Evidence map›Paper›PMID 22592307›Full record

ArticleJournal of neurophysiology2012

Methamphetamine produces bidirectional, concentration-dependent effects on dopamine neuron excitability and dopamine-mediated synaptic currents.

Sarah Y Branch, Michael J Beckstead

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

50 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Absence of TAAR1 function increases methamphetamine-induced excitability of dorsal raphe serotonin neurons and drives binge-level methamphetamine intake.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  5. Article
  6. Article
  7. A Mechanistic Review on Toxicity Effects of Methamphetamine.International journal of medical sciences · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Neurotensin Release from Dopamine Neurons Drives Long-Term Depression of Substantia Nigra Dopamine Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  12. Article
  13. Article
  14. Substance abuse and neurotransmission.Advances in pharmacology (San Diego, Calif.) · 2022
    Article
  15. Methamphetamine Dysregulation of the Central Nervous System and Peripheral Immunity.The Journal of pharmacology and experimental therapeutics · 2021
    Review
  16. Article
  17. Dopamine Transporter Is a Master Regulator of Dopaminergic Neural Network Connectivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  18. Article
  19. Article
  20. 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.

Sarah Y BranchDepartment of Physiology, University of Texas Health Science Center, San Antonio, Texas 78229, USA.
Michael J Beckstead
The University of Texas Health Science Center at San Antonio · US

Funding

Methamphetamine Effects on Dendrodendritic Dopamine Transmission in the VTAK01DA021699 · NIDA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BECKSTEAD, MICHAEL J · 2007 to 2011
$685k
NIDA NIH HHS K01 DA021699NIDA NIH HHS K01 DA21699
6 · The paper itself

Abstract

Amphetamine-like compounds are commonly used to enhance cognition and to treat attention deficit/hyperactivity disorder, but they also function as positive reinforcers and are self-administered at doses far exceeding clinical relevance. Many of these compounds (including methamphetamine) are substrates for dopamine reuptake transporters, elevating extracellular dopamine by inhibiting uptake and promoting reverse transport. This produces an increase in extracellular dopamine that inhibits dopamine neuron firing through autoreceptor activation and consequently blunts phasic dopamine neurotransmission, an important learning signal. However, these mechanisms do not explain the beneficial behavioral effects observed at clinically useful concentrations. In the present study, we have used patch-clamp electrophysiology in slices of mouse midbrain to show that, surprisingly, low concentrations of methamphetamine actually enhance dopamine neurotransmission and increase dopamine neuron firing through a dopamine transporter-mediated excitatory conductance. Both of these effects are reversed by higher concentrations of methamphetamine, which inhibit firing through dopamine D2 autoreceptor activation and decrease the peak amplitude of dopamine-mediated synaptic currents. These competing, concentration-dependent effects of methamphetamine suggest a mechanistic interplay by which lower concentrations of methamphetamine can overcome autoreceptor-mediated inhibition at the soma to increase phasic dopamine transmission.

Indexed as

AnimalsAutoreceptorsDopamine AgentsDopamine Plasma Membrane Transport ProteinsDopaminergic NeuronsMaleMesencephalonMethamphetamineMiceMice, Inbred C57BLReceptors, Dopamine D2Synaptic TransmissionAutoreceptorsDopamine AgentsDopamine Plasma Membrane Transport ProteinsMethamphetamineReceptors, Dopamine D2

Identifiers

PMID22592307
PMCPMC3424098
OpenAlexW2149439113

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.