title: Exploring temporospatial changes in glucose metabolic disorder, learning, and memory dysfunction in a rat model of diffuse axonal injury.
abstract: Diffuse axonal injury (DAI) is the predominant effect of severe traumatic brain injury and contributes significantly to cognitive deficits. The mechanisms underlying these cognitive deficits are often associated with complex metabolic alterations. However, the relationships between temporospatial alterations in cerebral glucose metabolism and the pathophysiology of DAI-related learning and memory dysfunction are not yet completely understood. We used a small animal positron emission tomography (PET) scanner with 2-[F-18]-fluoro-2-deoxy-D-glucose (¹⁸F-FDG) as a molecular probe to evaluate temporospatial glucose metabolism in vulnerable areas of rats with DAI. The Morris water maze (MWM) was used to evaluate the development and progression of learning and memory dysfunction. Compared to the sham-treated group, PET-MRI fusion images showed that glucose metabolism was reduced in animals with DAI. In addition, the standardized uptake value (SUV) of ¹⁸F-FDG was significantly decreased in the sensorimotor cortex, hippocampus, corpus callosum, caudate putamen, brain stem, and cerebellum at days 1, 3, and 7 after injury. SUV returned to baseline levels by 30 days after injury. The escape latency of the injured group was significantly increased, and the percentages of distance travelled and time spent in the target quadrant were significantly decreased 1 month after injury. These effects persisted for 3 months. SUVs in the hippocampus at the acute stage were significantly correlated with MWM performance during the recovery stage of DAI. These results demonstrate that microstructural injury-induced hypometabolism in the hippocampus at the acute stage are all significantly correlated with learning and memory dysfunctions during the recovery stage of DAI.
authors.affiliation: Department of Neurosurgery, No. 3 People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.
authors.forename: Jia
authors.initials: J
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Gu
authors.forename: Dong-Fu
authors.initials: DF
authors.lastname: Feng
authors.forename: Fang
authors.initials: F
authors.lastname: Ding
authors.forename: Guangyao
authors.initials: G
authors.lastname: Zhu
authors.forename: Jiandong
authors.initials: J
authors.lastname: Rong
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D020833:Diffuse Axonal Injury / Q000150:complications / Q000378:metabolism* / Q000523:psychology*; D019788:Fluorodeoxyglucose F18; D044882:Glucose Metabolism Disorders / Q000378:metabolism* / Q000523:psychology*; D006019:Glycolysis / Q000502:physiology; D006624:Hippocampus / Q000378:metabolism; D007091:Image Processing, Computer-Assisted; D007859:Learning Disabilities / Q000209:etiology / Q000523:psychology*; D016014:Linear Models; D008279:Magnetic Resonance Imaging; D008297:Male; D018782:Maze Learning / Q000502:physiology; D008569:Memory Disorders / Q000209:etiology / Q000523:psychology*; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals; D051381:Rats; D017207:Rats, Sprague-Dawley; D014057:Tomography, X-Ray Computed
chemical_list: D001786:Blood Glucose; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18