Reply to the commentary by Ben-Ari and Delpire: Bumetanide and neonatal seizures: Fiction versus reality.
GABA
KCC2
NKCC1
asphyxia
blood-brain barrier
diuretics
pharmacokinetics
Journal
Epilepsia
ISSN: 1528-1167
Titre abrégé: Epilepsia
Pays: United States
ID NLM: 2983306R
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
12
02
2021
accepted:
16
02
2021
pubmed:
26
3
2021
medline:
18
9
2021
entrez:
25
3
2021
Statut:
ppublish
Résumé
In this response to a commentary by Ben-Ari and Delpire on our recent study on the pharmacology of neonatal seizures in a novel, physiologically validated rat model of birth asphyxia, we wish to rectify their inaccurate descriptions of our model and data. Furthermore, because Ben-Ari and Delpire suggest that negative data on bumetanide from preclinical and clinical trials of neonatal seizures have few implications for (alleged) bumetanide actions on neurons in other brain disorders, we will discuss this topic as well. Based on the poor brain penetration of bumetanide, combined with the extremely wide cellular expression patterns of the target protein NKCC1, it is obvious that the numerous actions of systemically applied bumetanide described in the literature are not mediated by the drug's effects on central neurons.
Substances chimiques
Sodium Potassium Chloride Symporter Inhibitors
0
Solute Carrier Family 12, Member 2
0
Bumetanide
0Y2S3XUQ5H
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Comment
Langues
eng
Sous-ensembles de citation
IM
Pagination
941-946Commentaires et corrections
Type : CommentOn
Type : CommentOn
Informations de copyright
© 2021 The Authors. Epilepsia published by Wiley Periodicals LLC on behalf of International League Against Epilepsy.
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