Evidence map›Paper›PMID 9852609›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Glutamate inhibits GABA excitatory activity in developing neurons.

A N van den Pol, X B Gao, P R Patrylo, P K Ghosh, K Obrietan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Chloride imbalance in Fragile X syndrome.Frontiers in neuroscience · 2022
    Article
  6. Reduced Expression of GABAFrontiers in cell and developmental biology · 2021
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Cloning and characterization of GABAA α subunits and GABAB subunits in Xenopus laevis during development.Developmental dynamics : an official publication of the American Association of Anatomists · 2011
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Group III metabotropic glutamate receptors maintain tonic inhibition of excitatory synaptic input to hypocretin/orexin neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  18. 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

5 authors at 2 institutions in 1 country.

A N van den PolDepartment of Neurosurgery, Yale University, New Haven, Connecticut 06520, USA.
X B Gao
P R Patrylo
P K Ghosh
K Obrietan
Yale University · USStanford University · US

Funding

GABA: EXCITATORY TRANSMITTER IN DEVELOPING HYPOTHALAMUSR01NS034887 · NINDS · YALE UNIVERSITY · PI VAN DEN POL, ANTHONY N · 1995 to 2008
$2.6M
NINDS NIH HHS NS 34887NINDS NIH HHS R01 NS034887
6 · The paper itself

Abstract

In contrast to the mature brain, in which GABA is the major inhibitory neurotransmitter, in the developing brain GABA can be excitatory, leading to depolarization, increased cytoplasmic calcium, and action potentials. We find in developing hypothalamic neurons that glutamate can inhibit the excitatory actions of GABA, as revealed with fura-2 digital imaging and whole-cell recording in cultures and brain slices. Several mechanisms for the inhibitory role of glutamate were identified. Glutamate reduced the amplitude of the cytoplasmic calcium rise evoked by GABA, in part by activation of group II metabotropic glutamate receptors (mGluRs). Presynaptically, activation of the group III mGluRs caused a striking inhibition of GABA release in early stages of synapse formation. Similar inhibitory actions of the group III mGluR agonist L-AP4 on depolarizing GABA activity were found in developing hypothalamic, cortical, and spinal cord neurons in vitro, suggesting this may be a widespread mechanism of inhibition in neurons throughout the developing brain. Antagonists of group III mGluRs increased GABA activity, suggesting an ongoing spontaneous glutamate-mediated inhibition of excitatory GABA actions in developing neurons. Northern blots revealed that many mGluRs were expressed early in brain development, including times of synaptogenesis. Together these data suggest that in developing neurons glutamate can inhibit the excitatory actions of GABA at both presynaptic and postsynaptic sites, and this may be one set of mechanisms whereby the actions of two excitatory transmitters, GABA and glutamate, do not lead to runaway excitation in the developing brain. In addition to its independent excitatory role that has been the subject of much attention, our data suggest that glutamate may also play an inhibitory role in modulating the calcium-elevating actions of GABA that may affect neuronal migration, synapse formation, neurite outgrowth, and growth cone guidance during early brain development.

Indexed as

AnimalsAnimals, NewbornCalciumCells, CulturedCerebral CortexEmbryo, MammalianExcitatory Postsynaptic PotentialsGABA Antagonistsgamma-Aminobutyric AcidGene ExpressionGlutamic AcidGramicidinHypothalamusIn Vitro TechniquesNeuronsPatch-Clamp Techniques2-amino-4-phosphono-propinateCalciumGABA Antagonistsgamma-Aminobutyric AcidGlutamic AcidGramicidinmetabotropic glutamate receptor 3PropionatesReceptors, Metabotropic Glutamate

Identifiers

PMID9852609
PMCPMC6793361
OpenAlexW1850595514

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.