title: 17beta-Estradiol treatment following permanent focal ischemia does not influence recovery of sensorimotor function.
abstract: The development of therapy to aid poststroke recovery is essential. The female hormone 17beta-estradiol has been shown to promote synaptogenesis; the purpose of this study was to attempt to harness these mechanisms to promote repair and recovery in the peri-infarct zone. Rats were ovariectomized, tested for sensorimotor function, and the middle cerebral artery permanently occluded (MCAO). Infarct volumes were calculated using MRI, and damage was equivalent in all animals prior to implantation of either 17beta-estradiol or placebo pellets. Animals were tested for functional recovery for 28 days and tissue processed for synaptic marker syntaxin immunohistochemistry. The stroke induced a significant behavioral deficit, which persisted out to 28 days, and was not significantly different between 17beta-estradiol and placebo treatment groups. There was no difference in syntaxin immunostaining between groups in either the peri-infarct cortex or in the dendritic CA1 reference region. In conclusion, 17beta-estradiol treatment, delivered poststroke, did not influence recovery of function or synaptogenesis.
authors.affiliation: 7TMRI Facility and Wellcome Surgical Institute, Division of Clinical Neuroscience, University of Glasgow, Garscube Estate, Bearsden Road, Glasgow, Scotland G61 1QH, UK. t.farr.1@research.gla.ac.uk
authors.forename: Tracy D
authors.initials: TD
authors.lastname: Farr
authors.forename: Hilary V O
authors.initials: HV
authors.lastname: Carswell
authors.forename: Lindsay
authors.initials: L
authors.lastname: Gallagher
authors.forename: Barrie
authors.initials: B
authors.lastname: Condon
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Fagan
authors.forename: Jim
authors.initials: J
authors.lastname: Mullin
authors.forename: I Mhairi
authors.initials: IM
authors.lastname: Macrae
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D020520:Brain Infarction / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D004958:Estradiol / Q000097:blood / Q000494:pharmacology* / Q000627:therapeutic use; D005106:Exploratory Behavior / Q000187:drug effects / Q000502:physiology; D005260:Female; D020439:Growth Cones / Q000187:drug effects / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D009068:Movement / Q000187:drug effects / Q000502:physiology; D009069:Movement Disorders / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D010052:Ovariectomy; D017729:Presynaptic Terminals / Q000378:metabolism; D050765:Qa-SNARE Proteins / Q000378:metabolism; D051381:Rats; D020127:Recovery of Function / Q000187:drug effects* / Q000502:physiology; D014110:Touch / Q000187:drug effects / Q000502:physiology; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D018696:Neuroprotective Agents; D050765:Qa-SNARE Proteins; D004958:Estradiol