Anomalous properties of hippocampal lesion-induced retrograde amnesia

Abstract

Retrograde amnesia can result from transient or permanent insults to the central nervous system and is typically manifest as a temporally graded memory loss. This temporal gradient of retrograde amnesia has been considered evidence for memory consolidation, since newly acquired information is vulnerable to amnestic treatments, whereas older information is not. Although investigations of transient insult-induced retrograde amnesia have provided evidence against a consolidation interpretation, hippocampallesion-induced retrograde amnesia is still considered to represent a consolidation (or storage) failure. In order to investigate the consolidation interpretation of hippocampal lesion-induced retrograde amnesia, two experiments were undertaken. In the fIrSt, rats were reminded of "old" memories prior to hippocampal lesions, a procedure that produced retrograde amnesia This result is difficult to reconcile with current interpretations of retrograde amnesia, since consolidated memories are presumably not vulnerable to amnesia The second experiment explored the permanence of hippocampal lesioninduced retrograde amnesia by presenting amnestic rats with a portion of the training treatment (reactivation) prior to testing. The reactivation treatment successfully reversed retrograde amnesia Taken together, the results from these experiments indicate that hippocampal retrograde amnesia may not in all cases arise from storage failure and illuminate new circumstances under which damage to the hippocampus may affect memory.Insults to the central nervous system (CNS) can result in amnesia, or the inability to recall learned information. When the information was learned prior to the insult, the resulting deficit is referred to as retrograde amnesia. This manifestation of amnesia results from two broad classes of experimental treatments: transient disruptions ofCNS functioning or permanent damage to brain tissue. Transient insults include such treatments as electroconvulsive shock (ECS; Duncan, 1949), thermoregulatory disruption, concussive head injury, and electrical brain stimulation (see, e.g.,

Consolidation of Long-Term Memory: Evidence and Alternatives.

“…Reminder treatments can also make remote memories that normally survive hippocampal lesions vulnerable to hippocampal damage (Debiec et al, 2002;Land, Bunsey, & Riccio, 2000). Land et al (2000) trained rats to escape a footshock by moving to a lighted part of a Y-shaped apparatus (a signaled avoidance task). When rats were given a hippocampal lesion 30 days after training, performance on this task remained relatively intact, as it did in other studies (Kim & Fanselow, 1992).…”

“…Reminder treatments can also make remote memories that normally survive hippocampal lesions vulnerable to hippocampal damage (Debiec et al, 2002; Land, Bunsey, & Riccio, 2000). Land et al (2000) trained rats to escape a footshock by moving to a lighted part of a -shaped apparatus (a signaled avoidance task).…”

Cycloheximide impairs reconsolidation of a contextually reactivated memory in a conditioned taste aversion paradigm.

“…Research on what some have recently referred to as memory reconsolidation has grown in recent years (for some recent reviews see Miller & Matzel, 2006; Nader & Wang, 2006; Riccio, Millin, & Bogart, 2006; Rudy, Biedenkapp, Moineau, & Bolding, 2006; Sara & Hars, 2006). Reports from Nader, Schafe, and LeDoux (2000) and Land, Bunsey, and Riccio (2000) have demonstrated that reactivating previously consolidated memories renders them susceptible to the detrimental effects of protein synthesis inhibition (PSI) and hippocampus lesions, respectively.…”

“…Research with rats indicated that reconsolidation effects have been shown in a number of paradigms dependent on subcortical temporal lobe structures (Land et al, 2000; Morris et al, 2006; Nader et al, 2000; Suzuki et al, 2004). In contrast, conditioned taste aversion (CTA) training represents a distinct and biologically important form of learning that involves some of the same (e.g., amygdala) and some different (e.g., insular cortex and prefrontal cortex) neuroanatomical substrates (Reilly & Bornovalova, 2005).…”

Reconsolidation of appetitive odor discrimination requires protein synthesis only when reactivation includes prediction error.

“…A considerable literature on memory reconsolidation demonstrated the importance of “active” memory on vulnerability to amnesic agents (Dudai, 2004; Gonzales-Salinas et al, 2015; Land, Bunsey, & Riccio, 2000; Lewis, 1979; Mactutus, Riccio, & Ferek, 1979; Nader et al, 2000; Przybyslawski & Sara, 1997). That is, active memories are vulnerable memories.…”