Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13615
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dc.contributor.authorConway, Elizabeth Len
dc.date.accessioned2015-05-16T03:30:12Z
dc.date.available2015-05-16T03:30:12Z
dc.date.issued1998-07-27en
dc.identifier.citationBrain Research; 800(1): 10-20en
dc.identifier.govdoc9685571en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/13615en
dc.description.abstractThe effects of spermine on the acquisition and retention of spatial learning in the Morris water maze were studied. Spermine 25 and 125 nmol i.c.v. did not alter the ability of rats to find a hidden platform in the water maze when administered before training over 5 days. However, the inhibitory effect of the benzodiazepine, diazepam (3 mg/kg i.p., 30 min prior to training), on path length to target was markedly potentiated by the higher dose of spermine, consistent with spermine acting as a functional antagonist at the NMDA receptor. This drug combination did not affect performance on visible platform trials. Administration of doses of 125 and 250 nmol (but not 62.5 nmol) of spermine i.c.v. in the week prior to training (daily for 5 days) dose-dependently inhibited subsequent learning of a platform position in the absence of drug. These higher doses of spermine produced neuronal loss and increased [3H]PK11195 binding indicating microglial activation predominantly in the hippocampus and to a lesser extent in the striatum, septum, thalamus and amygdala. Spermine 125 nmol i.c.v. (daily for 7 days) also abolished retention of a previously learned platform position when administered in an interval between training and retention testing. The inhibitory effects of spermine 125 nmol i.c.v. (daily for 7 days) on subsequent spatial learning were not antagonised by concomitant administration of 30 nmol dizocilpine. These results demonstrate that spermine produces a delayed neurotoxic effect in particular neuronal populations in the brain that selectively impair spatial learning and recall.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherBrain.drug effects.metabolism.pathologyen
dc.subject.otherCerebral Ventricles.drug effects.pathology.physiologyen
dc.subject.otherDiazepam.pharmacologyen
dc.subject.otherInjections, Intraventricularen
dc.subject.otherIsoquinolines.metabolismen
dc.subject.otherKineticsen
dc.subject.otherLearning Disorders.chemically induced.physiopathologyen
dc.subject.otherMaleen
dc.subject.otherMaze Learning.drug effectsen
dc.subject.otherMemory.drug effectsen
dc.subject.otherRatsen
dc.subject.otherRats, Wistaren
dc.subject.otherReceptors, N-Methyl-D-Aspartate.antagonists & inhibitorsen
dc.subject.otherSpermine.administration & dosage.toxicityen
dc.subject.otherTime Factorsen
dc.titleBrain lesions and delayed water maze learning deficits after intracerebroventricular spermine.en
dc.typeJournal Articleen
dc.identifier.journaltitleBrain Researchen
dc.identifier.affiliationUniversity of Melbourne, Clinical Pharmacology and Therapeutics Unit, Department of Medicine, Austin and Repatriation Medical Centre, Heidelberg, Victoria 3084, Australiaen
dc.description.pages10-20en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/9685571en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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