A study on the facilitation of learning and memory elicited by food intake.

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(1) Intracerebroventricular (i.c.v.) infusion of some N-terminal fragments of acidic fibroblast growth factor (aFGF) such as aFGF (1-20) and aFGF (1-29) had no effect on food intake in rtas. However, infusion of [Ala^<16>] aFGF (1-29), in which a cysteine residue at position 16 was replaced by an alanine residue, significantly decreased food intake. In contrast, intrahypothalamic infusion of anti-FGF receptor-1 antibody increased food intake.(2) Intraperitoneal (i.p.) injection of glucose, which increases aFGF level in the cerebrospinal fluid, facilitates learning and memory in mice when tested by passive avoidance and Morris water maze tasks. This glucose effect was abolished by i.c.v.anti-aFGF antibody infusion 30 min before the i.p.glucose injection.(3) Effect of aFGF and aFGF(1-15) on neuronal activity in the parvocellular part of the paraventricular nucleus (PPPVN) in the hypothalamus was investigated in rat slice experiment. Both peptides increased the activity in more than half of PPPVN neurons. The result suggest that aFGF and aFGF (1-15) activate the hypothalamo-pituitary-adrenal axis, since PPPVN includes many CRF-containing neurons.(4) In senescence accelerated mouse (SAMP/8) which is known in deteriorating ability of learning and memory with age, subcutaneous injection of aFGF and [Ala^<16>] aFGF (1-29) was continued for 9 months at a frequency of once a week. In control SAMP/8, cell death and decrease of ChAT activity were observed in medial septum cholinergic neurons. These deficits were blocked in peptide-treated SAMP/8 and impairment of learning and memory seen in control SAMP/8 was ameliorated.