Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13102
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dc.contributor.authorGundlach, Andrew Len
dc.contributor.authorBurazin, T Cen
dc.contributor.authorJenkins, T Aen
dc.contributor.authorBerkovic, Samuel Fen
dc.date.accessioned2015-05-16T02:53:05Z
dc.date.available2015-05-16T02:53:05Z
dc.date.issued1995-02-20en
dc.identifier.citationBrain Research; 672(1-2): 214-27en
dc.identifier.govdoc7749743en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/13102en
dc.description.abstractNoradrenergic neurons are thought to be involved in the process of seizure development and long-term central nervous system plasticity associated with kindling and epilepsy. These processes involve actions of noradrenaline at alpha 1-, alpha 2- and beta 1-adrenergic receptors. In this study, quantitative in vitro autoradiography was used to investigate possible changes in the density of brain alpha 1-adrenergic receptors in a kindling model of epilepsy in the rat. Kindling was produced by daily unilateral stimulation of the amygdala. The alpha 1A+alpha 1B subtypes of adrenergic receptors were labelled with the alpha 1-selective antagonist, [3H]prazosin and alpha 1B receptors, detected in the presence of 10 nM WB4101 to selectively occupy alpha 1A receptors, accounted for 50% of total alpha 1 receptors in cerebral cortex. Autoradiographic studies identified significant and long-lasting, ipsilateral increases in specific [3H]prazosin binding throughout layers I-III of the cortex in sham-operated, unstimulated rats, presumably caused by the surgical implantation of the stimulating electrode within the basolateral amygdaloid nucleus. Binding to alpha 1A + alpha 1B receptors and alpha 1B receptors was increased by an average of 35 and 60%, respectively under these conditions. Stimulation-evoked seizures produced dramatic bilateral increases in specific [3H]prazosin binding to alpha 1A + alpha 1B receptors and particularly to alpha 1B receptors in layers I-III of all cortical areas examined. These changes were rapidly induced and the largest increases (range alpha 1A + alpha 1B 80-340%; alpha 1B 165-380%) occurred at 0.5-2 h after the last stage 5 kindled seizure. At 1 and 3 days after the last seizure, increases were measured for both alpha 1A + alpha 1B and alpha 1B receptors in layers I-III of particular cortical regions, but not overall (e.g. 60-210% increase in perirhinal cortex at both times, with increases also in retrosplenial, hindlimb, occipital, parietal and temporal cortices). Between 2-8 wk post-stimulation specific receptor binding levels were equivalent to those in sham-operated, unstimulated rats. In contrast to the large and widespread increases in outer cortical [3H]prazosin binding, smaller increases were detected in the inner cortex (layer V-VI) at individual times (65-75% increase at 30 min), while no significant changes occurred in several other brain regions examined, including thalamus, which contained a high density of alpha 1A and alpha 1B receptors, or hippocampus which has a low density of both alpha 1 receptor subtypes.(ABSTRACT TRUNCATED AT 400 WORDS)en
dc.language.isoenen
dc.subject.otherAmygdala.physiology.physiopathologyen
dc.subject.otherAnimalsen
dc.subject.otherAutoradiographyen
dc.subject.otherBinding Sitesen
dc.subject.otherCerebral Cortex.metabolismen
dc.subject.otherDiencephalon.metabolismen
dc.subject.otherKindling, Neurologicen
dc.subject.otherMaleen
dc.subject.otherMesencephalon.metabolismen
dc.subject.otherPrazosin.metabolismen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptors, Adrenergic, alpha.metabolismen
dc.subject.otherReference Valuesen
dc.subject.otherSeizures.etiology.metabolismen
dc.subject.otherTime Factorsen
dc.subject.otherTissue Distributionen
dc.subject.otherTritiumen
dc.titleSpatiotemporal alterations of central alpha 1-adrenergic receptor binding sites following amygdaloid kindling seizures in the rat: autoradiographic studies using [3H]prazosin.en
dc.typeJournal Articleen
dc.identifier.journaltitleBrain Researchen
dc.identifier.affiliationUniversity of Melbourne Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pages214-27en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/7749743en
dc.type.austinJournal Articleen
item.grantfulltextnone-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptEpilepsy Research Centre-
crisitem.author.deptNeurology-
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