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PubMed1992

Anisomycin and cycloheximide protect cerebellar neurons in culture from anoxia.

Protein synthesis inhibitors have recently been shown to protect from ischemia-induced neuronal death in the rat hippocampus in vivo. In an attempt to further investigate the mechanism of neuronal death resulting from anoxia, cerebellar neurons grown in culture were exposed to an anoxic atmosphere in the presence of protein synthesis inhibitors. Anisomycin and cycloheximide (100 micrograms/ml) offered, respectively, a 97 +/- 4% and 26 +/- 13% protection against anoxia-induced neuronal death.

Animals↗
PubMed1985

Effects of acetoxycycloheximide and anisomycin on approach and escape responses to hypothalamic stimulation.

The effects of acetoxycycloheximide (AXM) (7 mg/kg) and anisomycin (ANI) (25 and 150 mg/kg) on approach and escape responses induced by hypothalamic stimulation were studied in a situation in which male Swiss mice could initiate a continuous brain stimulation train by pressing a lever at one end of a box (ON-lever) and terminate this stimulation train by pressing a lever at the other end of the box (OFF-lever). AXM and ANI induced a large decrease in ON-OFF responses regardless of the level of stimulation presented (a low level just above the stimulation threshold and a high level which was twice the low level). Correspondingly, a significant increase was observed in the mean time during which animals remained unstimulated (NST) whereas mean time during which animals remained stimulated (ST) increased only slightly. The relative NST increase after treatment was always greater than the relative ST increase either at sites where before treatment NST was greater than ST or at sites where NST was shorter than ST. However, the animals in this latter electrode placement group (ST greater than NST) continued to shuttle and to make lever-pressing responses on the ON-lever, whereas the animals in the other placement group (ST less than NST) did not. These results are discussed in terms of possible interactions between disruptions of reinforcing systems induced by protein inhibitors and their effects on memory.

Animals↗
PubMed1982

Alleviation of anisomycin-induced amnesia by pre-test treatment with lysine- vasopressin.

Amnesia in mice for a passive avoidance response induced by anisomycin injection immediately after training was reversed by 40 micrograms of lysine-vasopressin given one hour before testing. Control groups receiving non-contingent shock instead of training were used to demonstrate that the effects of vasopressin were due to memory of shock received in a particular place, rather than non-specific suppression of locomotion. The effects of vasopressin on retention were not mimicked by either pentylenetetrazol or epinephrine suggesting that the enhanced latencies were probably not the result of increases in fear or arousal. These data support the hypothesis that the retrieval of memory can be facilitated by vasopressin. The possibility of a relationship between the effects of vasopressin and those of catecholamine manipulations on memory is discussed.

Animals↗
PubMed1986

The antagonistic effects of naloxone on cycloheximide and anisomycin-induced amnesia.

The amnesia induced by cycloheximide (CXM) injected SC and by CXM or anisomycin injected ICV immediately after the training test was antagonized in combination with an opiate antagonist, naloxone (NLX). This antagonism occurred on both the passive avoidance- and escape-learning responses in a dose-dependent manner in mice. NLX alone (0.3-10.0 mg/kg) did not alter the performances of these tasks. Furthermore, the decrease in retention performance on shuttle avoidance in rats induced by CXM was also antagonized by NLX. Treatment with CXM and/or NLX did not affect spontaneous locomotor activity. The interaction of these drugs on the performance of the passive avoidance- and escape-learning and the shuttle avoidance tasks may be related to neurochemical memory processes. These results suggest that an opioid system may participate in the amnesic actions induced by protein synthesis inhibitors in these models.

Amnesia↗
PubMed1993

Effect of anisomycin on the development of rapid tolerance to ethanol-induced motor impairment.

Male Wistar rats given a single moderate dose (1.7 g/kg, IP) of ethanol (EtOH), followed by six trials on the moving belt apparatus during the next hour, showed functional tolerance to the motor-impairing effects of a second dose given 24 h later if the first EtOH was preceded and followed by an injection of saline. The same EtOH dose and intoxicated practice did not produce tolerance if the saline injections were replaced by two doses of anisomycin (60 mg/kg each, SC) 15 min before and 105 min after the first dose of EtOH. This finding suggests that rapid tolerance, like chronic tolerance, requires de novo synthesis of protein during a short period immediately related to the test experience.

Animals↗
PubMed1989

Anisomycin and amnesia in the chick: state-dependent effects are not present with intracranial injections.

It has recently been suggested that intraperitoneal (IP) injection of anisomycin (ANI) in the chick produces amnesia for a one-trial passive avoidance task in a state-dependent manner. We have examined the behavioral and biochemical effects of IP and intracranial (IC) injections of ANI in chicks trained on a one-trial passive avoidance task. IC injection of ANI produced 35% brain protein synthesis inhibition whereas IP injection produced only negligible amounts of protein synthesis inhibition in the brain. IC injection of ANI produced amnesia and was not state-dependent. Patterns of behavior consistent with state-dependent effects were produced by IP injection of ANI. These experiments indicate that there are differences in the pattern of results produced by IP and IC injection of ANI and support the hypothesis that the expression of long-term memory in chicks is associated with protein synthesis.

Amnesia↗
PubMed1981

Reversal of anisomycin-induced amnesia by the ergot derivative hydergine.

The ergot alkaloid Hydergine was tested for its ability to reverse an amnesia for approach-avoidance training. Thirsty mice were trained to drink in a test chamber and then punished with brief electric shocks for drinking. Those mice injected with the protein-synthesis inhibitor anisomycin immediately after training were amnesic for the shock when tested 48 h later. Pre-test injection of 10.0 or 1.0 mg/kg of Hydergine effectively reversed the amnesia while 0.1 mg/kg was ineffective. Non-contingent shock control groups ruled out the possibility that the effect was due to non-specific effects of the drug or training stimuli.

Amnesia↗
PubMed1986

Anisomycin and cycloheximide, like growth factors, stimulate rapidly ATP turnover in 3T3 cells.

Addition of EGF and insulin to quiescent cultures of 3T3 cells induce a rapid stimulation of ATP turnover. We show that, like growth factors, anisomycin and cycloheximide, two inhibitors of protein synthesis, induce in 3T3 cells, a rapid increase in ATP turnover. However, this effect was not the result of the inhibition of protein synthesis since puromycin, in the same experimental conditions, did not stimulate ATP turnover.

Adenosine Triphosphate↗
PubMed1987

Amnesia produced by anisomycin in an appetitive task is not due to conditioned aversion.

Two experiments investigated the effects of lithium chloride (LiCl) and anisomycin (ANI) in a water reward Y-maze task. In Experiment 1, male CD-1 mice given weak or strong training were injected post-training with either saline or LiCl (150 mg/kg), which has been reported to produce conditioned aversion in mice. One day after training, both LiCl groups avoided the rewarded arm of the maze and drank less water than saline-injected controls. Two days after training, the strongly trained LiCl mice showed avoidance, while both LiCl groups drank less water. In Experiment 2, weakly trained mice given pre- and post-training ANI (30 mg/kg) were amnesic on the second test day compared to mice that received post-trial saline. However, water consumption was increased on the test day for both groups. LiCl produced a different pattern of results than ANI in this task. On the basis of these results, it is suggested that amnesia produced by ANI is due to impaired memory formation and not to conditioned aversion.

Amnesia↗
PubMed2002

Memory for context is impaired by injecting anisomycin into dorsal hippocampus following context exploration.

Pre-exposure to the context facilitates the small amount of contextual fear conditioning that is normally produced by immediate shock. This context pre-exposure facilitation effect provides a convenient way to study the rat's learning about context. We recently reported that anterograde damage to dorsal hippocampus prevents this facilitation. The present experiments strengthen this conclusion by showing that the protein synthesis inhibitor, anisomycin, injected bilaterally into the dorsal hippocampus following context pre-exposure also significantly reduces the facilitation effect. The same treatment given immediately after immediate shock, however, had no effect on facilitation. These results support theories that assume that, (a) contextual fear involves two processes, acquiring and storing a conjunctive representation of a context and associating that representation with fear; and (b) the hippocampus contributes to contextual fear by participating in the storage of the memory representation of the context.

Animals↗
PubMed2005

Stereodivergent syntheses of anisomycin derivatives from D-tyrosine.

[structures: see text] Enantiomerically pure 2-alkyl-3-acetoxy-4-iodopyrrolidines with all groups cis, and all adjacent groups trans (10 and 17), important precursors for the synthesis of pyrrolidinediols, have been prepared from D-tyrosine through regio- and diastereoselective reduction of a vinyl ketone and subsequent iodoamidation controlled by minimization of nonbonding steric interactions. Highly stereodivergent Woodward-Prevost methodology, applied to both iodopyrrolidines, yielded enantiomerically pure (2R,3R,4R)-, (2R,3R,4S)-, and (2R,3S,4R)-deacetylanisomycin (3, 4, and 5), each in excellent de. Incorporation of differential protection of the hydroxyl groups led to a one-pot synthesis of (2R,3R,4R)-anisomycin 2.

Anisomycin↗
PubMed2002

An aldol-based approach to the synthesis of the antibiotic anisomycin.

[reaction: see text] A new approach to the synthesis of the antibiotic anisomycin is reported that relies upon a key aldol disconnection. The glycolate aldol coupling proceeds in 75% yield and with >95% diastereoselectivity, which allows the 13-step synthesis to proceed in 35% overall yield.

Aldehydes↗
PubMed1985

Long-term working memory in the rat: effects of hippocampally applied anisomycin.

The extent to which protein synthesis is involved in working memory was investigated with the protein synthesis inhibitor anisomycin (ANI). Rats were trained to perform accurately on a 12-arm radial maze when delays of 240 min were interposed between choice 6 and choice 7. Bilateral hippocampal cannulas were then implanted. Accuracy on choices 7-12 was studied when ANI or saline was injected either 30 min before choice 1 or 5-10 min after choice 6 (Experiment 1). Pretrial injection of ANI significantly impaired performance following the 240-min delay, whereas ANI injected during the delay had no such effect. In Experiments 2 and 3, the ANI-induced amnesia was replicated, and the temporal course of development of the amnesia was determined. Pretrial administration of ANI did not significantly affect retention after a 2-min delay but did produce amnesia after delays of 15 min or longer. These data suggest that protein synthesis is important for the formation of temporary memories, provided the retention interval is long enough. It is suggested that working memory includes both short-term and long-term components. Protein synthesis appears to be important for formation of the long-term component, but not the short-term component, of working memory.

Animals↗
PubMed2002

Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells to Fas mediated apoptosis.

Treatment of the hormone refractory prostate cancer cell line DU 145 with sublethal concentrations of chemotherapeutic drugs has been reported to sensitise these cells to Fas mediated apoptosis. However, the mechanism by which this occurs has not been determined. Our group has shown that inhibition of JNK activity completely abrogates the effects of chemotherapeutic drugs. Using anisomycin, a potent JNK agonist, we have demonstrated a role for JNK in Fas mediated apoptosis in DU 145 cells. Inhibition of Caspase 8 and Caspase 9 completely inhibits this process which suggests that DU 145 cells require mitochondrial amplification of the Fas apoptotic signal. Furthermore, we have shown that inhibition of Fas mediated apoptosis is an early event in DU 145 cells, occurring upstream of Caspase 8 cleavage. It is hoped that identifying the target of JNK will allow novel therapies to be developed for the treatment of hormone refractory prostate cancer. Such therapies are especially important because no single or combined treatment to date has significantly prolonged survival in patients with hormone refractory prostate cancer.

Anisomycin↗
PubMed2003

Synthetic anisomycin analogues activating the JNK/SAPK1 and p38/SAPK2 pathways.

The synthesis of C(4)H and C(4)Me analogues of the JNK/p38 pathway activator anisomycin, based upon an aldol or Claisen construction of the C(3)-C(4) bond, has been demonstrated. The relative activation of the JNK/SAPK1 and p38/SAPK2 pathways in RAW macrophages by these analogues, and their synthetic precursors, has been assessed using immunoblot assays against phosphorylated c-Jun and MAPKAP-K2. These studies demonstrate that some of the synthetic C(4) analogues are also potent activators of these stress kinase pathways.

Animals↗
PubMed1998

Short communication: long- but not medium-term retention of olfactory memories in honeybees is impaired by actinomycin D and anisomycin.

Although work in a wide variety of species and paradigms has demonstrated that long-term memory is sensitive to the blocking of protein synthesis, previous studies have suggested that the honeybee might represent an exception to this rule. Retention tested one day after training was not impaired by the inhibition of translation by cycloheximide. Using blockers of either transcription (actinomycin D) or translation (anisomycin), we present experiments that reconcile this unusual finding by testing over longer retention periods. Honeybees were conditioned to associate an odourant with a sucrose reward. Typically, this leads to stable retention over days. However, injection of either drug led to lower retention after 4 days, whereas retention after 2 or sometimes even 3 days was unaffected. This dissociates two forms of memory: a protein synthesis-independent, medium-term memory (up to 3 days) and a protein synthesis-dependent, long-term memory lasting for at least 4 days.

Animals↗
PubMed1999

Okadaic acid and anisomycin are protective and stimulate the SAPK/JNK pathway.

We report that okadaic acid (OA), a known inhibitor of Ser/Thr phosphatases, protects pig myocardium against ischemic injury in an in vivo model and stimulates the activities of stress-activated protein kinases/c-Jun N-terminal kinases (SAPKs/JNKs). When OA was directly infused into the subsequently ischemic myocardium for 60 min before a 60-min period of coronary occlusion followed by reperfusion, infarct size was reduced from a control value of 83.4 +/- 2.8% of the risk region to 40.7 +/- 9.1%. When OA was infused for 10 min before a 5-min occlusion and during 45 min thereafter, infarct size was reduced to 26.5%. In a separate set of similar experiments, we pretreated pig hearts in vivo with the protein-synthesis inhibitor and known activator of SAPK/JNK, anisomycin (AN), and found that this compound also significantly reduced infarct size from 83.4 +/- 2.8.1% to 48.1 +/- 5.1%. For in vitro assays, OA (600 nM), AN (500 microM), or solvent (KHB) were locally infused into the left ventricular myocardium, and biopsies from in situ beating hearts were obtained after 10, 30, and 60 min of infusion. The activities of Ser/Thr phosphatases (PPases), especially PP-2A, were significantly decreased after OA infusion. OA infusion increased the activity (in-gel phosphorylation of N-terminal c-Jun1-135) of both 46- and 55-kDa SAPK/JNKs (twofold to threefold, 30 and 60 min of infusion), and this increase correlated well with the observed decrease of PPase activities. Western blot analysis with a phosphospecific SAPK/JNK (Thr 183/Tyr 185) antibody showed an increased content of the phosphorylated forms after OA treatment. We observed significant stimulation of SAPK/JNK activity also after AN treatment (threefold to fourfold, after 30 min of infusion). In contrast to the SAPK/JNKs, the infusion of both OA and AN did not significantly change the activities and phosphorylation of extracellular signal-related kinases (ERKs) and p38-MAPK. The findings that the protective effect of both OA and AN correlates with increased activity of SAPK/JNKs suggest the involvement of these enzymes in the mechanism of cardioprotection.

Animals↗