Access to abstract permanently restricted to Ball State community only / Access to thesis permanently restricted to Ball State community only / Department of Biology

Seizure activity is the primary symptom in a common but very serious neurological disorder known as epilepsy. Brain glycogen is utilized for neuronal function, prompting us to investigate the role of brain glycogen during seizure activity in mouse models. Seizures were induced with Pentylenetetrazole (PTZ) in both wild-type mice and mice lacking brain glycogen (MGSKO/GSL30 mice). A time course of brain glycogen utilization after onset of seizure activity revealed a reduction of brain glycogen in wild-type mice. The glycogen synthase activity ratio increased after onset of seizure activity, while the glycogen phosphorylase activity ratio remained constant. Brain and blood glucose levels increased after seizure onset in wild-type mice. Despite lacking brain glycogen, MGSKO/GSL30 mice exhibited acute seizure activity. No differences were observed in seizure intensity, onset time, and duration between genotypes. These findings suggest that brain glycogen is important, but not required for PTZ-induced acute seizure activity in mice. / Access to thesis permanently restricted to Ball State community only / Department of Biology

Thesis (M.S.)--University of Hawaii at Manoa, 2007. / Includes bibliographical references (leaves 45-55). / i, 92 leaves, bound ill. 29 cm

The brain evolved to control behavior, and locomotion is among the behaviors most critical to animal survival. The neural mechanisms of skilled locomotion have been studied for decades, yet recently developed technologies offer the opportunity to shine new light on this long studied behavior. I leveraged these technologies to develop a system for studying the behavioral strategies and neural mechanisms of skilled locomotion in mice. In Chapter 2, I use detailed 3D kinematic tracking and behavioral modelling to describe a rapid sensorimotor decision that determines the kinematic strategies used by mice to step over obstacles. Despite the whisker dependency of this behavior, performance is minimally affected by manipulations of whisker sensory cortex, whereas motor cortex manipulations impair but did not prevent obstacle clearance. Neither cortical manipulation substantially impacts the sensorimotor decision. In Chapter 3, we turn to the cerebellum. The cerebellum is thought to contribute to the coordination of movement, as evinced by the locomotor deficits that are a hallmark of cerebellar ataxia. However, much cerebellar research has focused on simple behaviors involving single body parts. Furthermore, the recent discovery of reward signals in the cerebellar cortex has drawn attention to its potential non-motor functions, but whether such signals exist in the output of the cerebellum is unknown. We conducted an electrophysiological survey of the deep cerebellar nuclei to characterize the signals communicated by the cerebellum to downstream structures. Preliminary analyses from this ongoing work suggest that cerebellar output is dominated by orofacial and locomotor signals, whereas reward related modulations are largely accounted for by the behavioral correlates of reward delivery. Collectively, these results demonstrate that quantitative whole body analyses of ethologically inspired behaviors can enhance our understanding of the neural control of sensorimotor behaviors.

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The purpose of this study was to investigate the effects of cocaine on spatial memory consolidation using the Morris water maze. Specifically, male and female C57BL/6 mice were trained on a spatial water task, and then administered a single posttraining injection of saline or cocaine (1.25, 2.5, 5.0, or 20.0 mg/kg).