Abstract
Numerous reports indicate that learning and memory of conditioned responses are accompanied by genesis of dendritic spines in the hippocampus, although there is a conspicuous lack of information regarding spine modifications after behavioral extinction. There is ample evidence that treatments that typically produce amnesia become innocuous when animals are submitted to a procedure of enhanced training. We now report that extinction of inhibitory avoidance (IA), trained with relatively low foot-shock intensities, induces pruning of dendritic spines along the length of the apical dendrites of hippocampal CA1 neurons. When animals are trained with a relatively high foot-shock there is a high resistance to extinction, and pruning in the proximal and medial segments of the apical dendrite are seen, while spine count in the distal dendrite remains normal. These results indicate that pruning is involved in behavioral extinction, while maintenance of spines is a probable mechanism that mediates the protecting effect against amnesic treatments produced by enhanced training.
Highlights
It has been reported that treatments that typically produce amnesia become innocuous when administered to animals that have been submitted to an enhanced learning experience
The hippocampus is involved in memory consolidation of inhibitory avoidance (IA) training, as shown by the deleterious effects of interference with hippocampal activity on retention of this task (Izquierdo et al, 1992; Ambrogi-Lorenzini et al, 1996; Stubley-Weatherly et al, 1996; Martínez et al, 2002), enhanced learning of this task protects against amnesia produced by reversible blockade of hippocampal activity (Quiroz et al, 2003)
The second main finding was that extinction produced pruning of spines in the three segments of the apical dendrite in the groups that had been trained with the lower foot-shock intensities (1.0 and 2.0 mA)
Summary
It has been reported that treatments that typically produce amnesia become innocuous when administered to animals that have been submitted to an enhanced learning experience. It was found that enhanced IA training prevented the typical amnesic effects of cycloheximide, a protein synthesis inhibitor (Díaz-Trujillo et al, 2009). In spite of this evidence, the neurobiological mechanisms of the protective effect of enhanced learning against amnesic treatments remain completely unknown. The hippocampus is involved in memory consolidation of IA training, as shown by the deleterious effects of interference with hippocampal activity on retention of this task (Izquierdo et al, 1992; Ambrogi-Lorenzini et al, 1996; Stubley-Weatherly et al, 1996; Martínez et al, 2002), enhanced learning of this task protects against amnesia produced by reversible blockade of hippocampal activity (Quiroz et al, 2003)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
