Pharmacologically induced absence seizures versus kindling in Wistar rats

dc.contributor.authorCarcak, Nihan
dc.contributor.authorSahiner, Melike
dc.contributor.authorAkman, Ozlem
dc.contributor.authorIdrizoglu, Medine Gulcebi
dc.contributor.authorCortez, Miguel A.
dc.contributor.authorSnead, O. Carter
dc.contributor.authorEskazan, Esat
dc.contributor.authorOnat, Filiz
dc.date.accessioned2023-02-21T12:39:20Z
dc.date.available2023-02-21T12:39:20Z
dc.date.issued2020-01-01
dc.description.abstractOBJECTIVE: This study aimed to investigate the effects of gamma-butyrolactone (GBL), a prodrug of gamma-Hydroxybutyric acid-induced absence seizures on the development of kindling in Wistar rats. METHODS: Three groups of adult male Wistar rats under anesthesia were implanted with bilateral cortical recording elec- trodes for the GBL group (GBL) and/or bipolar stimulation electrodes into the right basolateral amygdala for the Kindling group (KI) alone and Kindling plus GBL group (GBL+KI). Rats in the KI and GBL+KI groups were stimulated twice daily at the afterdischarge threshold until they reached Racine's stage 5 seizure state. The animals in the GBL + group had an i.p injection of GBL 20 minutes before each electrical stimulation, and the effects of GBL-induced seizures on the development of kindling were investigated. The animals in the GBL group were injected GBL twice daily i.p. for 15 days without receiving any electrical stimulation. RESULTS: The KI animals reached stage 5 seizure stage at 12th stimulations, whereas the GBL+KI rats reached at 27th stimulations. The mean numbers of stimulations needed for the development of the first stage 3, 4, or 5 generalized seizures were significantly higher in the GBL+KI group than the KI group. CONCLUSION: The resistance to amygdala kindling in the GBL model can be modulated by the absence seizure mechanism alone, without the intervention of an abnormal genetic background.
dc.description.issue1
dc.description.pages25-34
dc.description.volume7
dc.identifier.doi10.14744/nci.2019.80664
dc.identifier.urihttps://hdl.handle.net/11443/2496
dc.identifier.urihttp://dx.doi.org/10.14744/nci.2019.80664
dc.identifier.wosWOS:000514812200005
dc.publisherKARE PUBL
dc.relation.ispartofNORTHERN CLINICS OF ISTANBUL
dc.subjectAmygdala
dc.subjectgamma-butyrolactone
dc.subjectexperimental limbic epilepsy
dc.subjectgenetic absence epilepsy
dc.subjectkindling
dc.titlePharmacologically induced absence seizures versus kindling in Wistar rats
dc.typeArticle

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