Hypophagia is induced by intracerebroventricular administration of nerve growth factor
Hypophagia is induced by intracerebroventricular administration of nerve growth factor
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DOI：
10.1016/0014-4886(91)90143-z
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发表时间：
1991-07
影响因子：
5.3
通讯作者：
L. R. Williams
中科院分区：
文献类型：
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作者：
L. R. Williams
在先前检测脑室内NGF治疗对基底前脑胆碱乙酰转移酶(ChAT)活性的刺激作用的实验中，许多接受最大有效剂量NGF治疗的大鼠与赋形剂治疗的对照组动物相比显得面容憔悴。目前的实验确定，与未经治疗的动物和接受赋形剂治疗的动物相比，脑室注射1.2ng.g/d的神经生长因子可以显著减少整个治疗期间的食物消耗。注射NGF的雄性大鼠在开始注射NGF后的第一周平均减重约30g，在NGF治疗的第二周没有明显增加体重。NGF的降噬作用具有剂量依赖性、中枢调节和可逆性。NGF对基底前脑ChAT的刺激作用与NGF对体重增加的抑制作用之间无相关性。治疗阿尔茨海默病患者的NGF剂量与大鼠最大限度刺激中枢胆碱能神经元的剂量相当，每天接近1毫克。如果应用这种治疗方法，则可能存在作为NGF给药的副作用而导致吞噬功能低下的可能性。
In previous experiments examining the stimulatory effect of intracerebroventricular (icv) NGF treatment on basal forebrain choline acetyltransferase (ChAT) activity, many of the rats treated with the maximally effective dose of NGF appeared gaunt compared to the vehicle-treated control animals. The present experiments determined that icv infusion of NGF at a dose of 1.2 μg/day causes a significant reduction in food consumption during the entire period of treatment compared to untreated and vehicle-treated animals. Male rats infused with NGF lost an average of about 30 g of body wt during the first week after the start of infusion and did not gain appreciable weight during the second week of NGF treatment. The hypophagic effect of NGF is dose-dependent, centrally mediated, and reversible. There is no correlation between the stimulatory effect of NGF on basal forebrain ChAT and the inhibitory effect of NGF on weight gain. A therapeutic dose of NGF for Alzheimer's patients comparable to the rat dose for maximally stimulating central cholinergic neurons would approach 1 mg/day. If such therapy is applied, the potential exits for induction of hypophagia as a side effect of the NGF administration.