The pathology of Alzheimer's disease is characterized by neuritic plaques and neurofibrillary tangles. The core component of the plaques is an amino acid named Beta-amyloid (AB). A recent study done by Dornan, Kang, McCampbell, and Kang (1993) reported that bilateral injections of AB along with a subthreshold dose of ibotenic acid (IBO) into the hippocampus significantly impaired the acquisition of a spatial learning task in rats. Dornan et al suggest that the results seen in their study maybe due to AB+IBO working synergistically via NMDA receptors to cause calcium dyshomeostasis. Another way that calcium dyshomeostasis occurs in the brain is via glucocorticoids. In a study done by Sapolsky (1985), exposure to stress levels of glucpcorticoids exacerbated kianic acid damage to hippocampal neurons, suggesting the possibility that glucocorticoids may endanger neurons by making them more vulnerable to outside toxic insults. Therefore, in this study we assessed the effects of glucocorticoids (7mg of corticosterone in 1ml of sesame oil, injected daily for two weeks) on the retention of a spatial task in animals that received bilateral intrahippocampal injections of AB. Animals injected with 7mg of corticosterone along with bilateral injections of Beta-amyloid did not have significant differences in the retention of the spatial task as compared to control animals.
Wijeweera '94, Harinie, "The Effect of Exposure to Glucocorticoids on the Retention of a Spatial Task in Rats Injected Bilaterally with Beta-Amyloid into the Hippocampus" (1994). Honors Projects. Paper 49.