Evidence map›Paper›PMID 17597219›Full record

ReviewBrain research reviews2008

Modulation of glutamatergic transmission by sulfated steroids: role in fetal alcohol spectrum disorder.

C Fernando Valenzuela, L Donald Partridge, Manuel Mameli, Douglas A Meyer

Open access · greenAbstract readReview
In one paragraph

Review in Brain research reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Neurosteroid influences on sensitivity to ethanol.Frontiers in endocrinology · 2012
    Article
  14. Article
  15. Fetal alcohol spectrum disorders and abnormal neuronal plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2011
    Review
  16. Article
  17. Article
  18. Focus on: neurotransmitter systems.Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism · 2011
    Review
  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

4 authors at 1 institution in 1 country.

C Fernando ValenzuelaDepartment of Neurosciences, MSC08 4740, 1 University of New Mexico, Albuquerque, NM 87131-0001, USA. fvalenzuela@salud.unm.edu
L Donald Partridge
Manuel Mameli
Douglas A Meyer
University of New Mexico · US

Funding

Alcohol and Developing Neuronal CircuitsR01AA015614 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Carlos Fernando Valenzuela · 2005 to 2026
$3.9M
Age-dependent presynaptic action of pregnenolone sulfateR01MH070386 · NIMH · UNIVERSITY OF NEW MEXICO · PI PARTRIDGE, LLOYD DONALD · 2005 to 2009
$1.6M
NIAAA NIH HHS R01 AA015614NIMH NIH HHS R01 MH070386
6 · The paper itself

Abstract

It is well established that sulfated steroids regulate synaptic transmission by altering the function of postsynaptic neurotransmitter receptors. In recent years, evidence from several laboratories indicates that these agents also regulate glutamatergic synaptic transmission at the presynaptic level in an age-dependent manner. In developing neurons, pregnenolone sulfate (PREGS) increases the probability of glutamate release, as evidenced by an increase in the frequency of AMPA receptor-mediated miniature excitatory postsynaptic currents and a decrease in paired-pulse facilitation. In hippocampal slices from postnatal day 3-5 rats, this effect is mediated by an increase in Ca(2+) levels in the axonal terminal that depends on presynaptic NMDA receptors. This is followed by delayed potentiation of postsynaptic AMPA receptor currents. Importantly, depolarization of postsynaptic neurons, inhibition of hydroxysteroid sulfatase activity and acute exposure to ethanol mimics the effect of exogenous PREGS application. This developmental form of synaptic plasticity cannot be observed in slices from rats older than postnatal day 6, when presynaptic NMDA receptors are no longer expressed in CA1 hippocampal region. Both in the CA1 hippocampal region and the dentate gyrus of more mature rats, PREGS, dehydroepiandrosterone sulfate and hydroxysteroid sulfatase inhibitors increase paired-pulse facilitation, without affecting basal glutamate release probability. This effect depends on activation of sigma(1)-like receptors and G(i/o) and involves a target in the release machinery that is downstream of residual Ca(2+). These presynaptic actions of sulfated steroids could play important roles in physiological processes ranging from synapse maturation to learning and memory, as well as pathophysiological conditions such as fetal alcohol spectrum disorder.

Indexed as

AnimalsBrainDehydroepiandrosterone SulfateEthanolFemaleFetal Alcohol Spectrum DisordersGlutamineHumansNeuronsPregnancyPregnenoloneReceptors, N-Methyl-D-AspartateSteroidsSynaptic TransmissionDehydroepiandrosterone SulfateEthanolGlutaminePregnenolonepregnenolone sulfateReceptors, N-Methyl-D-AspartateSteroids

Identifiers

PMID17597219
PMCPMC2366116
OpenAlexW2076108722

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.