Dietary Omega-3 Fatty Acids Normalize BDNF Levels, Reduce Oxidative Damage, and Counteract Learning Disability after Traumatic Brain Injury in Rats

TLDR

Omega‑3 fatty acids regulate signal transduction, gene expression, and neuronal survival, while BDNF promotes synaptic transmission and learning through modulation of synapsin I and CREB. The study examined whether dietary omega‑3 fatty acid supplementation helps the brain cope with traumatic injury. Rats received either a standard diet or an omega‑3‑supplemented diet for four weeks prior to mild fluid percussion injury. Omega‑3 supplementation normalized BDNF, synapsin I, and CREB levels, reduced oxidative damage, and restored learning performance after fluid percussion injury, indicating protection against impaired plasticity.

Abstract

Omega-3 fatty acids (i.e., docosahexaenoic acid; DHA) regulate signal transduction and gene expression, and protect neurons from death. In this study we examined the capacity of dietary omega- 3 fatty acids supplementation to help the brain to cope with the effects of traumatic injury. Rats were fed a regular diet or an experimental diet supplemented with omega-3 fatty acids, for 4 weeks before a mild fluid percussion injury (FPI) was performed. FPI increased oxidative stress, and impaired learning ability in the Morris water maze. This type of lesion also reduced levels of brainderived neurotrophic factor (BDNF), synapsin I, and cAMP responsive element-binding protein (CREB). It is known that BDNF facilitates synaptic transmission and learning ability by modulating synapsin I and CREB. Supplementation of omega-3 fatty acids in the diet counteracted all of the studied effects of FPI, that is, normalized levels of BDNF and associated synapsin I and CREB, reduced oxidative damage, and counteracted learning disability. The reduction of oxidative stress indicates a benevolent effect of this diet on mechanisms that maintain neuronal function and plasticity. These results imply that omega-3 enriched dietary supplements can provide protection against reduced plasticity and impaired learning ability after traumatic brain injury.