Retrosplenial cortex damage produces retrograde and anterograde context amnesia using strong fear conditioning procedures

• Published in: Behavioural brain research 2019-09, Vol.369, p.111920-111920, Article 111920
• Main Authors: Fournier, Danielle I., Eddy, Meghan C., DeAngeli, Nicole E., Huszár, Roman, Bucci, David J.
• Format: Article
• Language: English
• Subjects: Amnesia, Anterograde - etiology; Amnesia, Anterograde - physiopathology; Amnesia, Retrograde - etiology; Amnesia, Retrograde - physiopathology; Animals; Association Learning - physiology; Associative learning; Auditory Perception - physiology; Conditioning, Psychological - physiology; Electroshock; Fear - physiology; Gyrus Cinguli - injuries; Gyrus Cinguli - physiopathology; Hippocampus - physiopathology; Male; Memory; Memory - physiology; Over-Training; Parahippocampal; Rats, Long-Evans
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2019.111920

•Damage to retrosplenial cortex produces anterograde and retrograde context amnesia.•Strong training procedures cannot overcome anterograde deficits.•The results differ from the effects of hippocampal damage using the same procedures. Contextual fear conditioning relies upon a network of cortical and subcortical structures, including the hippocampus and the retrosplenial cortex (RSC). However, the contribution of the hippocampus is parameter-dependent. For example, with “weak” training procedures, lesions of the hippocampus produce both retrograde and anterograde context amnesia. However, with “strong” training procedures (e.g., more trials and/or higher levels of footshock), lesions of the hippocampus produce retrograde context amnesia but not anterograde amnesia (Wiltgen et al., 2006). Likewise, prior studies have shown that with weak training, RSC lesions produce both retrograde and anterograde context amnesia (Keene & Bucci, 2008). The purpose of the current study was to examine the effects of RSC damage on contextual fear conditioning following strong training. In Experiment 1, lesions of the RSC resulted in both retrograde and anterograde context amnesia following strong training using the same unsignaled fear conditioning procedures described by Wiltgen et al. (2006). In Experiment 2, using a signaled fear conditioning procedure, we replicated these effects on context memory observing both retrograde and anterograde context amnesia. In contrast, there were no lesion effects on tone-fear memory. Thus, unlike lesions of the hippocampus, lesions of RSC produce both retrograde and anterograde context amnesia even when rats undergo strong fear conditioning. These findings suggest that the RSC has an essential role in contextual fear conditioning and that other systems or pathways are unable to compensate for the loss of RSC function.