Evidence map›Paper›PMID 25572531›Full record

ArticlePsychopharmacology2015

Psychostimulants and atomoxetine alter the electrophysiological activity of prefrontal cortex neurons, interaction with catecholamine and glutamate NMDA receptors.

Mathieu Di Miceli, Benjamin Gronier

Abstract read
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In one paragraph

Article in Psychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  5. Article
  6. Effects of Methylphenidate on the Dopamine Transporter and Beyond.Current topics in behavioral neurosciences · 2022
    Article
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  8. Profiling the structural determinants of aminoketone derivatives as hNET and hDAT reuptake inhibitors by field-based QSAR based on molecular docking.Technology and health care : official journal of the European Society for Engineering and Medicine · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Increased cortical neuronal responses to NMDA and improved attentional set-shifting performance in rats following prebiotic (B-GOSEuropean neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2018
    Article
  14. Disrupted Glutamatergic Transmission in Prefrontal Cortex Contributes to Behavioral Abnormality in an Animal Model of ADHD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Article
  15. Article
  16. 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

2 authors at 1 institution in 1 country.

Mathieu Di MiceliLeicester School of Pharmacy, De Montfort University, The Gateway, Leicester, LE1 9BH, UK.
Benjamin Gronier
De Montfort University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleAttention-deficit hyperactivity disorder (ADHD) is the most frequently diagnosed neuropsychiatric disorder in childhood. Currently available ADHD drugs include the psychostimulants methylphenidate (MPH) and D-amphetamine (D-AMP), acting on norepinephrine and dopamine transporters/release, and atomoxetine (ATX), a selective norepinephrine uptake inhibitor. Recent evidence suggests an involvement of glutamate neurotransmission in the pathology and treatment of ADHD, via mechanisms to be clarified.

objectiveWe have investigated how ADHD drugs could modulate, through interaction with catecholamine receptors, basal and glutamate-induced excitability of pyramidal neurons in the prefrontal cortex (PFC), a region which plays a major role in control of attention and impulsivity.

methodsWe have used the technique of extracellular single-unit recording in anaesthetised rats coupled with microiontophoresis.

resultsBoth MPH (1-3 mg/kg) and D-AMP (1-9 mg/kg) increased the firing activity of PFC neurons in a dopamine D1 receptor-dependent manner. ATX administration (1-6 mg/kg) also increased the firing of neurons, but this effect is not significantly reversed by D1 (SCH 23390) or alpha1 (prazosin) receptor antagonists but potentiated by alpha2 antagonist (yohimbine). All drugs induced a clear potentiation of the excitatory response of PFC neurons to the microiontophoretic application of the glutamate agonist N-methyl-D-aspartate (NMDA), but not to the glutamate agonist α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). The potentiating effect of D-AMP on NMDA-induced activation of PFC neurons was partially reversed or prevented by dopamine D1 receptor blockade.

conclusionOur data shows that increase in excitability of PFC neurons in basal conditions and via NMDA receptor activation may be involved in the therapeutic response to ADHD drugs.

Indexed as

AnimalsAtomoxetine HydrochlorideCentral Nervous System StimulantsDose-Response Relationship, DrugElectrophysiological PhenomenaMaleMethylphenidateNeuronsPrefrontal CortexPyramidal CellsRatsRats, Sprague-DawleyReceptors, AMPAReceptors, CatecholamineReceptors, Dopamine D1Receptors, N-Methyl-D-AspartateAtomoxetine HydrochlorideCentral Nervous System StimulantsMethylphenidateReceptors, AMPAReceptors, CatecholamineReceptors, Dopamine D1Receptors, N-Methyl-D-Aspartate

Identifiers

PMID25572531
OpenAlexW1973813011

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.