Amnesia induced by hypothermia as a function of treatment-test interval and recooling in rats

Hinderliter, Charles F.; Webster, Timothy; Riccio, David C.

doi:10.3758/bf03213441

Cited by 77 publications

(88 citation statements)

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“…The amnestic agent presumably creates an internal context that is not ordinarily present at the time of testing. This position readily accounts for the retrograde gradient of experimental amnesia and receives strong support from studies that demonstrate recovery when the subject is re-exposed to the amnestic agent just prior to testing (see Hinderliter et al 1975). Amnesia induced by an amnestic agent soon after reactivation of an old memory is viewed as the result of the old memory now being associated with the internal context created by the amnestic agent and that association interfering with the earlier acquired association between the internal training context and the target memory.…”

Section: Learning and Memory 493mentioning

confidence: 98%

Retrieval failure versus memory loss in experimental amnesia: Definitions and processes

Miller

Matzel²

2006

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For at least 40 years, there has been a recurring argument concerning the nature of experimental amnesia, with one side arguing that amnesic treatments interfere with the formation of enduring memories and the other side arguing that these treatments interfere with the expression of memories that were effectively encoded. The argument appears to stem from a combination of (1) unclear definitions and (2) real differences in the theoretical vantages that underlie the interpretation of relevant data. Here we speak to how the field might avoid arguments that are definitional in nature and how various hypotheses fare in light of published data. Existing but often overlooked data favor very rapid (milliseconds) synaptic consolidation, with experimental amnesia reflecting, at least in part, deficits in retrieval rather than in the initial storage of information.As most commonly conceived, "memory consolidation" refers uniquely to the processes by which newly acquired information, which is initially represented in ongoing synaptic transmission, comes over time to be encoded in a format that was independent of ongoing activity (and thus sensory stimulation) (Müller and Pilzecker 1900;McGaugh 1966). Fundamental to consolidation theory as it was originally formulated is that there were dual representational systems, one dependent upon ongoing neural transmission and the other dependent on enduring (i.e., structural/molecular) changes in the nervous system (e.g., pathway synthesis, facilitation of transmitter release, potentiation of sensitivity to transmitter binding, enhancement of membrane excitability) (for a review, see Matzel et al. 1998). Presumably there was a sequential dependence of the latter process (consolidation) on the former process (see Hebb 1949). Today it is widely recognized that there are a number of different molecular-structural representations that may be formed during memory storage, and that these representations become stable (i.e., "encoded") at very different rates and are dependent on different neuroanatomical sites (see Gibbs and Ng 1977;McGaugh 2000). This conceptualization of the consolidation process is often referred to as "system consolidation," although it should be noted that these different structural-molecular representations need not be sequentially linked (see Tully et al. 1994). Much recent attention has been devoted to system consolidation, which is relatively slow and measured in hours, days, or even months (see Kim and Fanselow 1992), as opposed to the earlier but still not fully answered questions of initial consolidation, which is generally assumed to occur in seconds or minutes. Although careless use of language has resulted in some confusion between these two related but different types of consolidation, some researchers distinguish them by using the expression "synaptic consolidation" (or "short-term molecular consolidation") for initial consolidation, which they differentiate from system consolidation (Nadel and Moscovitch 1997; Nader et al. 2000b;Dudai 2004). The focus of...

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Section: Learning and Memory 493mentioning

confidence: 98%

Retrieval failure versus memory loss in experimental amnesia: Definitions and processes

Miller

Matzel²

2006

Learn. Mem.

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“…These novel results showing that the RAs observed for both a reactivated memory and an extinction memory are reversible by reexposing the rats to the amnestic agent CHX can be accounted for by using a retrieval failure view of RA that invokes a postextinction state dependent effect (Hinderliter et al 1975;Millin et al 2001;Riccio et al 2003Riccio et al , 2006. According to this MSDR theory of RA, there is a short period after memory reactivation and extinction learning when the new information is processed.…”

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confidence: 99%

“…That old, well-established memories are once again vulnerable when activated challenges the storage failure view; however, other problematic evidence comes from findings that reexposure to the amnestic agent prior to testing alleviates RA (Thompson and Neely 1970;Hinderliter et al 1975;Mactutus and Riccio 1978;Bradley and Galal 1988;Millin and Newman 2008). This reversibility of RA favors a retrieval failure view of forgetting, which suggests forgetting is due to the inability to access the information that has been stored.…”

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confidence: 99%

“…Accordingly, since the forgotten information can be recovered when the appropriate cues are provided just prior to test (i.e., reexposure to the amnestic agent), the information was presumably stored and the RA results from the inability to access the information because of the lack of appropriate retrieval cues (Spear 1978;Riccio et al 2003Riccio et al , 2006. This retrieval failure view has been described using a modified state dependent retention (MSDR) theory of RA first proposed by Hinderliter et al (1975) (see also Millin et al 2001;Riccio et al 2003Riccio et al , 2006. Hinderliter et al (1975) demonstrated that RA for a Pavlovian fear-conditioning task produced by hypothermia could be reversed by recooling the amnestic rats prior to testing.…”

mentioning

confidence: 99%

“…This retrieval failure view has been described using a modified state dependent retention (MSDR) theory of RA first proposed by Hinderliter et al (1975) (see also Millin et al 2001;Riccio et al 2003Riccio et al , 2006. Hinderliter et al (1975) demonstrated that RA for a Pavlovian fear-conditioning task produced by hypothermia could be reversed by recooling the amnestic rats prior to testing. The results were explained by the MSDR view, which posits that when an amnestic agent (e.g., hypothermia) is administered during the processing or consolidation of the learned information, the information becomes encoded in the altered internal state (e.g., cool state).…”

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confidence: 99%

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Reexposure to the amnestic agent alleviates cycloheximide-induced retrograde amnesia for reactivated and extinction memories

Briggs

Olson

2013

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We investigated whether reexposure to an amnestic agent would reverse amnesia for extinction of learned fear similar to that of a reactivated memory. When cycloheximide (CHX) was administered immediately after a brief cue-induced memory reactivation (15 sec) and an extended extinction session (12 min) rats showed retrograde amnesia for both memories. CHX did not produce amnesia for a moderate extinction session (6 min). Re-administering CHX before testing reversed the amnestic effect for both memories (i.e., the memories were recovered). These results are discussed using a modified state dependent model of retrograde amnesia.

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A synaptic reinforcement‐based model for transient amnesia following disruptions of memory consolidation and reconsolidation

et al. 2008

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The observation of memory recovery following post-training amnestic interventions has historically caused controversy over the meaning of this finding, leading some authors to question the paradigm of a consolidation period for memories. Similarly, recent demonstrations of transient amnesia caused by interventions following memory reactivation have been used to question the existence of a retrieval-driven reconsolidation process. The present work aims to approach the phenomenon of transient amnesia following disruptions of consolidation and reconsolidation, discussing how memory recovery might be explained within a framework of systems consolidation, persistent synaptic reinforcement, and multiple memory traces. With these concepts in mind, we propose that long-term consolidation processes can underlie recovery from amnesia, demonstrating the feasibility of such a hypothesis in a two-structure computational model of learning in which consolidation is dependent upon synaptic reentry reinforcement. On the basis of this, we suggest that prolonged consolidation can account for experimental findings of transient amnesia, in a way that explains differences between disruptions of consolidation and reconsolidation without the need to dwell into the discussion between storage- and retrieval-based explanations for memory impairment.

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Amnesia induced by hypothermia as a function of treatment-test interval and recooling in rats

Cited by 77 publications

References 20 publications

Retrieval failure versus memory loss in experimental amnesia: Definitions and processes

Retrieval failure versus memory loss in experimental amnesia: Definitions and processes

Reexposure to the amnestic agent alleviates cycloheximide-induced retrograde amnesia for reactivated and extinction memories

A synaptic reinforcement‐based model for transient amnesia following disruptions of memory consolidation and reconsolidation

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