Evidence map›Paper›PMID 10066284›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Presynaptic inhibition of GABA(B)-mediated synaptic potentials in the ventral tegmental area during morphine withdrawal.

Y Shoji, J Delfs, J T Williams

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. VTA dopamine neuron plasticity - the unusual suspects.The European journal of neuroscience · 2016
    Review
  10. Pain and Poppies: The Good, the Bad, and the Ugly of Opioid Analgesics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Review
  11. Effects of the Mu opioid receptor polymorphism (OPRM1 A118G) on pain regulation, placebo effects and associated personality trait measures.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Opioid-sensitive GABA inputs from rostromedial tegmental nucleus synapse onto midbrain dopamine neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  17. Article
  18. Review
  19. PKG and PKA signaling in LTP at GABAergic synapses.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2009
    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

3 authors at 2 institutions in 1 country.

Y ShojiThe Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201, USA.
J Delfs
J T Williams
Oregon Health & Science University · USVollum Institute · US

Funding

BIOLOGICAL BASES OF DRUG-SEEKING BEHAVIORT32DA007262 · NIDA · OREGON HEALTH & SCIENCE UNIVERSITY · PI WILLIAMS, JOHN T · 1991 to 2022
$9.4M
CHRONIC MORPHINE--REGULATION OF ION CONDUCTANCESR01DA008163 · NIDA · OREGON HEALTH & SCIENCE UNIVERSITY · PI WILLIAMS, JOHN T · 1993 to 2021
$6.2M
NIDA NIH HHS DA07262NIDA NIH HHS DA08163NIDA NIH HHS R01 DA008163NIDA NIH HHS T32 DA007262
6 · The paper itself

Abstract

Opioids increase the firing of dopamine cells in the ventral tegmental area by presynaptic inhibition of GABA release. This report describes an acute presynaptic inhibition of GABAB-mediated IPSPs by mu- and kappa-opioid receptors and the effects of withdrawal from chronic morphine treatment on the release of GABA at this synapse. In slices taken from morphine-treated guinea pigs after washing out the morphine (withdrawn slices), a low concentration of a mu receptor agonist increased, rather than decreased, the amplitude of the GABAB IPSP. In withdrawn slices, after blocking A1-adenosine receptors with 8-cyclopentyl-1, 3-dipropylxantine, mu-opioid receptor activation inhibited the IPSP at all concentrations and increased the maximal inhibition. In addition, during withdrawal, there was a tonic increase in adenosine tone that was further increased by forskolin or D1-dopamine receptor activation, suggesting that metabolism of cAMP was the source of adenosine. The results indicate that during acute morphine withdrawal, there was an upregulation of the basal level of an opioid-sensitive adenylyl cyclase. Inhibition of this basal activity by opioids had two effects. First, a decrease in the formation of cAMP that decreased adenosine tone. This effect predominated at low mu receptor occupancy and increased the amplitude of the IPSP. Higher agonist concentrations inhibited transmitter release by both kinase-dependent and -independent pathways. This study indicates that the consequences of the morphine-induced upregulation of the cAMP cascade on synaptic transmission are dependent on the makeup of receptors and second messenger pathways present on any given terminal.

Indexed as

AdenosineAdenylyl CyclasesAnimalsDrug SynergismEnzyme ActivationGuinea PigsMorphineNarcoticsNeural InhibitionPhosphotransferasesPresynaptic TerminalsReceptors, Dopamine D1Receptors, GABA-BReceptors, Opioid, kappaReceptors, Opioid, muSubstance Withdrawal SyndromeAdenosineAdenylyl CyclasesMorphineNarcoticsPhosphotransferasesReceptors, Dopamine D1Receptors, GABA-BReceptors, Opioid, kappaReceptors, Opioid, mu

Identifiers

PMID10066284
PMCPMC6782572
OpenAlexW1775447930

What OpenQuestion holds

Texttitle and abstract
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.