ANALYSIS OF SYNAPTIC INTERACTION IN INFERIOR COLLICULUS

下丘是下丘的主要汇合点。 低位脑干听觉结构的听觉信息 因此，在集成和后续的 听觉信息的传输。最近的解剖学研究， 生理学和药理学研究已经开始 解开这个结构中正在发生的复杂的相互作用 电路仍然没有被很好地理解。多项研究 已经表明，集成电路不仅在正常情况下发挥着重要作用 但听觉功能也是非常重要的 感觉诱发听源性惊厥的传播和启动。 在啮齿动物中存在许多基因突变，特别是 遗传性癫痫易感大鼠(GEPR)，表现为癫痫发作 对强烈的听觉刺激的反应行为，这可能是 与IC中的功能异常有关，并可能 作为反射性或原发全身性癫痫的动物模型。 间接证据表明，许多具有相同潜力的 癫痫神经行为的机制 下位大脑皮质和海马区水平可能很活跃 丘脑。本研究将主要利用体外脑片 对丘脑进行研究的技术。其意图是开始一场 脑内细胞的固有和突触特征的表征 小丘的不同特定区域。我们会做出努力， 在细胞内水平上，观察特定的突触事件 由输入通路的激活引起的潜在的传递体 由这些途径使用，以及细胞的内在特征 可以帮助塑造对这些输入的反应。记录来自 正常IC脑片中神经传递改变的细胞 环境和来自GEPR突变体切片中的细胞 进行分析以确定哪些细胞类型能够出现异常 癫痫功能，这些功能是否会发生 自发地在突变切片中以及潜在的 机制/异常是导致这种活动的原因。终于来了 在体制备的推测的输出途径 来自IC的异常癫痫活动将更加彻底 特色化的。

The inferior colliculus (IC) serves as a major convergent site of auditory information for lower brainstem auditory structures and as such is of primary importance in the integration and subsequent transmission of auditory information. Recent anatomical, physiological and pharmacological investigations have begun to unravel the complex interactions taking place in this structure yet the circuitry is still not well understood. A number of studies have shown that the IC not only plays a major role in normal auditory function but also is of critical importance in the propagation and initiation of sensory evoked audiogenic seizures. A number of genetic mutants exist in rodents, in particular the genetically epilepsy prone rat (GEPR), that display seizure behavior in response to intense auditory stimuli which may be linked to functional abnormalities in the IC and which may serve as an animal model for reflex or primary generalized epilepsies. Indirect evidence indicates that many of the same potential mechanisms responsible for epileptic neural behavior at the cortical and hippocampal levels may be active in the inferior colliculus. This study will primarily utilize the in vitro brain slice technique to investigate the colliculus. The intent is to begin a characterization of the intrinsic and synaptic features of cells in various specific regions of the colliculus. An effort will be made, at the intracellular level, to look at specific synaptic events elicited by activation of input pathways the potential transmitters used by these pathways and the intrinsic features of the cells that could help to shape the response to these inputs. Records from cells in normal IC slices in altered neural transmission environments and from cells in slices from GEPR mutant will be analyzed to determine which cell types are capable of abnormal epileptic function, whether these functions can occur spontaneously in mutant slices and what the underlying mechanisms/abnormalities are causing this activity. Finally in the in vivo preparation the presumed output pathway of the abnormal seizure activity from the IC will be more thoroughly characterized.