Hohmann G F, Wenk G L, Lowenstein P, Brown M E, Coyle J T
Department of Psychiatry, Johns Hopkins University, School of Medicine, Baltimore, MD 21205.
Neurosci Lett. 1987 Dec 4;82(3):253-9. doi: 10.1016/0304-3940(87)90265-5.
Lesions of basal forebrain cholinergic nuclei projecting in neocortex have recently been employed as an animal model for the cholinergic deficits in Alzheimer's disease. However, unlike Alzheimer's patients, whose deterioration appears to be progressive and irreversible, basalis lesioned rats usually recover both behaviorally and neurochemically within several months after the lesion. We now demonstrate that this recovery may be a function of the age of the rat and that cholinergic deficits re-occur in the aged rat. Choline acetyltransferase (ChAT) activity and [3H]hemicholinium-3 ([3H]HCh-3) binding are reduced in cortex ipsilateral to ibotenic acid lesions in the 12-month postlesion rat following an initial recovery to normal levels by about 3 months postlesion. The recurrence of decrease of cholinergic markers is not a consequence of a non-specific age-related decline since the activity of glutamic acid decarboxylase remains constant between 3 and 12 months postlesion.
向新皮层投射的基底前脑胆碱能核团的损伤，最近已被用作阿尔茨海默病胆碱能缺陷的动物模型。然而，与阿尔茨海默病患者不同，后者的病情恶化似乎是渐进且不可逆的，基底核损伤的大鼠通常在损伤后的几个月内行为和神经化学方面都能恢复。我们现在证明，这种恢复可能是大鼠年龄的函数，并且胆碱能缺陷在老年大鼠中会再次出现。在损伤后约3个月最初恢复到正常水平后，损伤后12个月的大鼠中，与鹅膏蕈氨酸损伤同侧的皮层中胆碱乙酰转移酶（ChAT）活性和[3H]半胱氨酸-3（[3H]HCh-3）结合减少。胆碱能标志物下降的再次出现不是与年龄相关的非特异性下降的结果，因为谷氨酸脱羧酶的活性在损伤后3至12个月之间保持恒定。
