Oral Presentation The International Congress of Neuroendocrinology 2014

High fat / high sugar diet consumption reduces neuroplasticity and impairs hippocampus-dependent fear memories (#47)

Amy C Reichelt 1 2 , Fred Westbrook 1 2 , Jayanthi Maniam 1 , Margaret Morris 1 3
  1. University of New South Wales, Sydney, NSW, Australia
  2. School of Psychology, University of New South Wales, Sydney, NSW, Australia
  3. Pharmacology, School of Medical Sciences, UNSW Australia, Sydney, New South Wales, Australia

Over-consumption of palatable high fat / high sugar (HFHS) “cafeteria” diets in rats has been shown to induce cognitive deficits in learning and memory. In this study we utilised a hippocampus mediated memory task – trace fear conditioning. The trace interval requires the rats to remember information about the conditioned stimulus (CS) and animals also form associations between the context and the unconditioned stimulus (US - footshock). We assessed freezing both to the CS (flashing light) and in the context associated with footshock.

Adult male Sprague-Dawley rats were fed a diet that supplemented standard lab chow with palatable HFHS foods for 8 weeks, or regular lab chow. Overall, total levels of freezing did not differ between groups, however a dissociation was observed between freezing behaviour in the context and to the CS. HFHS diet fed rats froze less than control chow fed rats in the context associated with footshock (P<0.01), indicating that encoding of a hippocampus-dependent context representation was impaired in these rats. Conversely, HFHS diet fed rats froze more (P<0.05) to the CS than chow fed rats, indicating that for HFHS fed rats learnt about the CS but not the context.

Postmortem analysis indicated that HFHS diet fed rats had significantly greater white adipose tissue deposits (P<0.001). Hippocampal mRNA expression of inflammatory and neuroplasticity markers were analysed by RT qPCR. No change was observed in the inflammatory marker TNF-alpha, however significantly reduced levels of neuroplasticity-associated reelin mRNA was observed, which may contribute to the observed contextual fear memory deficits.