UVM Theses and Dissertations
Format:
Print
Author:
Lipatova, Olga
Dept./Program:
Psychology
Year:
2012
Degree:
MA
Abstract:
Numerous studies have investigated whether estrogen (E) enhances or impairs learning and memory. However, the type of memory affected by E and the mechanism involved in E's effects remain unclear. Indeed, studies attempting to examine this have been quite contradictory in their findings. The present experiments investigated the effects of E in the regulation of spatial learning and memory in female rats and how novel situations may alter the effect of E. In addition, we investigated E's regulation of specific serotonin type receptor (5-HT₆R) as well as the role this receptor plays in behavioral inhibition. Ovariectomized (OVX) female rats replaced with a physiological dose of E learned equally well as OVX non-replaced rats to navigate an open field maze in order to obtain a reward.
However, following a three-week period of absence from the maze, E-replaced rats had a significantly greater preservation of memory when returned to the maze environment compared to the non-treated animals. In contrast, once the non-replaced group was performing again at a similar level to the E-replaced group and a novel situation was introduced by placing the rat in a preViously non-experienced start location within the maze, E-replaced subjects showed a significant reduction in correct responses compared to the non-replaced OVX controls. Thus, E enhances the expression of spatial learning over time following a cessation of training, probably by maintaining memory systems. Introduction of novelty, however, disrupts the E effect on maze performance. These data suggest that the effect of E on spatial learning and memory is critically dependent on the familiarity of the task, and context, and can easily be offset by the stress or arousing properties of a novel situation.
We propose that the detrimental effect of novelty on spatial memory is induced by rats' inability to inhibit an emotional response to fearful stimuli. Additional findings show that even though 5-HT₆R was previously found to disrupt inhibition of fear response, the present experiment suggests that this receptor is not involved in appetitive conditioned-inhibition. Furthermore, a qPCR analysis indicates that E down-modulates 5-HT₆ mRNA expression in the bed nucleus of the stria terminalis (SST), however based on the autoradiography data E does not appear to modulate binding of a radiolabeled ligand to this receptor in the hippocampus, dorsal striatum or prefrontal cortex. Possible mechanisms and reasons for these results are discussed.
However, following a three-week period of absence from the maze, E-replaced rats had a significantly greater preservation of memory when returned to the maze environment compared to the non-treated animals. In contrast, once the non-replaced group was performing again at a similar level to the E-replaced group and a novel situation was introduced by placing the rat in a preViously non-experienced start location within the maze, E-replaced subjects showed a significant reduction in correct responses compared to the non-replaced OVX controls. Thus, E enhances the expression of spatial learning over time following a cessation of training, probably by maintaining memory systems. Introduction of novelty, however, disrupts the E effect on maze performance. These data suggest that the effect of E on spatial learning and memory is critically dependent on the familiarity of the task, and context, and can easily be offset by the stress or arousing properties of a novel situation.
We propose that the detrimental effect of novelty on spatial memory is induced by rats' inability to inhibit an emotional response to fearful stimuli. Additional findings show that even though 5-HT₆R was previously found to disrupt inhibition of fear response, the present experiment suggests that this receptor is not involved in appetitive conditioned-inhibition. Furthermore, a qPCR analysis indicates that E down-modulates 5-HT₆ mRNA expression in the bed nucleus of the stria terminalis (SST), however based on the autoradiography data E does not appear to modulate binding of a radiolabeled ligand to this receptor in the hippocampus, dorsal striatum or prefrontal cortex. Possible mechanisms and reasons for these results are discussed.