scholarly journals Different Training Procedures Recruit Either One or Two Critical Periods for Contextual Memory Consolidation, Each of Which Requires Protein Synthesis and PKA

1998 ◽  
Vol 5 (4) ◽  
pp. 365-374 ◽  
Author(s):  
Roussoudan Bourtchouladze ◽  
Ted Abel ◽  
Nathaniel Berman ◽  
Rachael Gordon ◽  
Kyle Lapidus ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Time Course ◽  
Contextual Fear Conditioning ◽  
Long Term Memory ◽  
Protein Synthesis Inhibitor ◽  
Critical Periods ◽  
Synthesis Inhibitor ◽  
Contextual Memory ◽  
Contextual Fear

We have used a combined genetic and pharmacological approach to define the time course of the requirement for protein kinase A (PKA) and protein synthesis in long-term memory for contextual fear conditioning in mice. The time course of amnesia in transgenic mice that express R(AB) and have genetically reduced PKA activity in the hippocampus parallels that observed both in mice treated with inhibitors of PKA and mice treated with inhibitors of protein synthesis. This PKA- and protein synthesis-dependent memory develops between 1 hr and 3 hr after training. By injecting the protein synthesis inhibitor anisomycin or the PKA inhibitor Rp-cAMPs at various times after training, we find that depending on the nature of training, contextual memory has either one or two brief consolidation periods requiring synthesis of new proteins, and each of these also requires PKA. Weak training shows two time periods of sensitivity to inhibitors of protein synthesis and PKA, whereas stronger training exhibits only one. These studies underscore the parallel dependence of long-term contextual memory on protein synthesis and PKA and suggest that different training protocols may recruit a common signaling pathway in distinct ways.

Enhanced inhibitory avoidance learning prevents the long-term memory-impairing effects of cycloheximide, a protein synthesis inhibitor

2009 ◽  
Vol 91 (3) ◽  
pp. 310-314 ◽  
Author(s):  
Arnulfo Díaz-Trujillo ◽  
Joey Contreras ◽  
Andrea C. Medina ◽  
Gerardo A. Silveyra-Leon ◽  
Anaid Antaramian ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Avoidance Learning ◽  
Inhibitory Avoidance ◽  
Long Term Memory ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor ◽  
Term Memory ◽  
Inhibitory Avoidance Learning

Drug inhibition of memory formation in chickens II. Short-term memory

1971 ◽  
Vol 178 (1053) ◽  
pp. 455-464 ◽  
Keyword(s):  
Protein Synthesis ◽  
Sodium Pump ◽  
Short Term Memory ◽  
Memory Loss ◽  
Protein Synthesis Inhibitor ◽  
Protein Synthesis Inhibitors ◽  
Short Term ◽  
Synthesis Inhibitor ◽  
Term Memory

1. Memory in day-old-chickens during the first few hours after learning can be made to decline by the prior intracranial injection of two classes of drugs. 2. Sodium pump inhibitors in increasing doses cause increasingly rapid loss of memory. 3. Protein synthesis inhibitors in increasing doses attain a maximum potency in causing memory decline and the rate may not be further accelerated by higher doses. 4. Adding a sodium pump inhibitor to the inhibition of protein synthesis increases memory loss. 5. Adding a protein synthesis inhibitor to a sodium pump inhibitor causes no further loss. 6. Therefore within a few minutes of learning a short-term memory of limited time span but independent of protein synthesis becomes supplemented and eventually replaced by a long-term storage requiring protein synthesis. The amount of long-term store is set by the amount of short-term memory. 7. The short-term store could be directly dependent on post-activation enhancement of Na + extrusion from neurons. Some physiological mechanisms by which this could be achieved and how this might activate protein synthesis are discussed.

Memory Reorganization by Synaptic Protein Degradation

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
B.-K. Kaang
Keyword(s):  
Protein Synthesis ◽  
Protein Degradation ◽  
Memory Retrieval ◽  
De Novo ◽  
Critical Role ◽  
Contextual Fear Conditioning ◽  
Synaptic Proteins ◽  
Protein Synthesis Inhibitor ◽  
Synaptic Protein

An accumulating body of evidence shows that the retrieval process of long-term memory is not static and requires de novo protein synthesis. Thus long-term memories are dynamic and particularly become fragile during its retrieval. Importantly, memory retrieval is regarded as a step necessary for incorporating new information into preexisting memories. We have examined whether protein degradation is involved in the memory reorganization or not. In this presentation I will present the evidence that synaptic proteins are degraded by polyubiquitination and proteasome pathway in the hippocampus after the retrieval of contextual fear conditioning. In addition, we found that the infusion of a proteasome inhibitor into the hippocampus prevented the memory impairment induced by anisomycin, a protein synthesis inhibitor. This indicates that ubiquitin/proteasome-dependent protein degradation is involved in destabilization processes accompanying the memory retrieval. It also supports our hypothesis that preexisting memory is disrupted by synaptic protein degradation before updated memory is strengthened by protein synthesis. Our data also showed that synaptic protein degradation plays a critical role in fear memory extinction, a simple form of memory reorganization. Taken together, synaptic protein degradation is critically involved in the reorganization of the preexisting memories.

Protein Synthesis–Dependent and mRNA Synthesis–Independent Intermediate Phase of Memory in Hermissenda

1999 ◽  
Vol 82 (1) ◽  
pp. 495-500 ◽  
Author(s):  
Terry Crow ◽  
Juan-Juan Xue-Bian ◽  
Vilma Siddiqi
Keyword(s):  
Protein Synthesis ◽  
Memory Consolidation ◽  
Transition Period ◽  
Intermediate Phase ◽  
Long Term Memory ◽  
Protein Synthesis Inhibitor ◽  
Mrna Synthesis ◽  
Synthesis Inhibitor ◽  
Short And Long Term ◽  
Mechanisms Of Memory

The conditioned stimulus pathway in Hermissenda has been used to examine the time-dependent mechanisms of memory consolidation following one-trial conditioning. Here we report an intermediate phase of memory consolidation following one-trial conditioning that requires protein synthesis, but not mRNA synthesis. In conditioned animals, enhanced excitability normally expressed during an intermediate phase of memory was reversed by the protein synthesis inhibitor anisomycin, but not by the mRNA synthesis inhibitor 5,6-dichloro-1-β-d-ribobenzimidazole (DRB). Associated with the intermediate phase of memory is an increase in the phosphorylation of a 24-kDa protein. Anisomycin present during the intermediate phase blocked the increased phosphorylation of the 24-kDa phosphoprotein, but did not block the increased phosphorylation of other proteins associated with conditioning or significantly change their baseline phosphorylation. DRB did not reverse enhanced excitability or decrease protein phosphorylation expressed during the intermediate phase of memory formation, but it did reverse enhanced excitability 3.5 h after conditioning. Phosphorylation of the 24-kDa protein may support enhanced excitability during the intermediate phase, in the transition period between short- and long-term memory.

Temporal phases of long-term potentiation (LTP): myth or fact?

2015 ◽  
Vol 26 (5) ◽  
pp. 507-546 ◽  
Author(s):  
Abdul-Karim Abbas ◽  
Agnès Villers ◽  
Laurence Ris
Keyword(s):  
Protein Synthesis ◽  
De Novo ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Long Term Memory ◽  
Protein Synthesis Inhibitor ◽  
Protein Synthesis Inhibitors ◽  
Early Protein ◽  
Term Potentiation

AbstractLong-term potentiation (LTP) remains the most widely accepted model for learning and memory. In accordance with this belief, the temporal differentiation of LTP into early and late phases is accepted as reflecting the differentiation of short-term and long-term memory. Moreover, during the past 30 years, protein synthesis inhibitors have been used to separate the early, protein synthesis-independent (E-LTP) phase and the late, protein synthesis-dependent (L-LTP) phase. However, the role of these proteins has not been formally identified. Additionally, several reports failed to show an effect of protein synthesis inhibitors on LTP. In this review, a detailed analysis of extensive behavioral and electrophysiological data reveals that the presumed correspondence of LTP temporal phases to memory phases is neither experimentally nor theoretically consistent. Moreover, an overview of the time courses of E-LTP in hippocampal slices reveals a wide variability ranging from <1 h to more than 5 h. The existence of all these conflictual findings should lead to a new vision of LTP. We believe that the E-LTP vs. L-LTP distinction, established with protein synthesis inhibitor studies, reflects a false dichotomy. We suggest that the duration of LTP and its dependency on protein synthesis are related to the availability of a set of proteins at synapses and not to the de novo synthesis of plasticity-related proteins. This availability is determined by protein turnover kinetics, which is regulated by previous and ongoing electrical activities and by energy store availability.

scholarly journals Induction of a rapidly responsive hepatic gene product by thyroid hormone requires ongoing protein synthesis.

1987 ◽  
Vol 7 (4) ◽  
pp. 1352-1357 ◽  
Author(s):  
D B Jacoby ◽  
J A Engle ◽  
H C Towle
Keyword(s):  
Protein Synthesis ◽  
Thyroid Hormone ◽  
Time Course ◽  
Primary Response ◽  
Receptor Interaction ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor ◽  
Spot 14 ◽  
Precursor Rna ◽  
Inhibitor Of Protein Synthesis

The regulation of a gene, designated spot 14, which is rapidly induced in rat liver in response to 3,5,3'-triiodo-L-thyronine (T3) was studied as a model for exploring the molecular basis of thyroid hormone action. The time course of induction of the nuclear precursor to spot 14 mRNA after intramuscular injection of T3 displayed a very short lag period of between 10 and 20 min. The rapidity of this effect suggests that the induction in gene expression occurs as a primary response to the hormone-receptor interaction. The protein synthesis inhibitor cycloheximide injected 15 min before T3 completely blocked the accumulation of nuclear precursor RNA 30 min after T3 treatment. Emetine, an inhibitor of protein synthesis which acts by a different mechanism than cycloheximide, also blocked the induction of the spot 14 nuclear precursor RNA. The increased rate of spot 14 gene transcription observed after T3 treatment, as measured by nuclear run-on assay, was similarly completely abolished in the presence of cycloheximide. In addition, ongoing protein synthesis was required for maintaining spot 14 nuclear precursor RNA at induced levels in animals previously treated with T3. On the other hand, cycloheximide had no effect on T3 uptake or binding to the nuclear receptor during the 45-min time frame studied. The paradox of the rapid kinetics of induction and the requirement of ongoing protein synthesis may be explained by a protein with an extremely short half-life which is necessary for T3 induction of the spot 14 gene.

scholarly journals Long-Lasting Effects of GABA Infusion Into the Cerebral Cortex of the Rat

2000 ◽  
Vol 7 (1-2) ◽  
pp. 1-8 ◽  
Author(s):  
Teresa Montiel ◽  
Daniel Almeida ◽  
Iván Arango ◽  
Eduardo Calixto ◽  
César Casasola ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Long Term Potentiation ◽  
Information Storage ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor ◽  
Receptor Stimulation ◽  
Paroxysmal Activity ◽  
The Brain

In electrophysiological terms, experimental models of durable information storage in the brain include long-term potentiation (LTP), long-term depression, and kindling. Protein synthesis correlates with these enduring processes. We propose a fourth example of long-lasting information storage in the brain, which we call the GABA-withdrawal syndrome (GWS). In rats, withdrawal of a chronic intracortical infusion of GABA, a ubiquitous inhibitory neurotransmitter, induced epileptogenesis at the infusion site. This overt GWS lasted for days. Anisomycin, a protein synthesis inhibitor, prevented the appearance of GWSin vivo. Hippocampal and neocortical slices showed a similar post-GABA hyperexcitabilityin vitroand an enhanced susceptibility to LTP induction. One to four months after the epileptic behavior disappeared, systemic administration of a subconvulsant dose of pentylenetetrazol produced the reappearance of paroxysmal activity. The long-lasting effects of tonicGABAAreceptor stimulation may be involved in long-term information storage processes at the cortical level, whereas the cessation ofGABAAreceptor stimulation may be involved in chronic pathological conditions, such as epilepsy. Furthermore, we propose that GWS may represent a common key factor in the addiction to GABAergic agents (for example, barbiturates, benzodiazepines, and ethanol). GWS represents a novel form of neurono-glial plasticity. The mechanisms of this phenomenon remain to be understood.

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