The Biochemical Basis of Long-Term Memory

Roberts, Richard B.; Flexner, Louis B.

doi:10.1017/s0033583500000937

Cited by 71 publications

(50 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our findings may provide an explanation for previous conflicting results on memory consolidation and reconsolidation, in which, in some cases, the amnesia produced by protein synthesis inhibitors appeared to be transient (Flexner et al, 1966;Roberts and Flexner, 1969;Judge and Quartermain, 1982;Anokhin et al, 2002;Lattal and Abel, 2004). It is possible that in these cases, the synthesis of proteins essential for the memory stabilization was blocked only transiently, and therefore memory re-emerged at a later time.…”

Section: Different Types Of Memory Reactivationmentioning

confidence: 49%

Persistent Disruption of an Established Morphine Conditioned Place Preference

Milekic¹,

Brown²,

Castellini³

et al. 2006

J. Neurosci.

200

184

View full text Add to dashboard Cite

In human addicts, craving and relapse are frequently evoked by the recall of memories connected to a drug experience. Established memories can become labile if recalled and can then be disrupted by several interfering events and pharmacological treatments, including inhibition of protein synthesis. Thus, reactivation of mnemonic traces provides an opportunity for disrupting memories that contribute to pathological states. Here, we tested whether the memory of a drug experience can be weakened by inhibiting protein synthesis after the reactivation of its trace. We found that an established morphine conditioned place preference (mCPP) was persistently disrupted if protein synthesis was blocked by either anisomycin or cycloheximide after the representation of a conditioning session. Unlike other types of memories, an established mCPP did not become labile after contextual recall, but required the concomitant re-experience of both the conditioning context and the drug. An established mCPP was disrupted after the conditioning session if protein synthesis was blocked selectively in the hippocampus, basolateral amygdala, or nucleus accumbens but not in the ventral tegmental area. This disruption seems to be permanent, because the preference did not return after further conditioning. Thus, established memories induced by a drug of abuse can be persistently disrupted after reactivation of the conditioning experience.

show abstract

Section: Different Types Of Memory Reactivationmentioning

confidence: 49%

Persistent Disruption of an Established Morphine Conditioned Place Preference

Milekic¹,

Brown²,

Castellini³

et al. 2006

J. Neurosci.

200

184

View full text Add to dashboard Cite

show abstract

“…As has been described in greater detail in a prior publication from our research group (Roberson and Sweatt 1999;Sweatt 2003), we are able to deduce that a certain, specific type of chemical reaction must be involved in long-term memory maintenance in order to overcome the problem of constant molecular turnover. This reaction has the following general form: X + X* → X* + X* In this equation, a mechanism associated with learning initially converts X from its basal state to an activated form (X*).…”

Section: Molecular Approach To Reconsolidationmentioning

confidence: 75%

Amnesia or retrieval deficit? Implications of a molecular approach to the question of reconsolidation

Miller¹,

Sweatt²

2006

Learn. Mem.

View full text Add to dashboard Cite

Post-retrieval interference with a memory has uncovered a phenomenon known to the field as reconsolidation. In this article, we will review the specific molecular mechanisms that have been implicated in reconsolidation. As a result of numerous studies over the past five years, it can now be said with a fair amount of certainty that reconsolidation is not a recapitulation of the mechanisms underlying consolidation, despite what the term “reconsolidation” may suggest. Therefore, in addition to reviewing the known mechanisms of reconsolidation, we will propose that two experimental approaches involving the targeting of specific molecular mechanisms, and the study of these mechanisms during retrieval, may serve useful to the field as it is now able to advance beyond comparisons between consolidation and reconsolidation.

show abstract

“…Even longterm structural changes whose initiation requires altered protein synthesis require an ongoing reinforcement mechanism that is self-perpetuating. This principle is discussed in more detail by Roberson andSweatt (1999), andSweatt (2003). Thus, there is no distinction along this line between protein synthesis-dependent models and the model of Routtenber and Rekart.…”

Section: A Comparison With the Post-translational Model Of Routtenbermentioning

confidence: 99%

Altered protein synthesis is a trigger for long-term memory formation

Klann

Sweatt

2008

Neurobiology of Learning and Memory

View full text Add to dashboard Cite

SummaryThere is ongoing debate concerning whether new protein synthesis is necessary for, or even contributes to, memory formation and storage. This review summarizes a contemporary model proposing a role for altered protein synthesis in memory formation and its subsequent stabilization. One defining aspect of the model is that altered protein synthesis serves as a trigger for memory consolidation. Thus, we propose that specific alterations in the pattern of neuronal protein translation serve as an initial event in long-term memory formation. These specific alterations in protein readout result in the formation of a protein complex that then serves as a nidus for subsequent perpetuating reinforcement by a positive feedback mechanism. The model proposes this scenario as a minimal but requisite component for long-term memory formation. Our description specifies three aspects of prevailing scenarios for the role of altered protein synthesis in memory that we feel will help clarify what, precisely, is typically proposed as the role for protein translation in memory formation. First, that a relatively short initial time window exists wherein specific alterations in the pattern of proteins translated (not overall protein synthesis) is involved in initializing the engram. Second, that a selfperpetuating positive feedback mechanism maintains the altered pattern of protein expression (synthesis or recruitment) locally. Third, that other than the formation and subsequent perpetuation of the unique initializing proteins, ongoing constitutive protein synthesis is all that is minimally necessary for formation and maintenance of the engram. We feel that a clear delineation of these three principles will assist in interpreting the available experimental data, and propose that the available data are consistent with a role for protein synthesis in memory.

show abstract

The Biochemical Basis of Long-Term Memory

Cited by 71 publications

References 54 publications

Persistent Disruption of an Established Morphine Conditioned Place Preference

Persistent Disruption of an Established Morphine Conditioned Place Preference

Amnesia or retrieval deficit? Implications of a molecular approach to the question of reconsolidation

Altered protein synthesis is a trigger for long-term memory formation

Contact Info

Product

Resources

About