Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats.
| dc.contributor.author | Sasaki, Toshihiro | |
| dc.contributor.author | Hoffmann, Ulrike | |
| dc.contributor.author | Kobayashi, Motomu | |
| dc.contributor.author | Sheng, Huaxin | |
| dc.contributor.author | Ennaceur, Abdelkader | |
| dc.contributor.author | Lombard, Frederick W | |
| dc.contributor.author | Warner, David S | |
| dc.date.accessioned | 2021-06-01T13:55:47Z | |
| dc.date.available | 2021-06-01T13:55:47Z | |
| dc.date.issued | 2016-10 | |
| dc.date.updated | 2021-06-01T13:55:46Z | |
| dc.description.abstract | BackgroundCognitive dysfunction can be a long-term complication following subarachnoid hemorrhage (SAH). Preclinical models have been variously characterized to emulate this disorder. This study was designed to directly compare long-term cognitive deficits in the context of similar levels of insult severity in the cisterna magna double-blood (DB) injection versus prechiasmatic blood (PB) injection SAH models.MethodsPilot work identified blood injectate volumes necessary to provide similar mortality rates (20-25 %). Rats were then randomly assigned to DB or PB insults. Saline injection and naïve rats were used as controls. Functional and cognitive outcome was assessed over 35 days.ResultsDB and PB caused similar transient rotarod deficits. PB rats exhibited decreased anxiety behavior on the elevated plus maze, while anxiety was increased in DB. DB and PB caused differential deficits in the novel object recognition and novel object location tasks. Morris water maze performance was similarly altered in both models (decreased escape latency and increased swimming speed). SAH caused histologic damage in the medial prefrontal cortex, perirhinal cortex, and hippocampal CA1, although severity of injury in the respective regions differed between DB and PB.ConclusionBoth SAH models caused long-term cognitive deficits in the context of similar insult severity. Cognitive deficits differed between the two models, as did distribution of histologic injury. Each model offers unique properties and both models may be useful for study of SAH-induced cognitive deficits. | |
| dc.identifier | 10.1007/s12028-016-0250-1 | |
| dc.identifier.issn | 1541-6933 | |
| dc.identifier.issn | 1556-0961 | |
| dc.identifier.uri | ||
| dc.language | eng | |
| dc.publisher | Springer Science and Business Media LLC | |
| dc.relation.ispartof | Neurocritical care | |
| dc.relation.isversionof | 10.1007/s12028-016-0250-1 | |
| dc.subject | Animals | |
| dc.subject | Rats | |
| dc.subject | Rats, Wistar | |
| dc.subject | Subarachnoid Hemorrhage | |
| dc.subject | Disease Models, Animal | |
| dc.subject | Behavior, Animal | |
| dc.subject | Maze Learning | |
| dc.subject | Male | |
| dc.subject | Cognitive Dysfunction | |
| dc.title | Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats. | |
| dc.type | Journal article | |
| duke.contributor.orcid | Sheng, Huaxin|0000-0002-4325-2940 | |
| pubs.begin-page | 293 | |
| pubs.end-page | 305 | |
| pubs.issue | 2 | |
| pubs.organisational-group | Faculty | |
| pubs.organisational-group | Duke | |
| pubs.organisational-group | School of Medicine | |
| pubs.organisational-group | Anesthesiology | |
| pubs.organisational-group | Clinical Science Departments | |
| pubs.organisational-group | Neurobiology | |
| pubs.organisational-group | Duke Institute for Brain Sciences | |
| pubs.organisational-group | Surgery | |
| pubs.organisational-group | Anesthesiology, Neuroanesthesia | |
| pubs.organisational-group | Basic Science Departments | |
| pubs.organisational-group | University Institutes and Centers | |
| pubs.organisational-group | Institutes and Provost's Academic Units | |
| pubs.publication-status | Published | |
| pubs.volume | 25 |
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