Anisomycin, an Inhibitor of Protein Synthesis, …

At the most basic level, these findings suggest that consolidation and reconsolidation are qualitatively different processes. For a reconsolidation account of memory to be viable, it will have to incorporate a mechanism that allows the original memory to be unaffected by manipulations after retrieval, which may mean abandoning the fundamental assumption that initial acquisition and retrieval act on the same underlying process. At the very least, one needs to be cautious about using the term “reconsolidation,” which inherently implies that the processes that occur after retrieval affect the consolidation of the original memory through the same consolidation process that operates after acquisition. Our experiments suggest that this is not true for the specific case of protein synthesis inhibition and contextual freezing. On a more general level, it is important to emphasize that a number of experiments using different preparations and manipulations, including anisomycin injections, have found recovery (, , -). These findings, however, have not been central to the recent development of reconsolidation theories, as others have noted (, ). Certainly, spontaneous recovery effects and the general idea that the original memory is preserved after postretrieval manipulations need to be incorporated into future theorizing and experimentation on reconsolidation.

Protein Synthesis and Memory - Springer

Anisomycin interferes with protein and DNA synthesis by inhibiting  or the 80S  system.

17/04/2014 · Protein Synthesis and ..

Anisomycin induces apoptosis of glucocorticoid resistant acute lymphoblastic leukemia CEM-C1 cells via activation of mitogen-activated protein kinases p38 and JNK.

An antibiotic that inhibits protein and DNA synthesis .

Although our results suggest that deficits caused by protein synthesis inhibition after memory retrieval reverse with time, deficits observed after initial acquisition appear to be long-lasting. This long-lasting impairment in acquisition has been observed in other studies with repeated anisomycin injections (), and the difference in persistence between initial acquisition and retrieval deficits also has been observed with other manipulations (, ). Of course, it is possible that the original acquisition memory was intact, but our method of unmasking that memory was unable to detect it. Indeed, as with putative deficits in reconsolidation, it is important to realize that there is no simple isomorphic relation between behavior and memory, meaning that the absence of a behavior should not by itself be taken as evidence for the absence of a memory. What is clear from our experiments is that the 21-day retention interval, although long enough to reverse a deficit after context retrieval, did not reverse a deficit after initial acquisition. These findings suggest that, at the very least, the effects of protein synthesis inhibition after acquisition and retrieval are quite different (, ).

c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) is required for mitoxantrone- and anisomycin-induced apoptosis in HL-60 cells.
T1 - Inhibition of protein synthesis and JNK activation are not required for cell death induced by anisomycin and anisomycin analogues

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N2 - The effects of anisomycin on dyskinetic head movements, circling, and locomotor activity were investigated in the IDPN-induced syndrome. Intracerebroventricular (ICV) injections of anisomycin in conjunction with IDPN caused exacerbation of all aspects of the syndrome, although circling and vertical head dyskinesias (retrocollis) were the most affected. Animals treated with only anisomycin showed persistent retrocollis but not latercollis or circling. Biochemical studies confirmed the increases in the concentration of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) previously observed in the striata of IDPN-treated rats two weeks after stopping administration of the drug. Rats treated with anisomycin alone also showed significant increases in striatal 5-HT and 5-HIAA concentrations which were somewhat higher on the side of the ICV infusions. Coadministration of IDPN and anisomycin did not cause any further increases in 5-HT or 5-HIAA. These results suggest that inhibition of protien synthesis by IDPN may be one of the processes involved in the development of the persistent dyskinetic syndrome.

Synergistic induction of TRAIL-mediated apoptosis by anisomycin in human hepatoma cells via the BH3-only protein Bid and c-Jun/AP-1 signaling pathway.

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Molecular accounts of memory suggest that memories are moved from a labile to a more fixed state in a protein synthesis-dependent consolidation process (-). Many experiments have demonstrated a role for protein synthesis during the consolidation of the learning that occurs after acquisition of a behavioral task, such as Pavlovian conditioning, in which a conditioned stimulus (such as a tone or a conditioning context) is paired with an unconditioned stimulus (such as a footshock; refs. and ). It also has been suggested that retrieval of the original association during reexposure to the conditioned stimulus induces another period of consolidation in which protein synthesis is needed for the original memory to be reconsolidated into a fixed state (, ). From this reconsolidation perspective, protein synthesis inhibition after retrieval, just like protein synthesis inhibition after acquisition, results in deficits in the consolidation of the original memory. The challenge for a reconsolidation account of memory is to demonstrate that impairments in behavior correspond to deficits in memory storage.

T1 - The protein synthesis inhibitor, anisomycin, causes exacerbation of the iminodipropionitrile-induced spasmodic dyskinetic syndrome in rats

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Administration of the protein synthesis inhibitor, anisomycin, induced both advance and delay phase-shifts in the circadian rhythm of locomotor activity in hamsters maintained in constant darkness. The magnitude and direction of the phase shift was dependent on the circadian time of drug treatment. A second protein synthesis inhibitor, cycloheximide, also induced phase-shifts in the circadian rhythm of activity, while two drugs which mimic some of the side effects of protein synthesis inhibitors had no significant effect on the activity rhythm. The phase-response curve generated by anisomycin injections in the hamster is similar to the response curves that have been measured for protein synthesis inhibitors in micro-organisms and invertebrates. Thus, the biochemical mechanisms generating circadian oscillations in mammals may share common features with those found in very distantly related phylogenetic groups.