Levodopa is a precursor to dopamine that has been shown to improve functional recovery following stroke partly achieved through mechanisms of brain plasticity. This study investigates if dopamine might affect plasticity by having a direct effect on synaptic plasticity through alterations in neurotransmitter release and re-uptake. Synaptogyrin is a synaptic vesicle protein that has been suggested to be involved in dopamine re-uptake in the synaptic terminal. Therefore, we investigated if levodopa has an effect on the expression of synaptogyrin 1. Thy1-YFP mice were subjected to photothrombosis as an experimental model of stroke. Starting two days after surgery they were treated with either levodopa or a vehicle solution (saline) on a daily basis until day seven following surgery. On day seven they were sacrificed and their brains stained for Dopamine 1 receptor (D1R), Dopamine 2 receptor (D2R) and Parvalbumin (PV). Neu-N stainings were used to estimate infarct size. A second group of mice were subjected to photothrombosis and also treated with either levodopa or a vehicle solution in the same manner as previously mentioned. On day seven they were then sacrificed, and samples of brain tissue were taken for protein determination. Western blots were carried out to investigate possible differences in synaptogyrin expression between the two groups. Immunofluorescent stains showed the presence of dopamine receptors on the YFP-positive neurons and on PV-expressing neurones. Our Western Blot analysis showed a significant decrease in the expression of synaptogyrin in levodopa-treated mice. Our stains showed co-localisation with Thy-1 neurones and PV-expressing neurones for both D1 and D2 receptors. This indicates that dopamine has the ability to bind to, and directly influence cortical neurons, as well as inhibitory interneurons. We discovered a considerable decrease in synaptogyrin expression through levodopa treatment, suggesting that this might be a mechanism for regulating brain plasticity.

中文翻译：

---

左旋多巴增强的功能恢复与老年小鼠中风后突触结合蛋白水平降低有关。

左旋多巴是多巴胺的前体，已显示可改善中风后部分通过脑可塑性机制实现的功能恢复。这项研究调查了多巴胺是否可能通过改变神经递质的释放和再摄取而直接影响突触可塑性，从而影响可塑性。突触结合蛋白是一种突触小泡蛋白，已被认为与突触末端的多巴胺再摄取有关。因此，我们研究了左旋多巴是否对突触结合蛋白1的表达有影响。将Thy1-YFP小鼠作为中风的实验模型进行了光血栓形成。手术后两天开始，每天用左旋多巴或溶媒溶液（盐水）治疗，直到手术后第七天。在第7天，将他们处死并对其大脑进行多巴胺1受体（D1R），多巴胺2受体（D2R）和小白蛋白（PV）染色。Neu-N染色用于估计梗塞面积。第二组小鼠进行光血栓形成，并以左旋多巴或赋形剂溶液以与前述相同的方式处理。然后在第七天将其处死，并取脑组织样品进行蛋白质测定。进行了蛋白质印迹以研究两组之间突触结合蛋白表达的可能差异。免疫荧光染色显示在YFP阳性神经元和表达PV的神经元上存在多巴胺受体。我们的蛋白质印迹分析表明，左旋多巴治疗的小鼠中突触结合蛋白的表达显着降低。对于D1和D2受体，我们的染色显示与Thy-1神经元和表达PV的神经元共定位。这表明多巴胺具有结合并直接影响皮层神经元以及抑制性中间神经元的能力。我们发现左旋多巴治疗后突触结合蛋白表达显着下降，表明这可能是调节大脑可塑性的一种机制。