Satiety Signal and Memory Enhancer

Science Signaling  19 May 2009:
Vol. 2, Issue 71, pp. ec165
DOI: 10.1126/scisignal.271ec165

Oleoylethanolamide (OEA) is a bioactive fatty acid produced by the gut in response to food intake, and it acts in the gut through the peroxisome proliferator-activated receptor α (PPAR-α) to stimulate expression of genes involved in lipid absorption. OEA is also involved in communicating satiety to the brain through stimulation of the vagus nerve. Campolongo et al. reasoned that because animals that could remember information associated with food sources would have an advantage in foraging in the wild, signals produced by feeding may also contribute to memory formation. In two different learning tasks, rats injected with OEA performed better than rats not receiving the fatty acid. Infusion of lidocaine to reversibly block nerve conduction in the nucleus tractus solitarius (NTS), which is the primary relay site of the vagus in the brain, blocked the memory-enhancing effects of OEA. Infusion of an adrenergic receptor blocker into the basolateral complex of the amygdala (BLA) to block signaling from the NTS to this site of emotional memory consolidation also prevented the memory-enhancing effects of OEA. Memory enhancement was absent in mice lacking PPARa and was reproduced in rats by treatment with two different PPAR-α agonists. Thus, eating not only may provide the brain with an energy supply but also, through the formation of OEA, may improve memory formation.

P. Campolongo, B. Roozendaal, V. Trezza, V. Cuomo, G. Astarita, J. Fu, J. L. McGaugh, D. Piomelli, Fat-induced satiety factor oleoylethanolamide enhances memory consolidation. Proc. Natl. Acad. Sci. U.S.A. 106, 8027–8031 (2009). [Abstract] [Full Text]