Antibiotics and memory.

Barraco, Robin A.; Stettner, Laurence J.

doi:10.1037/0033-2909.83.2.242

Cited by 98 publications

(32 citation statements)

References 136 publications

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“…The results obtained with propranolol pretreatment add to extensive evidence that a host of pharmacological agents can rescue memory from the effects of protein synthesis inhibitors (cf. Barraco and Stettner 1976;Martinez et al 1981;Davis and Squire 1984;Routtenberg and Rekart 2005;Gold 2006Gold , 2008. Substantial increases in the release of dopamine and acetylcholine were also seen after anisomycin treatment.…”

Section: Discussionmentioning

confidence: 88%

“…Despite the centrality of experience-induced protein synthesis in contemporary models of memory formation, the necessity of protein synthesis for memory consolidation and long-term potentiation (LTP) stabilization has been questioned since the beginning of experiments of this type (e.g., Flexner and Goodman 1975;Barraco and Stettner 1976;Flood et al 1978;Martinez et al 1981), and continues to be questioned in several recent reviews (Routtenberg and Rekart 2005;Gold 2006Gold , 2008Radulovic and Tronson 2008;Routtenberg 2008;Rudy 2008). There are many instances of intact memories formed in the presence of extensive inhibition of protein synthesis, and a wide range of behavioral and pharmacological manipulations can rescue memory impaired by protein synthesis inhibitors.…”

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confidence: 99%

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Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Qi¹,

Gold²

2009

Learn. Mem.

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Intra-amygdala injections of anisomycin produce large increases in the release of norepinephrine (NE), dopamine (DA), and serotonin in the amygdala. Pretreatment with intra-amygdala injections of the b-adrenergic receptor antagonist propranolol attenuates anisomycin-induced amnesia without reversing the inhibition of protein synthesis, and injections of NE alone produce amnesia. These findings suggest that abnormal neurotransmitter responses may be the basis for amnesia produced by inhibition of protein synthesis. The present experiment extends these findings to the hippocampus and adds acetylcholine (ACh) to the list of neurotransmitters affected by anisomycin. Using in vivo microdialysis at the site of injection, release of NE, DA, and ACh was measured before and after injections of anisomycin into the hippocampus. Anisomycin impaired inhibitory avoidance memory when rats were tested 48 h after training and also produced substantial increases in local release of NE, DA, and ACh. In an additional experiment, pretreatment with intrahippocampal injections of propranolol prior to anisomycin and training significantly attenuated anisomycininduced amnesia. The disruption of neurotransmitter release patterns at the site of injection appears to contribute significantly to the mechanisms underlying amnesia produced by protein synthesis inhibitors, calling into question the dominant interpretation that the amnesia reflects loss of training-initiated protein synthesis necessary for memory formation. Instead, the findings suggest that proteins needed for memory formation are available prior to an experience, and that post-translational modifications of these proteins may be sufficient to enable the formation of new memories.A dominant view of the molecular basis for memory is that the formation of long-term memory for an experience depends on de novo protein synthesis initiated by that experience (Davis and Squire

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Section: Discussionmentioning

confidence: 88%

mentioning

confidence: 99%

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Qi¹,

Gold²

2009

Learn. Mem.

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“…A popular approach involved the systemic infusion of pharmacological protein-synthesis inhibitors (PSIs; for review see Barraco & Stettner, 1976;Davis & Squire, 1984), such as anisomycin (ANI), and cycloheximide (CXM).…”

Section: Protein-synthesis Inhibitorsmentioning

confidence: 99%

Persistence and plasticity in the human memory system: An empirical investigation of the overwriting hypothesis

Hardwicke¹

2017

Preprint

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The human memory system must resolve a critical tension, ensuring that knowledge endures over time (persistence), whilst simultaneously retaining a capacity for updating when knowledge is outdated or erroneous (plasticity). In this thesis, I examine the provocative idea that memory traces can be overwritten with new information, especially during transient periods of retrieval-induced plasticity that occur when a trace undergoes reconsolidation. A systematic review of human reconsolidation studies finds that the evidentiary support for this claim is remarkably tenuous. Furthermore, the theory fails to survive several strong empirical tests. In Experiments 1-7, I do not replicate a previous finding that is widely cited as a convincing demonstration of human reconsolidation. In Experiments 8-10, I revisit the ‘destructive updating’ account of the classic ‘misinformation effect’ in the context of reconsolidation theory. These experiments show that the effect can be eliminated when an appropriate recognition test is used, demonstrating that event traces are not irrecoverably lost, and therefore cannot have been overwritten during reconsolidation. In Experiment 11, I examine whether prior retrieval will help or hinder the correction of naturally occurring semantic misconceptions. Contrary to reconsolidation theory, I find that knowledge updating is not contingent on memory retrieval, nor does it result in the overwriting of prior knowledge.Finally, in the context of media ‘breaking news’ reports (Experiment 12), I find that the provision of an explicit retraction message, coupled with an alternative account with high causal coverage, is insufficient to eliminate reliance on false information. Finally, I contend that the widespread proliferation of ad hoc hypotheses, and the absence of systematic direct replication, has caused the field of reconsolidation to descend into a theoretical quagmire.I make several recommendations based on the principles of open science that may help to restore mechanisms of self-correction and foster genuine theoretical progress.

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“…Studies carried out in the 1970s proved that stronger memories require longer (stronger) inhibition of protein synthesis to be permanently disrupted, suggesting that, in fact, a partial inhibition may exactly be the reason why a transient amnesia can be seen (Barraco & Stettner, 1976;Davis & Rosenzweig, 1978;Flood, Bennett, Orme, & Rosenzweig, 1975;Flood, Rosenzweig, Bennett, & Orme, 1973).…”

Section: Requirement For Protein Synthesis During Memory Formation: Tmentioning

confidence: 99%

The role of protein synthesis during the labile phases of memory: Revisiting the skepticism

Alberini

2008

Neurobiology of Learning and Memory

157

111

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Despite the fact that extensive evidence supports the view that phases of de novo protein synthesis are necessary for memory formation and maintenance, doubts are still raised. Skeptics generally argue that amnesia and the disruption of long-term synaptic plasticity are caused by "non-specific effects" of the reagents or approaches used to disrupt protein synthesis. This paper attempts to clarify some of these issues by reviewing, discussing and providing results addressing some of the major critiques that argue against the idea that de novo protein synthesis is necessary for the stabilization of long-term memory.

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Antibiotics and memory.

Cited by 98 publications

References 136 publications

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Persistence and plasticity in the human memory system: An empirical investigation of the overwriting hypothesis

The role of protein synthesis during the labile phases of memory: Revisiting the skepticism

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