Evidence map›Paper›PMID 17651419›Full record

ArticleEpilepsia2007

Structural consequences of Kcna1 gene deletion and transfer in the mouse hippocampus.

H Jürgen Wenzel, Helene Vacher, Eliana Clark, James S Trimmer, Angela L Lee, Robert M Sapolsky, Bruce L Tempel, Philip A Schwartzkroin

Open access · greenAbstract read
In one paragraph

Article in Epilepsia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

42 citing papers in PubMed, 74 citations in OpenAlex.

  1. Renal TRPM6 but not Kv1.1 is required for magnesium homeostasis in mice.American journal of physiology. Renal physiology · 2026
    Article
  2. Article
  3. In vitro human ion channel assays predictive of drug-induced seizure.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  4. Article
  5. Article
  6. Adam, amigo, brain, and K channel.Biophysical reviews · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. KScientific reports · 2021
    Article
  12. Article
  13. Changes in lipid profiles of epileptic mouse model.Metabolomics : Official journal of the Metabolomic Society · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

8 authors at 3 institutions in 1 country.

H Jürgen WenzelDepartment of Neurological Surgery, School of Medicine, University of California-Davis, 1515 Newton Court, Davis, CA 95618, USA.
Helene Vacher
Eliana Clark
James S Trimmer
Angela L Lee
Robert M Sapolsky
Bruce L Tempel
Philip A Schwartzkroin
University of California, Davis · USStanford University · USUniversity of Washington · US

Funding

GENETIC MODEL FOR CONGENITAL DEAFNESSR01DC002739 · NIDCD · UNIVERSITY OF WASHINGTON · PI TEMPEL, BRUCE L · 1995 to 2013
$4.1M
K+ CHANNEL ALPHA AND BETA SUBUNIT INTERACTIONSR37NS034383 · NINDS · UNIVERSITY OF CALIFORNIA DAVIS · PI TRIMMER, JAMES S · 2000 to 2006
$2.6M
K+ Channel Alpha & Beta Subunit InteractionR01NS034383 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI TRIMMER, JAMES S · 1995 to 2012
$1.7M
NIDCD NIH HHS DC 002739NIDCD NIH HHS R01 DC002739NINDS NIH HHS R01 NS034383NINDS NIH HHS R37 NS034383PHS HHS NE 034383
6 · The paper itself

Abstract

purposeMice lacking the Kv1.1 potassium channel alpha subunit encoded by the Kcna1 gene develop recurrent behavioral seizures early in life. We examined the neuropathological consequences of seizure activity in the Kv1.1(-/-) (knock-out) mouse, and explored the effects of injecting a viral vector carrying the deleted Kcna1 gene into hippocampal neurons.

methodsMorphological techniques were used to assess neuropathological patterns in hippocampus of Kv1.1(-/-) animals. Immunohistochemical and biochemical techniques were used to monitor ion channel expression in Kv1.1(-/-) brain. Both wild-type and knockout mice were injected (bilaterally into hippocampus) with an HSV1 amplicon vector that contained the rat Kcna1 subunit gene and/or the E. coli lacZ reporter gene. Vector-injected mice were examined to determine the extent of neuronal infection.

resultsVideo/EEG monitoring confirmed interictal abnormalities and seizure occurrence in Kv1.1(-/-) mice. Neuropathological assessment suggested that hippocampal damage (silver stain) and reorganization (Timm stain) occurred only after animals had exhibited severe prolonged seizures (status epilepticus). Ablation of Kcna1 did not result in compensatory changes in expression levels of other related ion channel subunits. Vector injection resulted in infection primarily of granule cells in hippocampus, but the number of infected neurons was quite variable across subjects. Kcna1 immunocytochemistry showed "ectopic" Kv1.1 alpha channel subunit expression.

conclusionsKcna1 deletion in mice results in a seizure disorder that resembles--electrographically and neuropathologically--the patterns seen in rodent models of temporal lobe epilepsy. HSV1 vector-mediated gene transfer into hippocampus yielded variable neuronal infection.

Indexed as

Gene DeletionGene Transfer TechniquesAnimalsColoring AgentsElectroencephalographyGene ExpressionGenetic VectorsHerpesvirus 1, HumanHippocampusImmunohistochemistryKv1.1 Potassium ChannelMiceMice, KnockoutMonitoring, PhysiologicSeizuresSeverity of Illness IndexColoring AgentsKcna1 protein, mouseKv1.1 Potassium Channel

Identifiers

PMID17651419
PMCPMC2752664
OpenAlexW2044975802

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.