title: Evaluation of effects of T and N type calcium channel blockers on the electroencephalogram recordings in Wistar Albino Glaxo/Rij rats, an absence epilepsy model.
abstract: OBJECTIVE
  It is suggested that excessive calcium entry into neurons is the main triggering event in the initiation of epileptic discharges. We aimed to investigate the role of T and N type calcium channels in absence epilepsy experimental model.
  
  
  METHODS
  Wistar Albino Glaxo/Rij (WAG/Rij) rats (12-16 weeks old) were randomly allocated into four groups; sham, mibefradil (T type calcium channel blocker), w-Conotoxin MVIIA (N type calcium channel blocker), and mibefradil + w-Conotoxin MVIIA. Beta, alpha, theta, and delta wave ratios of EEG recordings and frequency and duration of spike wave discharges (SWDs) were analyzed and compared between groups.
  
  
  RESULTS
  Beta and delta recording ratios in 1 μM/5 μl mibefradil group was significantly different from basal and other dose-injected groups. Beta, alpha, and theta recordings in 0.2 μM/5 μl w-Conotoxin MVIIA group was significantly different from basal and other dose-injected groups. In w-Conotoxin MVIIA after mibefradil group, beta, alpha, and theta recording ratios were significantly different from basal and mibefradil group. Mibefradil and w-Conotoxin MVIIA significantly decreased the frequency and duration of SWDs. The decrease of frequency and duration of SWDs in mibefradil group was significantly different from w-Conotoxin MVIIA group. The frequency and duration of SWDs significantly decreased in w-Conotoxin MVIIA after mibefradil group compared with basal, mibefradil, and w-Conotoxin MVIIA groups.
  
  
  CONCLUSIONS
  We concluded that both T and L type calcium channels play activator roles in SWDs and have positive effects on frequency and duration of these discharges. These results are related with their central effects more than peripheral effects.
authors.affiliation: Department of Medical Pharmacology, Hacettepe University Medical Faculty, Ankara, Turkey.
authors.forename: Nedim
authors.initials: N
authors.lastname: Durmus
authors.affiliation: Department of Physiology, Cumhuriyet University Medical Faculty, Sivas, Turkey.
authors.forename: Sefa
authors.initials: S
authors.lastname: Gültürk
authors.affiliation: Department of Medical Pharmacology, Katip Celebi University Medical Faculty, İzmir, Turkey.
authors.forename: Tijen
authors.initials: T
authors.lastname: Kaya
authors.affiliation: Department of Physiology, Gaziantep University Medical Faculty, Gaziantep, Turkey.
authors.forename: Tuncer
authors.initials: T
authors.lastname: Demir
authors.affiliation: Department of Medical Pharmacology, Cumhuriyet University Medical Faculty, Sivas, Turkey.
authors.forename: Mesut
authors.initials: M
authors.lastname: Parlak
authors.affiliation: Department of Medical Pharmacology, Cumhuriyet University Medical Faculty, Sivas, Turkey.
authors.forename: Ahmet
authors.initials: A
authors.lastname: Altun
mesh_terms: D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D058256:Brain Waves / Q000187:drug effects*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D020864:Calcium Channels, N-Type / Q000187:drug effects* / Q000378:metabolism; D020747:Calcium Channels, T-Type / Q000187:drug effects* / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects; D004195:Disease Models, Animal; D004569:Electroencephalography; D004832:Epilepsy, Absence / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D020748:Mibefradil / Q000494:pharmacology*; D017208:Rats, Wistar; D013997:Time Factors; D020960:omega-Conotoxins / Q000494:pharmacology*
chemical_list: D000927:Anticonvulsants; D002121:Calcium Channel Blockers; D020864:Calcium Channels, N-Type; D020747:Calcium Channels, T-Type; D020960:omega-Conotoxins; D020748:Mibefradil; C078452:ziconotide
keywords: Epilepsy; T and N type calcium channels; Wistar Albino Glaxo/Rij rats; mibefradil; w-Conotoxin MVIIA
references.citation: Eur J Pharmacol. 2000 Oct 20;406(3):381-9
references.pmid: 11040345
references.citation: Vet Q. 2012;32(3-4):159-67
references.pmid: 23163553
references.citation: Behav Genet. 2003 Nov;33(6):635-55
references.pmid: 14574120
references.citation: Pol J Pharmacol. 2004 Jan-Feb;56(1):29-41
references.pmid: 15047975
references.citation: Electroencephalogr Clin Neurophysiol. 1969 Oct;27(4):444
references.pmid: 4186745
references.citation: Med Clin North Am. 1988 Jan;72(1):83-115
references.pmid: 3276988
references.citation: J Neural Transm Suppl. 1992;35:37-69
references.pmid: 1512594
references.citation: Neuroscience. 1992 Dec;51(4):755-8
references.pmid: 1336826
references.citation: Science. 1993 Oct 29;262(5134):679-85
references.pmid: 8235588
references.citation: Epilepsia. 1995 Jan;36(1):86-92
references.pmid: 7528137
references.citation: Trends Pharmacol Sci. 1995 Feb;16(2):43-9
references.pmid: 7762082
references.citation: Annu Rev Physiol. 1996;58:329-48
references.pmid: 8815798
references.citation: Arch Pediatr Adolesc Med. 1997 Feb;151(2):152-8
references.pmid: 9041870
references.citation: Annu Rev Neurosci. 1997;20:185-215
references.pmid: 9056712
references.citation: J Neurosci. 1998 Jul 1;18(13):4842-53
references.pmid: 9634550
references.citation: Brain Res. 1998 Jun 15;796(1-2):311-4
references.pmid: 9689485
references.citation: Hum Mol Genet. 1999;8(10):1907-12
references.pmid: 10469844
references.citation: Epilepsia. 2005 Nov;46(11):1796-801
references.pmid: 16302860
references.citation: Epilepsia. 2005;46 Suppl 9:34-47
references.pmid: 16302874
references.citation: Pharmacol Ther. 2006 Jul;111(1):288-325
references.pmid: 16832874
references.citation: Neuropharmacology. 2007 Sep;53(3):431-46
references.pmid: 17675191
references.citation: Neuropsychol Rev. 2007 Dec;17(4):427-44
references.pmid: 17963043
references.citation: Epilepsia. 2012 Nov;53(11):1868-76
references.pmid: 23061663
references.citation: Epilepsia. 2003;44 Suppl 2:7-15
references.pmid: 12752456