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Cav2.3 (R-Type) Calcium Channels are Critical for Mediating Anticonvulsive and Neuroprotective Properties of Lamotrigine In Vivo.

Authors
  • Dibué-Adjei, Maxine1, 2, 3
  • Kamp, Marcel A1, 3
  • Alpdogan, Serdar1
  • Tevoufouet, Etienne E1
  • Neiss, Wolfram F4
  • Hescheler, Jürgen1
  • Schneider, Toni1
  • 1 Institute for Neurophysiology, Cologne, Germany. , (Germany)
  • 2 Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany. , (Germany)
  • 3 Department of Neurosurgery, University Hospital, Heinrich-Heine-University, Düsseldorf, Germany. , (Germany)
  • 4 Institute for Anatomy I, University of Cologne, Cologne, Germany. , (Germany)
Type
Published Article
Journal
Cellular Physiology and Biochemistry
Publisher
S. Karger AG
Publication Date
Jan 01, 2017
Volume
44
Issue
3
Pages
935–947
Identifiers
DOI: 10.1159/000485361
PMID: 29176325
Source
Medline
Keywords
License
Unknown

Abstract

These findings give first in vivo evidence for an essential role for Cav2.3 in LTG pharmacology and shed light on a paradoxical effect of LTG in their absence. Furthermore, LTG appears to promote ictal activity in Cav2.3-deficient mice resulting in increased neurotoxicity in the CA1 region. This paradoxical mechanism, possibly reflecting rebound hyperexcitation of pyramidal CA1 neurons after increased inhibition, may be key in understanding LTG-induced seizure aggravation, observed in clinical practice.

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