PHARMACOLOGY, BIOCHEMISTRY AND PHYSIOLOGY OF CENTRAL NEUROTRANSMITTERS

1.晚期帕金森病患者的运动反应并发症 疾病似乎很大程度上归因于非生理性波动 突触内的多巴胺。持续的多巴胺仿制疗法限制了这些 并发症。 2.对一种原型多巴胺激动剂的研究发现，一种抗帕金森症 疗效只有左旋多巴的一半，尽管有同等的诱导能力 运动障碍。由于该药物主要作用于D-多巴胺受体，激动剂 开发现在将集中在导致DL AS的化合物上，如左旋多巴 以及D2多巴胺受体的刺激。 3.帕金森病动物模型的纹状体多巴胺感受器系统 慢性左旋多巴疗法和 治疗方案的连续性或间歇性：DL输出 通过纹状体黑质系统减少，而D2通过 纹状体苍白球通路增加。左旋多巴替代药物，特别是当 因此，间歇给药并不能简单地逆转多巴胺的作用 去神经，但创造了一种新的功能状态，与 可能导致运动并发症的正常和失神经状态。 4.神经心理学研究比较了老年痴呆患者的认知障碍 阿尔茨海默病与帕金森病患者病情同等严重 痴呆症：两组的语义和情景记忆都受到了损害，但 阿尔茨海默病患者的程度相对较高，而精神错乱 帕金森氏症患者在执行任务上相对更容易妥协。

1. Motor response complications in patients with advanced Parkinson's disease appear largely attributable to nonphysiologic fluctuations in intrasynaptic dopamine. Continuous dopaminomimetic therapies limit these complications. 2. Studies of one prototypic dopamine agonist revealed an antiparkinsonian efficacy only half that of levodopa, despite an equal ability to induce dyskinesias. Since this drug acts main y on D dopamine receptors, agonist development will now focus on compounds, like levodopa, that lead to Dl as well as D2 dopamine receptor stimulation. 3. Striatal dopaminoceptive systems in an animal model of Parkinson's disease are differentially affected by chronic levodopa therapy and by the continuous or intermittent nature of the therapeutic regimen: Dl output through the striatonigral system decreases while D2 output through the striatopallidal pathway increases. Levodopa replacement, especially when given intermittently, thus does not simply reverse the effects of dopamine denervation but creates a new functional state differing from both the normal and denervated states that could contribute to motor complications. 4. Neuropsychologic studies compared cognitive deficits in patients with Alzheimer's disease with those in Parkinsonian patients with equally severe dementia: Semantic and episodic memory were impaired in both groups, but to a relatively greater degree in Alzheimer patients, while demented Parkinsonian patients were relatively more compromised on executive tasks.