Evidence map›Paper›PMID 22434675›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2012

A mouse kindling model of perimenstrual catamenial epilepsy.

Doodipala Samba Reddy, Jordan Gould, O Gangisetty

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.3field-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.

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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
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  7. Review
  8. Article
  9. Article
  10. 3The Journal of pharmacology and experimental therapeutics · 2018
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Clinical Potential of Neurosteroids for CNS Disorders.Trends in pharmacological sciences · 2016
    Review
  16. A Treatment Approach to Catamenial Epilepsy.Current treatment options in neurology · 2016
    Review
  17. Article
  18. Article
  19. Review
  20. Antiseizure Activity of Midazolam in Mice Lacking δ-Subunit Extrasynaptic GABA(A) Receptors.The Journal of pharmacology and experimental therapeutics · 2015
    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

3 authors at 1 institution in 1 country.

Doodipala Samba ReddyDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, 8447 State Highway 47, MREB Building Room 1005, Bryan, TX 77807-3260, USA. reddy@medicine.tamhsc.edu
Jordan Gould
O Gangisetty
Texas A&M Health Science Center · US

Funding

Progesterone Receptors and Seizure SusceptibilityR01NS051398 · NINDS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI REDDY, DOODIPALA SAMBA · 2007 to 2011
$1.5M
NINDS NIH HHS NS051398NINDS NIH HHS R01 NS051398
6 · The paper itself

Abstract

Catamenial epilepsy is caused by fluctuations in progesterone-derived GABA(A) receptor-modulating anticonvulsant neurosteroids, such as allopregnanolone, that play a significant role in the pathophysiology of epilepsy. However, there is no specific mouse model of catamenial epilepsy. In this study, we developed and characterized a mouse model of catamenial epilepsy by using the neurosteroid-withdrawal paradigm. It is hypothesized that seizure susceptibility decreases when neurosteroid levels are high (midluteal phase) and increases during their withdrawal (perimenstrual periods) in close association with GABA(A) receptor plasticity. A chronic seizure condition was created by using the hippocampus kindling model in female mice. Elevated neurosteroid levels were induced by sequential gonadotropin treatment, and withdrawal was induced by the neurosteroid synthesis inhibitor finasteride. Elevated neurosteroid exposure reduced seizure expression in fully kindled mice. Fully kindled mice subjected to neurosteroid withdrawal showed increased generalized seizure frequency and intensity and enhanced seizure susceptibility. They also showed reduced benzodiazepine sensitivity and enhanced neurosteroid potency, similar to the clinical catamenial seizure phenotype. The increased susceptibility to seizures and alterations in antiseizure drug responses are associated with increased abundance of the α4 and δ subunits of GABA(A) receptors in the hippocampus. These findings demonstrate that endogenous neurosteroids protect against seizure susceptibility and their withdrawal, such as that which occurs during menstruation, leads to exacerbation of seizure activity. This is possibly caused by specific changes in GABA(A) receptor-subunit plasticity and function, therefore providing a novel mouse model of human perimenstrual catamenial epilepsy that can be used for the investigation of disease mechanisms and new therapeutic approaches.

Indexed as

Disease Models, Animal5-alpha Reductase InhibitorsAnimalsDiazepamEpilepsyFemaleFinasterideGonadotropinsHippocampusKindling, NeurologicMenstrual CycleMiceMice, Inbred C57BLPregnanoloneProgesteroneRats5-alpha Reductase InhibitorsDiazepamFinasterideGonadotropinsPregnanoloneProgesteroneReceptors, GABA-ARNA, Messenger

Identifiers

PMID22434675
PMCPMC3362885
OpenAlexW2160297083

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.