EXCITATORY SYNAPTIC TRANSMISSION IN NEOSTRIATUM

这项研究的目的是为了进一步了解 其中多巴胺能和多巴胺能突触传递有助于 新纹状体的功能 之前的实验已经证明 离子型和代谢型谷氨酸受体在 皮质纹状体突触传递 此外，两种形式的突触 抑郁症（STD和LTD）已经在这些突触中观察到。 实验 旨在确定：1）涉及的突触改变位点 皮质纹状体和黑质纹状体传入的作用 在诱发纹状体LTD的输入; 3）参与的机制， 代谢型谷氨酸受体对传递的突触前调节。 谷氨酸或相关的氨基酸是主要的兴奋性神经递质 在哺乳动物的中枢神经系统。 在尾状核和壳核内，谷氨酸- 包含来自皮质和可能丘脑的纤维， 神经元，尤其是中型多刺神经元。 激活这些 突触使纹状体神经元去极化， 或者增加它们被其它输入激活的可能性。 一 进一步了解的生理和药理学特性， 这些突触对功能性新纹状体的识别至关重要， 电路 多巴胺能黑质纹状体通路也起着重要的作用。 在调节纹状体功能中的作用，并与 帕金森病和其他神经系统疾病的神经病理学 包括基底神经节 然而，人们对它的了解相对较少。 在细胞水平上激活该途径的后果 生理学和突触传递。 我们假设 阐明多巴胺能皮质纹状体传递的作用， 纹状体功能中的多巴胺能黑质纹状体传递将有助于 发展治疗涉及损伤的疾病的方法 纹状体的功能

The aim of the proposed research is to further our understanding of the way in which glutamatergic and dopaminergic synaptic transmission contribute to the function of the neostriatum. Previous experiments have demonstrated roles for both ionotropic and metabotropic glutamate receptors in corticostriatal synaptic transmission. In addition, two forms of synaptic depression (STD and LTD) have been observed at these synapses. Experiments are designed to determine: 1) The synaptic locus of alterations involved in striatal LTD; 2) The role of corticostriatal and nigrostriatal afferent inputs in eliciting striatal LTD; 3) The mechanisms involved in presynaptic modulation of transmission by metabotropic glutamate receptors. Glutamate or a related amino acid is the major excitatory neurotransmitter in the mammalian CNS. Within the caudate nucleus and putamen, glutamate- containing fibers from the cortex and possibly thalamus form synapses with neurons, most notably the medium spiny neurons. Activation of these synapses depolarizes striatal neurons which activates the neurons directly or increases the likelihood of their being activated by other inputs. A further understanding of the physiologic and pharmacologic properties of these synapses is critical to the appreciation of functional neostriatal circuitry. The dopaminergic nigrostriatal pathway also plays a prominent role in regulation of striatal function, and is critically involved in the neuropathology of Parkinson's disease and other neurological disorders involving the basal ganglia. However, relatively little is known about the consequences of activation of this pathway at the level of cellular physiology and synaptic transmission. It is our hypothesis that elucidation of the role of glutamatergic corticostriatal transmission and dopaminergic nigrostriatal transmission in striatal function will aid in the development of therapeutic approaches to disorders involving impairment of striatal function.