ANALYSIS OF SYNAPTIC INTERACTION IN INFERIOR COLLICULUS

下丘（IC）是一个主要的会聚部位， 下脑干听觉结构的听觉信息， 因此，在整合和随后的 听觉信息的传递。 最近的解剖学， 生理学和药理学研究已经开始， 解开这个结构中复杂的相互作用 电路仍然没有被很好地理解。 多项研究 已经表明，IC不仅在正常的 听觉功能也是至关重要的 感觉诱发的听源性癫痫发作的传播和起始。 啮齿类动物中存在许多基因突变体，特别是 遗传性癫痫易感大鼠（GEPR），显示癫痫发作 对强烈听觉刺激的反应行为， 与IC的功能异常有关， 作为反射性或原发性全身性癫痫的动物模型。 间接证据表明，许多相同的潜在 负责癫痫神经行为的机制 皮质和海马水平可能在下丘脑活跃， 丘 本研究将主要利用体外脑切片 技术来研究丘。 目的是开始一个 细胞的内在和突触特征的表征， 丘的各个特定区域。 我们会做出努力， 在细胞内水平，观察特定的突触事件， 通过激活输入通路引起潜在的递质 这些途径所使用的，以及细胞的内在特征， 可以帮助塑造对这些输入的反应。 记录从 正常IC切片中的细胞在改变的神经传递中 环境和来自GEPR突变体切片中的细胞将被 分析以确定哪些细胞类型能够异常 癫痫功能，这些功能是否可以发生 在突变体切片中自发发生， 机制/异常导致该活动。 终于在 体内制备假定的输出途径 异常的癫痫活动从IC将更彻底 表征了

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.