Retrograde Amnesia and the "Reminder Effect": An Alternative Interpretation

Gold, Paul E.; Haycock, John W.; Macri, John; McGaugh, James L.

doi:10.1126/science.180.4091.1199

Cited by 71 publications

(53 citation statements)

References 11 publications

(7 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Second, if the systemic anisomycin injections produced specific effects in the study by Lattal and Abel (2004), it is well established that the probability of recovery from consolidation blockade is an inverse function of the behavioral impairment induced by the amnesic treatment (Cherkin, 1972;Gold et al, 1973;Davis and Rosenzweig, 1978). This increased tendency to observe recovery from smaller behavioral impairments can explain the differential recovery in the study by Lattal and Abel (2004).…”

Section: Discussionmentioning

confidence: 87%

“…This is because it is unclear whether the observed recovery from the reconsolidation impairment occurred because of the different levels of amnesia between the reconsolidation and consolidation experiments or whether recovery is more likely to result from a reconsolidation impairment, regardless of how profound the amnesia is. Given that it is already established that recovery from consolidation blockade is a function of the magnitude of amnesia (Cherkin, 1972;Gold et al, 1973;Davis and Rosenzweig, 1978), the former interpretation would seem most likely. We should not forget that there are some reports of spontaneous recovery from amnesia induced by consolidation blockade (Kohlenberg and Trabasso, 1968;Quartermain and McEwen, 1970;Serota, 1971;Young and Galluscio, 1971).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Characterization of Fear Memory Reconsolidation

Duvarci¹,

Nader²

2004

J. Neurosci.

352

293

View full text Add to dashboard Cite

Reactivation of consolidated memories returns them to a protein synthesis-dependent state. One interpretation of these findings is that the memory reconsolidates after use. Two alternative interpretations are that protein synthesis inhibition facilitates extinction and that postreactivation protein synthesis inhibition leads to an inability to retrieve the consolidated memory. First, using two different approaches, we report that reconsolidation cannot be reduced down to facilitated extinction. We show that the reconsolidation deficit does not show renewal after a contextual shift, whereas an extinguished auditory fear memory does under the same conditions and the deficit occurs regardless of whether the memory is reactivated with an extinction [conditioned stimulus (CS) alone] or a reinforced trial (CS-unconditioned stimulus). To address the issue of whether postreactivation anisomycin leads to an inability to retrieve the consolidated memory, we used two traditional assays for retrieval deficits. First, we demonstrate that the amnesia induced by blockade of reconsolidation does not show any spontaneous recovery. Second, we show that application of reminder shock does not result in the reinstatement of the memory. These findings support the idea that reactivation of consolidated memories initiates a second timedependent memory formation process.

show abstract

Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Characterization of Fear Memory Reconsolidation

Duvarci¹,

Nader²

2004

J. Neurosci.

352

293

View full text Add to dashboard Cite

show abstract

“…"Experimental amnesia is viewed as a failure to retrieve information from longterm memory rather than a failure of the information to be consolidated in long-term memory." Yet attenuation of amnesia by reminder treatments does not contradict a storage view of amnesia (Cherkin 1972;Gold et al 1973;Haycock et al 1973). An amnestic treatment need not have an all-or-none effect, and a reminder treatment might summate with a weak memory to raise it above threshold for behavioral expression.…”

Section: Reminder Treatmentsmentioning

confidence: 99%

“…Yet these weakly trained animals, similar to the animals with ECS-produced amnesia, improved their performance scores following the noncontingent footshock. As Gold et al (1973) wrote: ". .…”

Section: Reminder Treatmentsmentioning

confidence: 99%

See 1 more Smart Citation

Lost forever or temporarily misplaced? The long debate about the nature of memory impairment

Squire

2006

Learn. Mem.

View full text Add to dashboard Cite

Studies of memory impairment in humans and experimental animals have been fundamental to learning about the organization of memory and its cellular and molecular substrates. When memory impairment occurs, especially after perturbations of the nervous system, the question inevitably arises whether the impairment reflects impaired information storage or impaired accessibility. This topic has been the subject of considerable commentary and experimental work over the years. In this reappraisal, I first consider four broad areas of behavioral study from the 1970s and 1980s that led to a dominant and compelling view of memory impairment as a deficit of information storage. Second, I identify some ambiguities that arise about how the terms “storage” and “retrieval” are applied, especially when the evidence is somewhat indirect and based on a behavioral-psychological level of analysis. I then review neurobiological findings that have been largely overlooked in these discussions. The relevant studies are ones where it has been possible to monitor neurons and synapses in direct relation to behavioral memory, for example, in animals with simple nervous systems and in single cell recordings from behaving monkeys. This work provides a straightforward and illuminating perspective on the question and confirms the view that first emerged from less direct evidence.

show abstract