Title

The effects of severity of traumatic brain injury on cognitive performance and hippocampal electrophysiology

Date of Award

1998

Availability

Article

Degree Name

Doctor of Philosophy (Ph.D.)

First Committee Member

Edward Green, Committee Chair

Abstract

The experiments presented here were designed to investigate the effects of severity of traumatic brain injury on learning and hippocampal electrophysiology in rats during both acute and chronic periods. Traumatic brain injury presents a significant challenge to the health sciences. Head trauma results in immediate destruction of brain tissue and long-term dysfunction in surviving neurons. Brain injured individuals show dramatic deficits in learning and memory for chronic periods. The fluid-percussion model of injury (using rodent subjects) has been developed to investigate the neuronal and psychological effects of traumatic brain injury. In the present studies, rats were subjected to traumatic injury and then tested for learning and physiological deficits. In these experiments, performance on traditional "spatial" and "nonspatial" water maze learning tasks was affected differentially by traumatic injury. Performance on the hidden platform and cued platform versions of the water maze presumably measure spatial and nonspatial cognition, respectively. Fluid-percussive injury of increasing severity resulted in increased deficits in hidden platform learning at one week without corresponding deficits in cued platform learning. In contrast, injury resulted in significant cued platform learning deficits at 8 weeks coincident with reduced deficits in hidden platform learning. Thus deficits in hidden platform learning had recovered somewhat by 8 weeks while deficits in cued platform learning had intensified. Data thus indicate that neural processes subserving spatial and nonspatial teaming are affected differently by traumatic injury and that "recovery" of these processes follows different time courses. Traumatic injury resulted in an impairment of CA1 hippocampal synaptic plasticity at 8 weeks but not at 1 week. Whereas injury severity was predictive of the magnitude of cognitive deficits at 8 weeks, severity was not predictive of the magnitude of plasticity deficits. Finally, measures of synaptic plasticity were not predictive of measures of cognitive performance. In conclusion, although they both are affected negatively by injury, long-term potentiation in hippocampal CA1 and cognitive performance in the water maze do not covary after trauma.

Keywords

Biology, Neuroscience; Psychology, Psychobiology; Psychology, Cognitive

Link to Full Text

http://access.library.miami.edu/login?url=http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:9934270