A saturated-fat diet aggravates the outcome of traumatic brain injury on hippocampal plasticity and cognitive function by reducing brain-derived neurotrophic factor

• Published in: Neuroscience 2003-01, Vol.119 (2), p.365-375
• Main Authors: Wu, A, Molteni, R, Ying, Z, Gomez-Pinilla, F
• Format: Article
• Language: English
• Subjects: Animals; BDNF; Behavior, Animal; Biological and medical sciences; Blotting, Western; Brain Injuries - metabolism; Brain Injuries - pathology; Brain Injuries - physiopathology; Brain-Derived Neurotrophic Factor - genetics; Brain-Derived Neurotrophic Factor - metabolism; cognition; Cognition - drug effects; CREB; Cyclic AMP Response Element-Binding Protein - metabolism; Dietary Fats - adverse effects; Dietary Sucrose - adverse effects; Enzyme-Linked Immunosorbent Assay; Fatty Acids - adverse effects; fluid percussion injury; Fluoresceins; Fluorescent Dyes - pharmacokinetics; Hippocampus - drug effects; Hippocampus - metabolism; Immunohistochemistry; Injuries of the nervous system and the skull. Diseases due to physical agents; Male; Maze Learning - drug effects; Medical sciences; Neuronal Plasticity - drug effects; neuroplasticity; Organic Chemicals; Percussion - methods; Rats; Rats, Sprague-Dawley; Reaction Time - drug effects; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - biosynthesis; synapsin I; Synapsins - biosynthesis; Synapsins - metabolism; Time Factors; Traumas. Diseases due to physical agents
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/S0306-4522(03)00154-4

We have conducted studies to determine the potential of dietary factors to affect the capacity of the brain to compensate for insult. Rats were fed with a high-fat sucrose (HFS) diet, a popularly consumed diet in industrialized western societies, for 4 weeks before a mild fluid percussion injury (FPI) or sham surgery was performed. FPI impaired spatial learning capacity in the Morris water maze, and these effects were aggravated by previous exposure of the rats to the action of the HFS diet. Learning performance decreased according to levels of brain-derived neurotrophic factor (BDNF) in individual rats, such that rats with the worst learning efficacy showed the lowest levels of BDNF in the hippocampus. BDNF immunohistochemistry localized the decreases in BDNF to the CA3 and dentate gyrus of the hippocampal formation. BDNF has a strong effect on synaptic plasticity via the action of synapsin I and cAMP-response element-binding protein (CREB), therefore, we assessed changes in synapsin I and CREB in conjunction with BDNF. Levels of synapsin I and CREB decreased in relation to decreases in BDNF levels. The combination of FPI and the HFS diet had more dramatic effects on the active state (phosphorylated) of synapsin I and CREB. There were no signs of neurodegeneration in the hippocampus of any rat group assessed with Fluoro-Jade B staining. The results suggest that FPI and diet impose a risk factor to the molecular machinery in charge of maintaining neuronal function under homeostatic and challenging situations.