Amygdaloid Kindling and the GABA System
dc.contributor.author | Myslobodsky, Michael S. | en_US |
dc.contributor.author | Valenstein, Elliot S. | en_US |
dc.date.accessioned | 2010-04-01T15:37:29Z | |
dc.date.available | 2010-04-01T15:37:29Z | |
dc.date.issued | 1980-04 | en_US |
dc.identifier.citation | Myslobodsky, Michael S.; Valenstein, Elliot S. (1980). "Amygdaloid Kindling and the GABA System." Epilepsia 21(2): 163-175. <http://hdl.handle.net/2027.42/66112> | en_US |
dc.identifier.issn | 0013-9580 | en_US |
dc.identifier.issn | 1528-1167 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/66112 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=7358042&dopt=citation | en_US |
dc.description.abstract | The effect of increased brain GABA levels on fully kindled amygdala seizures was investigated in Long-Evans rats. The newly synthesized GABA-transaminase inhibitor, -Γ-acetylenic GABA (GAG) administered on four consecutive days (100 mg/kg, followed by 50 mg/kg, i.p.) was found to either significantly reduce, or eliminate entirely, the behavioral seizures normally produced by amygdala stimulation. The effect is seen after the first injection of GAG although its magnitude was greater on subsequent days. Behavioral seizures reappeared 2 to 3 days after termination of GAG treatment. The duration of electrographic seizures (self-sustained amygdala after-discharge) was either unchanged or greater on the first day of GAG treatment, but was briefer on subsequent days. The duration of afterdischarges returned to normal levels 1 to 2 days earlier than the behavioral seizures after the termination of GAG. Picrotoxin (1.5-2 mg/kg, i.p.) did not antagonize either electrographic or behavioral effects of inhibition produced with GAG. Electrical stimulation of amygdala delivered during the initial sedation stage induced by picrotoxin resulted in further regression of kindled seizures in the majority of animals. Although in doses employed, GAG alleviates amygdaloid-kindled seizures its use requires caution in view of its ability to reduce arousal level. RÉSUMÉ L'effet de l'ÉlÉvation des taux cÉrÉbraux de GABA sur les crises amygdaliennes par effet d'embrasement complet a ÉtÉÉtudiÉ chez des rats Long-Evans. l'injection pendant 4 jours consÉcutifs de 100 mg/kg suivis de 50 mg/kg i.p. d'un inhibiteur de la GABA. Transaminase nouvellement synthÉtisÉ (Γ-acetylenic GABA ou GAG) a significativement rÉduit ou mÊme supprimÉ les crises normalement provoquÉes par la stimulation amygdalienne. l'effet est observÉ aprÈs la premiere injection de GAG, mais son importance s'accroit les jours suivants. Les crises rÉapparaissent 2 ou 3 jours aprÈs la fin du traitement au GAG. Du point de vue Électrographique, la durÉe de la postdÉcharge amygdalienne autoentretenue est inchingÉe ou accrue le premier jour du traitement, mais elle diminue les jours suivants pour retourner À la normale un ou deux jours avant que les crises ne rÉapparaissent aprÈs la fin de ('administration du GAG. l'injection de picrotoxine (1.5-2 mg/kg i.p.) ne s'oppose pas aux effets inhibiteurs du GAG sur les crises ou leur accompagnement EEG. La stimulation Électrique de l'amygdala pendant l'Étape sÉdative initiate induite par la picrotoxine provoque une rÉgression supplÉmentaire des crises d'embrasement chez la majoritÉ des animaux. Bien que, aux doses utilisÉes, le GAG attÉnue les crises amyg-daliennes d'embrasement, son utilisation nÉcessite des prÉcautions compte tenu de sa tendance À rÉduire le niveau d'Éveil. RESUMEN En ratas Long-Evans se ha investigado el efecto del aumento de los niveles cerebrales de GABA, sobre los ataques originados en la amÍgdala totalmente condicionada, (Kindling). El recientemente sintetizado in-hibidor de la GABA transaminasa, Γ-acetilÉnico GABA (GAG), redujo significativamente o eliminÓ totalmente las crisis de comportamiento que habitualmente se producen con la estimulaciÓn de la amÍgdala. El efecto se observa despuÉs de la primera in-yecciÓn de GAG pero su magnitud aumentÓ en dias subsiguientes. Las crisis de comportamiento reaparecieron a los 2–3 dÍas de la interrupciÓn del tratamiento con GAG. La duraciÓn de los ataques electrogrÁficos (perservaciÓn de la post-descarga de la amigdala) no se modificÓ, o incluso aumentÓ, en el primer dia de la administraciÓn de GAG pero se redujo en los dias siguientes. La duraciÓn de las post-descargas volviÓ a sus niveles normales 1 o 2 dias antes que la reapariciÓn de las crisis de comportamiento una vez terminado el tratamiento con GAG. La picrotoxina (1.5-2 mg/kg, i.p.) no antagonizÓ los efectos inhibitorios producidos por el GAG sobre el electroencefalograma o las crisis de comportamiento. La estimulaciÓn elÉctrica sobre la amÍgdala, aplicada durante la fase de sedaciÓn inicial inducida por la picrotoxina, condujo a una regresiÓn aÚn mÁs intensa de las crisis condicionadas, en la mayorÍa de los animales. A pesar de que, con las dosis utilizadas, el GAG alivia las crisis de la amÍgdala previamente condicionada, se requiere gran precauciÓn en su utilizaciÓn en vista de su propiedad de reducir el nivel del despertar. ZUSAMMENFASSUNG Die Wirkung erhÖhter GABA-Spiegel des Gehirns auf AmygdalonkrÄmpfe nach Kindling wurden bei Long-Evans-Ratten untersucht. Der neuerdings synthetisierte GABA-TYansaminasen-Inhibitor, Gamma-Acetylen-GABA (GAG) wurde an 4 aufeinander-folgenden Tagen in einer Dosis von 100 mg/kg und anschlieliend 50 mg/kg i.p. verabfolgt. Er reduzierte entweder signifikant oder eliminierte vÖllig die anfalls-weisen VerhaltensÄnderungen, die normalerweise durch Stimulation des Amygdalon produziert wurden. Die Wirkung ist nach der Erstinjektion des GAG zu beobachten, obgleich ihr Ausmaß an folgenden Tagen grÖßer war. Die VerhaltensanfÄlle kamen 2 bis 3 Tagen nach Beendigung der GAG-Behandlung wieder. Die Dauer der elektrographischen AnfÄlle (sich selbst un-terhaltende Amydalonnachentladungen) blieben entweder gleich oder sie wurden grÖßer am 1. Tag der GAG-Behandlung, wurden aber kÜrzer an folgenden Tagen. Die Dauer der Nachentladungen nor-malisierte sich 1 bis 2 Tage frÜher als die VerhaltensanfÄlle nach Beendigung des GAG verschwanden. Picrotoxin (1.5 bis 2 mg/kg i.p.) wirken nicht als Antagonist gegenÜber der durch GAG produzierten Hemmung der elektrographischen-oder Verhalten-seffekte. Die elektrische Stimulierung des Amygdalon wÄhrend der initialen Sedierung nach Picrotoxin ver-ursachte bei der Mehrzahl der Tiere einen weiteren RÜckgang der durch Kindling entstandenen AnfÄlle. Obgleich das GAG in den verwandten Dosen, die durch Kindling des Amygdalon erzeugten KrÄmpfe leichter ablaufen lUßt, erfordert seine Anwendung Vorsicht hinsichtlich seiner FÄhigkeit, das Erreg-barkeitsniveau zu senken. | en_US |
dc.format.extent | 1640633 bytes | |
dc.format.extent | 3110 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Blackwell Publishing Ltd | en_US |
dc.rights | 1980 International League Against Epilepsy | en_US |
dc.subject.other | Amygdala | en_US |
dc.subject.other | Kindling | en_US |
dc.subject.other | GABA | en_US |
dc.subject.other | Picrotoxin | en_US |
dc.subject.other | GAG | en_US |
dc.subject.other | Seizures | en_US |
dc.title | Amygdaloid Kindling and the GABA System | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Medicine (General) | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Psychology and Neuroscience Laboratory, University of Michigan, Ann Arbor, Michigan 48109 | en_US |
dc.identifier.pmid | 7358042 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/66112/1/j.1528-1157.1980.tb04058.x.pdf | |
dc.identifier.doi | 10.1111/j.1528-1157.1980.tb04058.x | en_US |
dc.identifier.source | Epilepsia | en_US |
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