Evidence map›Paper›PMID 10518582›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Resistance to excitotoxin-induced seizures and neuronal death in mice lacking the preprotachykinin A gene.

H Liu, Y Cao, A I Basbaum, A M Mazarati, R Sankar, C G Wasterlain

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 113 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Substance P Regulation in Epilepsy.Current neuropharmacology · 2018
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Layer-specific CREB target gene induction in human neocortical epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  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

6 authors at 2 institutions in 1 country.

H LiuEpilepsy Research Laboratory, Veterans Administration Medical Center, Sepulveda, CA 91343, USA. htliu@ucla.edu
Y Cao
A I Basbaum
A M Mazarati
R Sankar
C G Wasterlain
University of California, San Francisco · USW. M. Keck Foundation · US

Funding

BRAINSTEM CONTROL OF PAIN TRANSMISSIONR01NS014627 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BASBAUM, ALLAN I. · 1985 to 2016
$3.9M
Brainstem control of pain transmissionR37NS014627 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BASBAUM, ALLAN I. · 2008 to 2014
$3.6M
BRAIN DEVELOPMENT IN EXPERIMENTAL EPILEPSY: STATUSR01NS013515 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WASTERLAIN, CLAUDE G · 1986 to 2006
$2.2M
NINDS NIH HHS NS01792NINDS NIH HHS NS14627NINDS NIH HHS R01 NS013515NINDS NIH HHS R01 NS014627NINDS NIH HHS R37 NS014627
6 · The paper itself

Abstract

Epileptic seizures are associated with increases in hippocampal excitability, but the mechanisms that render the hippocampus hyperexcitable chronically (in epilepsy) or acutely (in status epilepticus) are poorly understood. Recent evidence suggests that substance P (SP), a peptide that has been implicated in cardiovascular function, inflammatory responses, and nociception, also contributes to hippocampal excitability and status epilepticus, in part by enhancing glutamate release. Here we report that mice with disruption of the preprotachykinin A gene, which encodes SP and neurokinin A, are resistant to kainate excitoxicity. The mice show a reduction in the duration and severity of seizures induced by kainate or pentylenetetrazole, and both necrosis and apoptosis of hippocampal neurons are prevented. Although kainate induced the expression of bax and caspase 3 in the hippocampus of wild-type mice, these critical intracellular mediators of cell death pathways were not altered by kainate injection in the mutant mice. These results indicate that the reduction of seizure activity and the neuroprotection observed in preprotachykinin A null mice are caused by the extinction of a SP/neurokinin A-mediated signaling pathway that is activated by seizures. They suggest that these neurokinins are critical to the control of hippocampal excitability, hippocampal seizures, and hippocampal vulnerability.

Indexed as

ApoptosisProto-Oncogene Proteins c-bcl-2Animalsbcl-2-Associated X ProteinCaspase 3CaspasesConvulsantsHippocampusIn Situ Nick-End LabelingMiceMice, KnockoutMicroscopy, VideoNeuronsNeurotoxinsPentylenetetrazoleProtein PrecursorsBax protein, mousebcl-2-Associated X ProteinCasp3 protein, mouseCaspase 3CaspasesConvulsantsNeurotoxinsPentylenetetrazolepreprotachykininProtein PrecursorsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Tachykinins

Identifiers

PMID10518582
PMCPMC18418
OpenAlexW2008074758

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.