Open AccessCav2.3 (R-Type) Calcium Channels are Critical for Mediating Anticonvulsive and Neuroprotective Properties of Lamotrigine In Vivo
Author(s) -
Maxine Dibué-Adjei,
Marcel A. Kamp,
Serdar Alpdogan,
Etienne E. Tevoufouet,
Wolfram F. Neiss,
Jürgen Hescheler,
Toni Schneider
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000485361
Subject(s) - lamotrigine , lacosamide , topiramate , pharmacology , anticonvulsant , in vivo , epilepsy , kainic acid , neuroprotection , chemistry , ictal , tiagabine , zonisamide , medicine , anesthesia , glutamate receptor , receptor , biology , microbiology and biotechnology , psychiatry
Lamotrigine (LTG) is a popular modern antiepileptic drug (AED), however, its mechanism of action has yet to be fully understood, as it is known to modulate many members of several ion channel families. In heterologous systems, LTG inhibits Cav2.3 (R-type) calcium currents, which contribute to kainic-acid- (KA) induced epilepsy in vivo. To gain insight into the role of R-type currents in LTG drug action in vivo, we compared the effects of LTG to topiramate and lacosamide in Cav2.3-deficient mice and controls on KA-induced seizures.