Evidence map›Paper›PMID 10414998›Full record

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

Glutamate inhibits thalamic reticular neurons.

C L Cox, S M Sherman

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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Article
  3. Post cardiac arrest physical exercise mitigates cell death in the septal and thalamic nuclei and ameliorates contextual fear conditioning deficits in rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. mGluR1 and mGluR5 Synergistically Control Cholinergic Synaptic Transmission in the Thalamic Reticular Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  10. Article
  11. Article
  12. Article
  13. The function of metabotropic glutamate receptors in thalamus and cortex.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2014
    Review
  14. Modulation of short-term plasticity in the corticothalamic circuit by group III metabotropic glutamate receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  15. Article
  16. Article
  17. Article
  18. Activity-dependent regulation of retinogeniculate signaling by metabotropic glutamate receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  19. Article
  20. Glutamatergic inhibition in sensory neocortex.Cerebral cortex (New York, N.Y. : 1991) · 2009
    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 2 institutions in 1 country.

C L CoxDepartment of Neurobiology, State University of New York, Stony Brook, New York 11794-5230, USA.
S M Sherman
State University of New York · USStony Brook University · US

Funding

VISUAL DEPRIVATION OF THE VISUAL SYSTEMR01EY003038 · NEI · UNIVERSITY OF CHICAGO · PI SHERMAN, S. MURRAY · 1985 to 2007
$3.4M
NEI NIH HHS EY03038
6 · The paper itself

Abstract

Activation of metabotropic glutamate receptors (mGluRs) can result in long-lasting modulation of neuronal excitability. Multiple mGluR subtypes are localized within the rat thalamic reticular nucleus (TRN), and we have examined the effects of activating these different receptor subtypes on the excitability of these neurons using an in vitro slice preparation. Typical of most mGluR-sensitive preparations, the general mGluR agonist, (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (ACPD) produced a robust, long-lasting excitatory response. Surprisingly, ACPD produced a membrane hyperpolarization in some neurons. Using selective mGluR agonists, we found that activation of group II mGluRs produces the hyperpolarization, whereas the depolarization is mediated by group I mGluRs. While the polarity of the postsynaptic response (hyperpolarization vs depolarization) was dependent on the mGluR subtype activated, both actions appear to result from modification of a linear K(+) conductance. The inhibitory action of Glutamate, via group II mGluRs, provides an avenue for a disinhibitory effect that could have interesting consequences upon a well-investigated, model neuronal circuit, turning its assumed functional role upside down.

Indexed as

AnimalsElectrophysiologyGlutamic AcidIn Vitro TechniquesNeural InhibitionNeuronsRatsRats, Sprague-DawleyReceptors, Metabotropic GlutamateThalamic NucleiGlutamic AcidReceptors, Metabotropic Glutamate

Identifiers

PMID10414998
PMCPMC6782814
OpenAlexW2098560768

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.