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

(1)脑室内输注酸性成纤维细胞生长因子（aFGF）的某些n端片段，如aFGF（1-20）和aFGF(1-29)，对大鼠的食物摄取量没有影响。然而，输注[Ala^<16>] aFGF(1-29)，其中16位的半胱氨酸残基被丙氨酸残基取代，显著减少了食物摄入量。相反，下丘脑内注射抗fgf受体-1抗体增加了食物摄入量。(2)在被动回避和Morris水迷宫实验中，腹腔注射葡萄糖可提高脑脊液中aFGF水平，促进小鼠的学习和记忆。在静脉滴注葡萄糖前30分钟静脉滴注抗afgf抗体可消除这种葡萄糖效应。(3)采用大鼠切片实验研究了aFGF和aFGF（1-15）对下丘脑室旁核（PPPVN）旁细胞部分神经元活性的影响。两种多肽均增加了半数以上PPPVN神经元的活性。结果表明，aFGF和aFGF（1-15）激活了下丘脑-垂体-肾上腺轴，因为PPPVN包含许多含crf的神经元。(4)衰老加速小鼠（SAMP/8）的学习和记忆能力随着年龄的增长而恶化，以每周一次的频率皮下注射aFGF和[Ala^<16>] aFGF(1-29)，持续9个月。对照SAMP/8时，大鼠中隔胆碱能神经元细胞死亡，ChAT活性降低。这些缺陷在肽处理的SAMP/8中被阻断，并且在对照SAMP/8中看到的学习和记忆障碍得到改善。

(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.