Evidence map›Paper›PMID 10718099›Full record

ReviewDrugs2000

Pharmacology of AMPA/kainate receptor ligands and their therapeutic potential in neurological and psychiatric disorders.

G J Lees

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Drugs, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04676659 (Phase II Dose-finding Open Study of Recombinant Human TNK Tissue-type Plasminogen Activator), which is not on this map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.1field-weighted citation impact, top 5% 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.

NCT04676659 phase2completednot on this mapstarted 2018, after this paper: background citation

Phase II Dose-finding Open Study of Recombinant Human TNK Tissue-type Plasminogen Activator (rhTNK-tPA) Injection Administered Within 3 Hours After Onset of Hyperacute Ischemic Stroke

TypeinterventionalSponsorBeijing Tiantan HospitalRan2018 to 2020Enrolled240ConditionsAcute Ischemic StrokeArmsTNK-tPA
3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 136 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Recent developments on triazole nucleus in anticonvulsant compounds: a review.Journal of enzyme inhibition and medicinal chemistry · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Brain-derived neurotrophic factor mRNA and protein are targeted to discrete dendritic laminas by events that trigger epileptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  19. Structure and function of AMPA receptors.The Journal of physiology · 2004
    Review
  20. Review
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

1 author at 1 institution in 1 country.

G J LeesDepartment of Psychiatry and Behavioural Science, University of Auckland School of Medicine, New Zealand. gj.lees@auckland.ac.nz
Auckland University of Technology · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been postulated, consistent with the ubiquitous presence of glutamatergic neurons in the brain, that defects in glutamatergic neurotransmission are associated with many human neurological and psychiatric disorders. This review evaluates the possible application of ligands acting on glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) and kainate (KA) receptors to minimise the pathology and/or symptoms of various diseases. Glutamate activation of AMPA receptors is thought to mediate most fast synaptic neurotransmission in the brain, while transmission via KA receptors contributes only a minor component. Variants of the protein subunits forming these receptors greatly extend the pharmacological and electrophysiological properties of AMPA/KA receptors. Disease and drug use can differentially affect the expression of the subunits and their variants. Ligands bind to AMPA receptors by competing with glutamate at the glutamate binding site, or non-competitively at other sites on the proteins (allosteric modulators). Ligands showing selective competitive antagonist actions at the AMPA/ KA class of glutamate receptors were first reported in 1988, and the systemically active antagonist 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline (NBQX) was first shown to have useful therapeutic effects on animal models of neurological diseases in 1990. Since then, newer antagonists with increased potency, higher specificity, increased water solubility, and a longer duration of action in vivo have been developed. Negative allosteric modulators such as the prototype GYKI-52466 also block AMPA receptors but have little action at KA receptors. Positive allosteric modulators enhance glutamatergic neurotransmission at AMPA receptors. Polyamines and adamantane derivatives bind within the ion channel of calcium-permeable AMPA receptors. The latest developments include ligands selective for KA receptors containing Glu-R5 subunits. Evidence for advantages of AMPA receptor antagonists over N-methyl-D-aspartate (NMDA) receptor antagonists for symptomatic treatment of neurological and psychiatric conditions, and for minimising neuronal loss occurring after acute neurological diseases, such as physical trauma, ischaemia or status epilepticus, have been shown in animal models. However, as yet AMPA receptor antagonists have not been shown to be effective in clinical trials. On the other hand, a limited number of clinical trials have been reported for AMPA receptor ligands that enhance glutamatergic neurotransmission by extending the ion channel opening time (positive allosteric modulators). These acute studies demonstrate enhanced memory capability in both young and aged humans, without any apparent serious adverse effects. The use of these allosteric modulators as antipsychotic drugs is also possible. However, the long term use of both direct agonists and positive allosteric modulators must be approached with considerable caution because of potential adverse effects.

Indexed as

AnimalsArousalBrain DiseasesCognitionHumansKainic Acid ReceptorsMemoryMental DisordersReceptors, AMPAKainic Acid ReceptorsReceptors, AMPA

Identifiers

PMID10718099
OpenAlexW1974835335

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.