title: The effects of L type calcium channels on the electroencephalogram recordings in WAG/RIJ rat model of absence epilepsy.
abstract: BACKGROUND
  Epilepsy is one of the most important central nervous system disorder and 1% of the total world population suffers from this disorder which require a chronic drug treatment. Most of the researchers suggested that excessive calcium entry into neurons is the main triggering event in the initiation of epileptic discharges but the role of L type calcium channels has not been clarified in absence epilepsy.
  
  
  OBJECTIVE
  In this study, it is aimed to investigate the antiepileptic effects of nifedipine, an L type calcium channel blocker and BAY K8644, an L type calcium channel opener in a genetic model of absence epilepsy in WAG/Rij rats.
  
  
  METHODS
  Thirty two WAG/Rij rats were allocated into four groups; sham (only saline injected), only nifedipine (an L type calcium channel blocker) injected group (40 µg/2 µl; 60 µg/2 µl; 80 µg/2 µl), only BAY K8644 (1,4 Dihydro-2,6-dimethyl-5-nitro-4-trifluoromethyl- phenyl-3-pyridine carboxylic acid methyl ester) (L-type Ca2+-channel activator) injected group (40 µg/2 µl; 60 µg/2 µl; 80 µg/2 µl) and combination of their most effective doses BAY K8644 (60 µg/2 µl) after nifedipine (60 µg/2 µl) injected group. All agents were given by intracerebroventricular injection. The beta, alpha, theta and delta wave ratios of electroencephalogram recordings and the frequency and duration of SWDs (spike and wave discharges) were analyzed and compared between four groups.
  
  
  RESULTS
  Nifedipine increased the number and duration of spike wave discharges whereas BAY K8644 decreased both of them. When BAY K8644 was given after nifedipine, there was no significant difference with control group.
  
  
  CONCLUSIONS
  L type calcium channels play an activator role on spike wave discharges and have positive effects on the duration and frequency.
authors.affiliation: Turkish Medicines and Medical Devices Agency, Ankara, Turkey. drnedimdurmus@gmail.com
authors.forename: N
authors.initials: N
authors.lastname: Durmus
authors.forename: T
authors.initials: T
authors.lastname: Kaya
authors.forename: S
authors.initials: S
authors.lastname: Gültürk
authors.forename: T
authors.initials: T
authors.lastname: Demir
authors.forename: M
authors.initials: M
authors.lastname: Parlak
authors.forename: A
authors.initials: A
authors.lastname: Altun
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000513:Alpha Rhythm / Q000187:drug effects; D000818:Animals; D001611:Beta Rhythm / Q000187:drug effects; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000502:physiology*; D003700:Delta Rhythm / Q000187:drug effects; D004569:Electroencephalography; D004832:Epilepsy, Absence / Q000503:physiopathology*; D009543:Nifedipine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine