Davis K L, Hollister L E, Berger P A, Barchas J D
Psychopharmacol Commun. 1975;1(5):533-43.
It has been proposed that the etiologies of tardive dyskinesia and Huntington's chorea and of some forms of schizophrenia and the affective disorders involve a cholinergic imbalance with respect to a second neurotransmitter. This relative over- or underactivity of the cholinergic system could result from altered synthesis, storage, release, degradation, or reuptake or from a variety of receptor interactions. Under these hypotheses, clinical symptoms would reflect both the brain region in which the imbalance occurs and the neurotransmitter with which acetylcholine is interacting. Effective treatments could involve the correction of this hypothetical imbalance by changing the relative availability of either one or both of the neurotransmitters. Both precursor loading with choline or dimethylaminoethanol and cholinesterase inhibition may be useful in evaluating the effects of increased cholinergic activity in these disease states; the relative merits of these strategies are discussed.
有人提出,迟发性运动障碍、亨廷顿舞蹈症以及某些形式的精神分裂症和情感障碍的病因涉及一种胆碱能与另一种神经递质的失衡。胆碱能系统这种相对的活性过高或过低可能源于合成、储存、释放、降解或再摄取的改变,或者源于多种受体相互作用。在这些假设下,临床症状将反映失衡发生的脑区以及与乙酰胆碱相互作用的神经递质。有效的治疗可能涉及通过改变一种或两种神经递质的相对可利用性来纠正这种假设的失衡。用胆碱或二甲基氨基乙醇进行前体负荷以及抑制胆碱酯酶在评估这些疾病状态下胆碱能活性增加的效果方面可能都有用;本文讨论了这些策略的相对优点。