CellularA saturated-fat diet aggravates the outcome of traumatic brain injury on hippocampal plasticity and cognitive function by reducing brain-derived neurotrophic factor
Section snippets
Experimental design and tissue preparation
Eighty male Sprague–Dawley rats (Charles River Laboratories, Inc., Wilmington, MA) weighing between 200 and 240 g were housed in cages (two rats per cage) and maintained in environmentally controlled rooms (22–24 °C) with a 12 h light/dark cycle. After acclimatization for 1 week on standard rat chow, the rats were randomly assigned to HFS diet or regular diet (RD) for 4 weeks. The diets, fed ad libitum, were provided in powder (TestDiet Inc., Richmond, IN) in large bowl and contained a standard
Spatial learning
Animals were maintained on HFS diet or RD for 4 weeks and some of them received a FPI and were killed 1 week later. We performed the Morris water maze test daily for three consecutive days before and after FPI to assess spatial memory function. The escape latency to find the platform was about the same in HFS versus RD intact rats (Fig. 1A). FPI resulted in longer escape latencies in RD and HFS rats compared with animals receiving sham surgery, and the latency of HFS rats was longer than that
Discussion
Current results demonstrate that FPI significantly impaired learning and memory performance in rats. Moreover, consumption of a HFS diet for 1 month before the injury, potentiated the deleterious effects of FPI on cognitive function and neuronal plasticity. BDNF and its downstream effectors on synaptic plasticity, synapsin I and CREB, appear to be involved with the effects of the HFS diet. The HFS diet and trauma reduce levels of CREB and synapsin I and the efficiency of crucial molecular
Acknowledgements
We thank Dr. Grace Griesbach for help with the TBI experiments. This study was supported by awards from the Alzheimer’s Association, the UCLA Brain Injury Research Center, and NIH (NINDS 38978 and 39522).
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