PHARMACOLOGY, BIOCHEMISTRY AND PHYSIOLOGY OF CENTRAL NEUROTRANSMITTERS

1.晚期帕金森病患者的运动反应并发症 疾病似乎主要归因于非生理波动， 突触内多巴胺 连续的多巴胺模拟疗法限制了这些 并发症 2.对一种原型多巴胺激动剂的研究显示， 功效仅为左旋多巴的一半，尽管诱导 运动障碍 由于该药主要作用于D多巴胺受体， 开发现在将集中在化合物，如左旋多巴，导致DI作为 以及D2多巴胺受体刺激。 3.帕金森病动物模型的纹状体多巴胺感受系统 慢性左旋多巴治疗和 治疗方案的连续或间歇性质：DI输出 通过纹状体黑质系统的输出减少，而D2通过纹状体黑质系统的输出减少。 纹状体苍白球通路增加。 左旋多巴替代品，特别是当 因此，间歇性地给予多巴胺并不能简单地逆转多巴胺的作用， 去神经支配，但创建不同于神经支配和去神经支配两者的新的功能状态。 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 阿尔茨海默病与那些同样严重的帕金森病患者 痴呆：两组的语义和情景记忆都受损，但 在阿尔茨海默病患者中， 帕金森病患者在执行任务时相对更妥协。

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.