Evidence map›Paper›PMID 26975318›Full record

ArticleNeurochemical research2016

Frequency-Dependent Modulation of Dopamine Release by Nicotine and Dopamine D1 Receptor Ligands: An In Vitro Fast Cyclic Voltammetry Study in Rat Striatum.

W Goutier, J P Lowry, A C McCreary, J J O'Connor

Open access · greenAbstract read
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In one paragraph

Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. The Role of CaMKII and ERK Signaling in Addiction.International journal of molecular sciences · 2021
    Review
  7. Nicotinic Acetylcholine Receptor Signaling in the Hypothalamus: Mechanisms Related to Nicotine's Effects on Food Intake.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020
    Review
  8. Article
  9. Complex Control of Striatal Neurotransmission by Nicotinic Acetylcholine Receptors via Excitatory Inputs onto Medium Spiny Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

W GoutierAbbott Healthcare Products B.V. (formerly Solvay Pharmaceuticals B.V.), C.J. van Houtenlaan 36, 1381 CP, Weesp, The Netherlands.
J P LowryMaynooth University Department of Chemistry, Maynooth University, Maynooth, Co. Kildare, Ireland.
A C McCrearyAbbott Healthcare Products B.V. (formerly Solvay Pharmaceuticals B.V.), C.J. van Houtenlaan 36, 1381 CP, Weesp, The Netherlands.
J J O'ConnorMaynooth University Department of Chemistry, Maynooth University, Maynooth, Co. Kildare, Ireland. john.oconnor@ucd.ie.
Abbott (Netherlands) · NLNational University of Ireland, Maynooth · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nicotine is a highly addictive drug and exerts this effect partially through the modulation of dopamine release and increasing extracellular dopamine in regions such as the brain reward systems. Nicotine acts in these regions on nicotinic acetylcholine receptors. The effect of nicotine on the frequency dependent modulation of dopamine release is well established and the purpose of this study was to investigate whether dopamine D1 receptor (D1R) ligands have an influence on this. Using fast cyclic voltammetry and rat corticostriatal slices, we show that D1R ligands are able to modulate the effect of nicotine on dopamine release. Nicotine (500 nM) induced a decrease in dopamine efflux at low frequency (single pulse or five pulses at 10 Hz) and an increase at high frequency (100 Hz) electrical field stimulation. The D1R agonist SKF-38393, whilst having no effect on dopamine release on its own or on the effect of nicotine upon multiple pulse evoked dopamine release, did significantly prevent and reverse the effect of nicotine on single pulse dopamine release. Interestingly similar results were obtained with the D1R antagonist SCH-23390. In this study we have demonstrated that the modulation of dopamine release by nicotine can be altered by D1R ligands, but only when evoked by single pulse stimulation, and are likely working via cholinergic interneuron driven dopamine release.

Indexed as

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepineAnimalsBenzazepinesCorpus StriatumDopamineElectric StimulationIn Vitro TechniquesLigandsMaleNicotineRats, WistarReceptors, Dopamine D12,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepineBenzazepinesDopamineLigandsNicotineReceptors, Dopamine D1SCH 23390Dopamine D1 receptorDopamine releaseFast cyclic voltammetryNicotineSCH-23390SKF-38393

Identifiers

PMID26975318
OpenAlexW2234914150

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.