from mesocorticolimbic dopaminergic projections and corticostriatal glutamatergic innervation. Cocaine-primed reinstatement can also be attenuated by systemic administration of dopamine β-hydroxylase (DBH) inhibitors, which prevent norepinephrine (NE) synthesis, or by α1-adrenergic receptor (α1AR) antagonists, indicating functional modulation by the noradrenergic system. In the present study, we sought to further discern the role of NE in cocaine-seeking behavior by determining whether α1AR activation can induce reinstatement on its own or is sufficient to permit cocaine-primed reinstatement in the absence of all other AR signaling, and identifying the neuroanatomical substrate within the mesocorticolimbic reward system harboring the critical α1ARs. We found that while intracerebroventricular infusion of the α1AR agonist phenylephrine did not induce reinstatement on its own, it did overcome the blockade of cocaine-primed reinstatement by the DBH inhibitor nepicastat. Furthermore, administration of the α1AR antagonist terazosin in the medial prefrontal cortex (mPFC), but not the ventral tegmental area (VTA) or nucleus accumbens (NAc) shell, attenuated cocaine-primed reinstatement. Combined, these data indicate that α1AR activation in the mPFC is required for cocaine-primed reinstatement, and suggest that α1AR antagonists merit further investigation as pharmacotherapies for cocaine dependence.
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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.