科研人員發(fā)現(xiàn)了從前腦到腦干的一個直接神經(jīng)路徑的證據(jù),，揭示了神經(jīng)遞質(zhì)多巴胺用以控制運動的一種機制。根據(jù)目前的法則,，運動依賴于通過多巴胺神經(jīng)元傳遞的信號,，這些神經(jīng)元向基底核發(fā)出向上的突起。在基底核,，這些突起向下延伸到腦干的一個運動控制中心,。人們已經(jīng)把這些上升的突起的喪失與帕金森疾病的運動缺陷聯(lián)系在了一起。近來在猴子和大鼠身上的發(fā)現(xiàn)提示存在從多巴胺細胞直接向下通往運動控制中心的突起,，Réjean Dubuc及其同事根據(jù)這些發(fā)現(xiàn)進行了研究,。這組作者在一個七鰓鰻脊椎動物模型中使用紅色、綠色和藍色標記對投射到大腦不同區(qū)域的神經(jīng)元進行了區(qū)分,。這些發(fā)現(xiàn)表明許多多巴胺神經(jīng)元繞過了基底核,，直接投向運動控制中心，在那里,，這些神經(jīng)元的激活導致多巴胺的釋放,。這組作者說，這些發(fā)現(xiàn)改變了目前關于多巴胺如何控制運動的理解,，而且可能對于帕金森疾病的運動相關癥狀有治療意義,。（生物谷 Bioon.com）
生物谷推薦的英文摘要
PNAS doi: 10.1073/pnas.1301125110
Forebrain dopamine neurons project down to a brainstem region controlling locomotion
Dimitri Ryczkoa, Swantje Grätscha, François Auclaira, Catherine Dubéa, Saskia Bergeronb, Michael H. Alpertc, Jackson J. Conec, Mitchell F. Roitmanc, Simon Alfordc, and Réjean Dubuca,b,1
The contribution of dopamine (DA) to locomotor control is traditionally attributed to ascending dopaminergic projections from the substantia nigra pars compacta and the ventral tegmental area to the basal ganglia, which in turn project down to the mesencephalic locomotor region (MLR), a brainstem region controlling locomotion in vertebrates. However, a dopaminergic innervation of the pedunculopontine nucleus, considered part of the MLR, was recently identified in the monkey. The origin and role of this dopaminergic input are unknown. We addressed these questions in a basal vertebrate, the lamprey. Here we report a functional descending dopaminergic pathway from the posterior tuberculum (PT; homologous to the substantia nigra pars compacta and/or ventral tegmental area of mammals) to the MLR. By using triple labeling, we found that dopaminergic cells from the PT not only project an ascending pathway to the striatum, but send a descending projection to the MLR. In an isolated brain preparation, PT stimulation elicited excitatory synaptic inputs into patch-clamped MLR cells, accompanied by activity in reticulospinal cells. By using voltammetry coupled with electrophysiological recordings, we demonstrate that PT stimulation evoked DA release in the MLR, together with the activation of reticulospinal cells. In a semi-intact preparation, stimulation of the PT elicited reticulospinal activity together with locomotor movements. Microinjections of a D1 antagonist in the MLR decreased the locomotor output elicited by PT stimulation, whereas injection of DA had an opposite effect. It appears that this descending dopaminergic pathway has a modulatory role on MLR cells that are known to receive glutamatergic projections and promotes locomotor output.
