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.