Diabetes exacerbates the loss of basilar dendritic spines after ischemic stroke
| dc.contributor.author | Sweetnam Holmes, Andrew | |
| dc.contributor.supervisor | Brown, Craig E. | |
| dc.date.accessioned | 2014-01-09T21:16:58Z | |
| dc.date.available | 2014-01-09T21:16:58Z | |
| dc.date.copyright | 2013 | en_US |
| dc.date.issued | 2014-01-09 | |
| dc.degree.department | Program: Neuroscience | |
| dc.degree.department | Division of Medical Sciences | |
| dc.degree.department | School of Medical Sciences | |
| dc.degree.level | Master of Science M.Sc. | en_US |
| dc.description.abstract | Most stroke survivors recover some degree of lost function after an ischemic event. Recovery however, is negatively affected by comorbid conditions such as diabetes. Successful recovery is dependent on the ability of adjacent surviving cortical tissue and functionally related areas to take over functions lost by the stroke. Recently our lab has shown that diabetes interferes with the remapping of sensory function to peri-infarct areas after photothrombotic stroke. Given this result, it is crucial to understand how diabetes affects the structure of neurons following stroke, particularly at the level of dendritic spines, which receive the vast majority of excitatory synaptic inputs. Type I diabetes was pharmacologically induced in transgenic mice expressing yellow fluorescent protein (YFP) in a subset of cortical neurons 4 weeks prior to receiving unilateral photothrombotic stroke in the forelimb area of the primary somatosensory cortex (FLS1). Spine density measurements were made on the apical and basilar dendrites of layer-5 pyramidal neurons at 1 and 6 weeks after stroke. Our analysis indicated that diabetes was associated with fewer apical and basilar dendritic spines in the peri-infarct region 1 week after stroke. At 6 weeks of recovery, peri-infarct dendritic spine density in both control and diabetic animals returned to baseline levels. These changes were specific to the peri-infarct cortex, as spine density in distant cortical areas such as the forelimb sensorimotor region of the contralateral hemisphere, were not affected by stroke. In order to relate changes in spine density to the recovery of forepaw function, we re-analyzed data from a previous study that employed the forepaw adhesive-tape-removal test (Sweetnam et al 2012). This analysis revealed that diabetes significantly increased the latency of tape removal from the impaired forepaw (when normalized to the unaffected paw) at 1 but not 6 weeks of recovery. Collectively, these findings indicate that diabetes exacerbates forepaw impairments and basilar spine loss initially after stroke, but does not affect the ability of the brain to replace lost spines over weeks of recovery. | en_US |
| dc.description.proquestcode | 0317 | en_US |
| dc.description.scholarlevel | Graduate | en_US |
| dc.identifier.bibliographicCitation | Sweetnam D, Holmes A, Tennant K a, Zamani A, Walle M, Jones P, Wong C, Brown CE (2012) Diabetes impairs cortical plasticity and functional recovery following ischemic stroke. The Journal of Neuroscience 32:5132–5143 | en_US |
| dc.identifier.uri | http://hdl.handle.net/1828/5152 | |
| dc.language.iso | en | en_US |
| dc.rights.temp | Available to the World Wide Web | en_US |
| dc.subject | plasticity | en_US |
| dc.subject | dendritic spines | en_US |
| dc.subject | Stroke | en_US |
| dc.subject | behaviour | en_US |
| dc.title | Diabetes exacerbates the loss of basilar dendritic spines after ischemic stroke | en_US |
| dc.type | Thesis | en_US |