ANALYSIS OF SYNAPTIC INTERACTION IN INFERIOR COLLICULUS

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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.