ArticleBrain and behavior2015
Selective inhibition of dopamine-beta-hydroxylase enhances dopamine release from noradrenergic terminals in the medial prefrontal cortex.
Article in Brain and behavior, 2015. 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, 30 citations in OpenAlex.
- Exploring Nepicastat Activity: Beyond DβH.International journal of molecular sciences · 2025Article
- Monoaminergic Modulation of Learning and Cognitive Function in the Prefrontal Cortex.Brain sciences · 2024Review
- Genetic disruption of dopamine β-hydroxylase dysregulates innate responses to predator odor in mice.Neurobiology of stress · 2024Article
- Genetic disruption of dopamine β-hydroxylase dysregulates innate responses to predator odor in mice.bioRxiv : the preprint server for biology · 2024Article
- Norepinephrine and dopamine contribute to distinct repetitive behaviors induced by novel odorant stress in male and female mice.Hormones and behavior · 2022Article
- A role for cortical dopamine in the paradoxical calming effects of psychostimulants.Scientific reports · 2022Article
- Treatment with dopamine β-hydroxylase (DBH) inhibitors prevents morphine use and relapse-like behavior in rats.Pharmacological reports : PR · 2021Article
- Both Prelimbic and Infralimbic Noradrenergic Neurotransmissions Modulate Cardiovascular Responses to Restraint Stress in Rats.Frontiers in physiology · 2021Article
- Treatment With Nepicastat Decreases Contextual Traumatic Memories Persistence in Post-traumatic Stress Disorder.Frontiers in molecular neuroscience · 2021Article
- Combined Optogenetic Approaches Reveal Quantitative Dynamics of Endogenous Noradrenergic Transmission in the Brain.iScience · 2020Article
- Noradrenergic Source of Dopamine Assessed by Microdialysis in the Medial Prefrontal Cortex.Frontiers in pharmacology · 2020Article
- Noradrenergic depletion causes sex specific alterations in the endocannabinoid system in the Murine prefrontal cortex.Neurobiology of stress · 2019Article
- Dopamine and Noradrenaline in the Brain; Overlapping or Dissociate Functions?Frontiers in molecular neuroscience · 2019Article
- Dopamine: Functions, Signaling, and Association with Neurological Diseases.Cellular and molecular neurobiology · 2019Review
- Limited modulation of the abuse-related behavioral effects of d-methamphetamine by disulfiram.Experimental and clinical psychopharmacology · 2018Article
- Maternal Immune Activation Disrupts Dopamine System in the Offspring.The international journal of neuropsychopharmacology · 2016Article
- Neurobiology of KB220Z-Glutaminergic-Dopaminergic Optimization Complex [GDOC] as a Liquid Nano: Clinical Activation of Brain in a Highly Functional Clinician Improving Focus, Motivation and Overall Sensory Input Following Chronic Intake.Clinical medical reviews and case reports · 2016Article
- Selective inhibition of dopamine-beta-hydroxylase enhances dopamine release from noradrenergic terminals in the medial prefrontal cortex.Brain and behavior · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionDisulfiram has been claimed to be useful in cocaine addiction therapy, its efficacy being attributed to dopamine-beta-hydroxylase (DBH) inhibition. Our previous results indicate that disulfiram and the selective DBH inhibitor nepicastat increase extracellular dopamine (DA) in the rat medial prefrontal cortex (mPFC), and markedly potentiated cocaine-induced increase. Concomitantly, in rats with cocaine self-administration history, cocaine-seeking behavior induced by drug priming was prevented, probably through overstimulation of D1 receptors due to the DA increase. The present research was aimed at studying the neurochemical mechanisms originating the enhanced DA release.
methodsNoradrenergic system ablation was attained by intracerebroventricular (i.c.v.) administration of the neurotoxin anti-DBH-saporin (aDBH-sap). DA, noradrenaline (NA), and DOPAC were assessed by HPLC after ex vivo tissue extraction or in vivo microdialysis. Control and denervated rats were subjected to microdialysis in the mPFC and caudate nucleus to evaluate the effect of nepicastat-cocaine combination on extracellular DA levels and their regulation by α2-adrenoceptors.
resultsFifteen days after neurotoxin or its vehicle administration, tissue and extracellular NA were reduced to less than 2% the control value, while extracellular DA was increased by approximately 100%. In control rats, nepicastat given alone and in combination with cocaine increased extracellular DA by about 250% and 1100%, respectively. In denervated rats, nepicastat slightly affected extracellular DA, while in combination with cocaine increased extracellular DA by 250%. No differences were found in the caudate nucleus. Clonidine almost totally reversed the extracellular DA elevation produced by nepicastat-cocaine combination, while it was ineffective in denervated rats.
conclusionsThis research shows that the increase of extracellular DA produced by nepicastat alone or in combination with cocaine was prevented by noradrenergic denervation. The results indicate that nepicastat enhances DA release from noradrenergic terminals supposedly by removing NA from α2-autoreceptors. In addition to the inhibition of DA uptake, the latter mechanism may explain the synergistic effect of cocaine on nepicastat-induced DA release.
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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.