Memory facilitation educed by food intake

Abstract

Acidic fibroblast growth factor (aFGF) in rat CSF increased 1000 times in the 2-h period after food intake, or IP, or ICV glucose infusion. The ICV application of aFGF dose dependently depresses and anti-aFGF antibody facilitates food intake. aFGF is produced in the ependymal cells and released into the CSF in response to increased glucose in the CSF caused by food intake. Released aFGF diffused into the brain parenchyma and was taken up into neurons in the hypothalamus, hippocampus, amygdala, etc. IP injection of glucose 2 h before a task that combined acquisition with passive avoidance significantly increased retention of avoidance by mice tested 24 h later. In a Morris water maze task, IP glucose injection 2 h before a first trial block reduced time to find and climb onto a platform hidden just below the water surface. The glucose facilitation of these affective and spatial memory were abolished by pretreatment with anti-aFGF antibody applied ICV. Continuous ICV infusion of aFGF into rats also significantly increased the reliability of passive avoidance for several days. After food intake, centrally released aFGF reaches the hippocampus and facilitates memory; peripherally released cholecystokinin reaches the endings of the afferent vagal nerves in the portal vein and changes their activity, which modulates hippocampal activity, to lead to memory facilitation. This, however, is blocked by vagotomy below the diaphragm. The results indicate the importance of food intake, not only to maintain homeostasis, but also to prepare a readiness state for memory facilitation.