Dixon C E, Bao J, Bergmann J S, Johnson K M
Department of Neurosurgery, University of Texas, Houston 77030.
Neurosci Lett. 1994 Oct 24;180(2):127-30. doi: 10.1016/0304-3940(94)90503-7.
Hippocampal cholinergic hypofunction may contribute to memory deficits following experimental traumatic brain injury. These studies examined two important factors in acetylcholine synthesis: choline availability and neuronal uptake. No reductions in basal extracellular choline levels, using microdialysis, were observed 2 weeks after cortical impact injury. However, studies of high affinity [3H]choline uptake in the hippocampus, measured in a synaptosomal preparation, found a reduction in the maximum velocity of choline uptake (Vmax), while no differences in affinity constants (Km) were found. The results suggest that post-traumatic cholinergic deficits are not attributable to decreased availability of choline, but may be associated with either a decreased ability of cholinergic neurons to take up choline and/or a loss of cholinergic neurons.
海马胆碱能功能减退可能导致实验性创伤性脑损伤后的记忆缺陷。这些研究考察了乙酰胆碱合成中的两个重要因素：胆碱可用性和神经元摄取。使用微透析法，在皮质撞击损伤后2周未观察到基础细胞外胆碱水平降低。然而，在突触体制备中测量海马中高亲和力[3H]胆碱摄取的研究发现，胆碱摄取的最大速度（Vmax）降低，而亲和力常数（Km）没有差异。结果表明，创伤后胆碱能缺陷并非由于胆碱可用性降低，而是可能与胆碱能神经元摄取胆碱的能力下降和/或胆碱能神经元丢失有关。
