Sara S J
Département de Psychophysiologie, C.N.R.S., Gif-sur-Yvette, France.
Arch Gerontol Geriatr Suppl. 1989;1:99-108.
Over the past 10 years, cholinergic deficits have been strongly correlated with memory dysfunction. On the other hand the lack of efficacy of direct or indirect cholinergic drugs has led to research in other neurotransmitter systems. Several authors have found miscellaneous results in NE and metabolites levels and in monoamine enzyme activities. These discrepancies have lead to discussions about the homogeneity of the disease. Animal lesion studies point out the importance of the septo-hippocampal cholinergic pathway and the interrelations between ACh and NE in the hippocampal formation. The author performed a series of experiments in rats in which hippocampal ACh activity was reduced (fornix section or destruction of cells in the medial septum) and the NE system modified by clonidine or neurotoxic lesions. The hypothesis was that a lesion of the cholinergic pathway leads to an enhancement of NE activity which inhibits spared ACh neurons. The alpha-2 agonist clonidine would interrupt this loop by decreasing of NE release. Results provide arguments for the author's theory.
在过去的10年里，胆碱能缺陷与记忆功能障碍密切相关。另一方面，直接或间接胆碱能药物疗效欠佳促使人们对其他神经递质系统展开研究。多位作者在去甲肾上腺素（NE）及其代谢产物水平以及单胺酶活性方面得到了各种各样的结果。这些差异引发了关于该疾病同质性的讨论。动物损伤研究指出了隔海马胆碱能通路的重要性以及海马结构中乙酰胆碱（ACh）与NE之间的相互关系。作者对大鼠进行了一系列实验，其中降低了海马ACh活性（穹窿切断或破坏内侧隔区的细胞），并通过可乐定或神经毒性损伤对NE系统进行了改造。其假设是胆碱能通路损伤会导致NE活性增强，从而抑制剩余的ACh神经元。α-2激动剂可乐定将通过减少NE释放来中断这一循环。结果为作者的理论提供了依据。
