Ca(v)3.2 T-type calcium channel mutation influences kindling-induced thalamic neuronal firing patterns in Genetic Absence Epilepsy Rats From Strasbourg

Carcak N., Ali I., Powell K., Zheng T., ONAT F., O'Brien T. J.

EPILEPSIA, vol.60, no.7, pp.1378-1386, 2019 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 60 Issue: 7
  • Publication Date: 2019
  • Doi Number: 10.1111/epi.16076
  • Journal Name: EPILEPSIA
  • Journal Indexes: Science Citation Index Expanded, Scopus
  • Page Numbers: pp.1378-1386
  • Keywords: amygdala kindling, Cav3.2 mutation, GAERS, thalamic reticular nucleus, ELECTRICAL-STIMULATION, SEIZURE EXPRESSION, MODEL, CACNA1H


Objective: Recent data indicate that amygdala kindling leads to significant changes in interictal neuronal firing patterns of thalamic reticular nucleus (TRN) neurons by decreasing the spontaneous firing rate and increasing burst firing in nonepileptic control (NEC) rats. Genetic Absence Epilepsy Rats From Strasbourg (GAERS) were resistant to these kindling-induced firing changes in TRN neurons, and are also resistant to the progression of kindling. We investigated whether a homozygous, missense, single nucleotide mutation (R1584P) in the Ca(v)3.2 T-type Ca2+ channel gene, which has been correlated with the expression of absence seizures in GAERS, influenced kindling progression and TRN firing patterns.