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Protein synthesis requirement of the Aplysia circadian clock. Tested by active and inactive derivatives of the inhibitor anisomycin.

1. The circadian rhythm of compound action potential frequency recorded from the isolated eye of Aplysia in culture medium and darkness was subjected to 6 h pulse treatments with either anisomycin, a protein synthesis inhibitor, or inactive derivatives of anisomycin. 2. Anisomycin caused phase-dependent phase shifts of the rhythm as expected from previous experiments, but none of the derivative molecules caused phase shifts or perturbed the rhythm. 3. Anisomycin inhibited eye-protein synthesis by 75% at the concentrations (10(-6) M) used in the phase shifting experiments but none of the derivatives inhibited synthesis. 4. Only those molecules that actually inhibited protein synthesis caused phase shifts of the clock, although the inactive derivatives differed from anisomycin by only an acetyl group. 5. The results strengthen the conclusion that the inhibition of protein synthesis caused by anisomycin is important in perturbing the timing of the circadian clock and not some other characteristic effect of the inhibitor molecule. Together with the results from other systems, these findings imply that the daily synthesis of protein is a general requirement for circadian clocks.

Animals↗

Critical role of p42/44(MAPK) activation in anisomycin and hepatocyte growth factor-induced LDL receptor expression: activation of Raf-1/Mek-1/p42/44(MAPK) cascade alone is sufficient to induce LDL receptor expression.

The protein synthesis inhibitor anisomycin activates stress-related mitogen-activated protein kinases (MAPKs), namely, c-jun NH(2)-terminal kinase (p46/54(JNK)) and p38(MAPK) in mammalian cells. In this paper, we show that although exposure to anisomycin resulted in rapid and strong activation of p46/54(JNK) and p38(MAPK), with a delayed low level dual-phosphorylation of mitogen/extracellular protein kinase (p42/44(MAPK)), low density lipoprotein (LDL) receptor induction depends solely on the mild activation of p42/44(MAPK) signaling cascade in HepG2 cells. Unlike hepatocyte growth factor (HGF) which caused LDL receptor induction via rapid, strong, and Ras-dependent p42/44(MAPK) activation, anisomycin-induced p42/44(MAPK) activity and increased LDL receptor expression in a Ras-independent manner. Finally, we examined the role of the p42/44(MAPK) signaling cascade in LDL receptor induction by activating this kinase independently of anisomycin or HGF. By using estrogen-dependent human Raf-1 protein kinase in transient transfection assays, we show that the exclusive activation of the Raf-1/MEK-1/p42/44(MAPK) signaling cascade with antiestrogen ICI 182, 780 caused induction of LDL receptor expression to the same level as observed with either HGF or anisomycin. Consistent with the role of p42/44(MAPK), induction was strongly inhibited by pretreatment with the MEK-1/2 inhibitor PD98059. Our observation that anisomycin can use p42/44(MAPK) signaling cascade is a departure from established thinking, and the results presented shows that activation of the p42/44(MAPK) alone is sufficient to fully induce LDL receptor transcription.

Anisomycin↗

Effect of anisomycin on stimulation-induced changes in dendritic spines of the dentate granule cells.

Tetanic stimulation of the entorhinal area induces significant enlargement of the average dendritic spine area and perimeter in the middle and distal thirds of the dentate molecular layer 4 and 90 min following stimulation. Four minutes after stimulation, the differences between the stimulated and control animals were 20% for the dendritic spine area and 9% for the perimeter in the middle third, and in the distal third 32 and 14%, respectively. Ninety minutes after stimulation the differences were 28 and 11% for the area and perimeter in the middle third, and 33 and 18% in the distal third, respectively. Anisomycin at a dose of 25 mg/kg had no significant effect on the average spine area or perimeter in the various thirds of the dentate molecular layer in the 19 and 105 min post-application intervals. This dose of anisomycin given 15 min prior to the stimulation suppresses the stimulation-induced spine changes in the 4 min interval. In the 90 min interval when the effect of anisomycin on protein synthesis is largely terminated, spine enlargement reappears, being 21% higher than the controls in the middle and distal thirds. The differential effect of anisomycin on dendritic spines in the two post-stimulation intervals is discussed in relation to the effect of anisomycin on protein synthesis. The present experiments thus demonstrate that the stimulation-induced spine enlargement in the dentate fascia can be suppressed by a protein synthesis blocking drug.

Animals↗

Phase response curve to anisomycin in tau mutant hamsters.

Administration of the protein synthesis inhibitor, anisomycin, to wild type hamsters produces phase shifts in their circadian rhythms that have similarities to shifts produced by non-photic behavioral stimulation. A mutation that shortens the period of rhythms in hamsters results in altered responsiveness to non-photic input. However, responses of the mutants to anisomycin are unaffected: their phase response curve (PRC) for anisomycin is similar to that of wild types. This suggests that 1) anisomycin is not acting on mechanisms specifically involved in non-photic behavioral phase shifting, and 2) the mutation affects the non-photic input pathway or the pacemaker itself at a point that is upstream from anisomycin's site of action.

Animals↗

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

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 laterocollis 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 protein synthesis by IDPN may be one of the processes involved in the development of the persistent dyskinetic syndrome.

Animals↗

Intrathecal infusions of anisomycin impact the learning deficit but not the learning effect observed in spinal rats that have received instrumental training.

Previous research has shown that spinally transected rats will learn to maintain a flexion response when administered shock contingent upon leg position. In short, a contingency is arranged between shock delivery and leg extension so that Master rats exhibit an increase in flexion duration that lasts throughout the training session. Furthermore, when Master rats are later tested they reacquire the flexion response in fewer trials, indicative of some savings. As a control, a second group of spinal rats (Yoked rats) are given shock irrespective of leg position (noncontingent shock). These animals fail to show the same increase in leg flexion duration. Interestingly, when Yoked rats are later tested with a shock contingency in place, they still fail to learn (learning deficit). The present experiments were designed to determine whether both forms of instrumental learning in spinal animals require de novo protein synthesis. As such, we administered various doses of anisomycin intrathecally prior to training. Additionally, spinal rats were trained and tested either immediately or 24 h after test. We found that only the highest dose of anisomycin (125 microg/microl) had an effect in Yoked animals that were tested 24 h after training. Specifically, the highest dose of anisomycin reversed the learning deficit in those animals. Moreover, anisomycin had a similar effect when administered prior to training and immediately following training, but not 6 h after training. Finally, the results demonstrated that the observed effect of anisomycin was not due to state-dependency.

Animals↗

Ha-Ras sensitizes transformed mouse skin cells to Anisomycin-induced apoptosis.

Efforts have been made to develop a chemoprevention that selectively triggers apoptosis in malignant cancer cells. Here, we demonstrated that a mutated Ha-Ras activity is required in Anisomycin-induced apoptosis in transformed keratinocytes. Anisomycin stimulates JNK activity and apoptosis in oncogenic Ha-Ras positive cells, but not in normal keratinocytes. This effect was demonstrated in stably transfected cells with dominant negative Ha-Ras, that protected transformed cells, and oncogenic Ha-Ras that sensitized non-transformed cells to Anisomycin-induced apoptosis. Lastly, the treatment of cells with inhibitors of the JNK displayed resistance to Anisomycin induced apoptosis. These data suggests that the oncogenic Ha-Ras is important for Anisomycin-induced JNK activation and apoptosis in transformed keratinocytes.

Animals↗

Behavioral impairments caused by injections of the protein synthesis inhibitor anisomycin after contextual retrieval reverse with time.

Recent accounts of memory suggest that retrieval of a learning experience transforms that memory into a labile state that requires a period of protein synthesis to be reconsolidated into a fixed state. In this article, we show that the impairments in behavior caused by the protein synthesis inhibitor anisomycin given after retrieval are temporary and are thus not likely to reflect disruptions in a protein synthesis-dependent reconsolidation process. Mice received injections of anisomycin after either initial acquisition or retrieval of contextual fear conditioning. When anisomycin injections followed acquisition, freezing was impaired during memory tests the next day and 21 days later. When anisomycin injections followed normal retrieval of contextual fear conditioning, freezing was impaired the next day but recovered to levels of control mice when testing occurred 21 days later. This recovery effect occurred after short or long durations of exposure during the retrieval period and was specific to the conditioning context. These results suggest that anisomycin injections after retrieval do not retroactively affect the memory from conditioning.

Animals↗

Two time windows of anisomycin-induced amnesia for inhibitory avoidance training in rats: protection from amnesia by pretraining but not pre-exposure to the task apparatus.

We have studied the effect of training conditions on hippocampal protein synthesis-dependent processes in consolidation of the inhibitory avoidance task. Adult male Wistar rats were trained and tested in a step-down inhibitory avoidance task (0.4 mA foot shock, 24 hr training-test interval). Fifteen minutes before or 0, 3, or 6 hr after training, animals received a 0.8-microl intrahippocampal infusion of the protein-synthesis inhibitor anisomycin (80 microg) or vehicle (PBS, pH 7.4). The infusion of anisomycin impaired retention test performance in animals injected 15 min before and 3 hr after the training session, but not at 0 or 6 h post-training. Pretraining with a low foot shock intensity (0.2 mA) 24 hr before training, prevented the amnestic effect of anisomycin injected at 15 min before or 3 hr after training. However, simple pre-exposure to the inhibitory avoidance apparatus did not alter the amestic effects of anisomycin. The results suggest that hippocampal protein synthesis is critical in two periods, around the time of, and 3 hr after training. A prior weak training session, however, which does not itself alter step-down latencies, is sufficient to prevent the amnestic effect of anisomycin, suggesting that even if not behaviorally detectable, weak training must be sufficient to produce some lasting cellular expression of the experience.

Age Factors↗

Blockade of progesterone-activated estrous behavior in rats by intracerebral anisomycin is site specific.

The hypothesis that progesterone (P) activates estrous behavior in estrogen-primed female rats via a protein synthetic mechanism was examined. The protein synthesis inhibitor anisomycin was applied intracerebrally via 28-gauge bilateral implants to neural sites implicated in the mediation of estrous responsiveness. Results showed that anisomycin blockade of P-activated estrous behavior was neural site specific. Animals with anisomycin placed in the ventromedial hypothalamus (VMH) (n = 27) showed low levels of lordosis and solicitation behavior 4 h after the subcutaneous administration of 500 micrograms P, whereas animals with anisomycin implants in the preoptic area (n = 11) or the midbrain area in the region of the interpeduncular nucleus (n = 11) displayed high levels of estrous behavior. No deficits in open-field activity were observed following localized anisomycin treatment, and all animals appeared to be healthy. Results of the present study are consistent with the hypothesis that P acts to promote estrous behavior via a receptor-mediated genomic protein synthetic mechanism, and provide additional evidence that the VMH is the primary site of P action.

Animals↗

p53-independent anisomycin induced G1 arrest and apoptosis in L1210 cell lines.

An L1210 cell line selected for resistance to deoxyadenosine (Y8) has been shown to have barely detectable levels of p53 mRNA and no measurable p53 protein in comparison to the parental mouse wild-type (WT) L1210 cells. We now show that the protein synthesis inhibitors, anisomycin and cycloheximide, arrest WT cells in the G1 phase of the cell cycle and induce apoptosis in Y8 cells via a p53-independent mechanism. There was a decrease in Rb phosphorylation but without the induction of WAF1 protein. Anisomycin treatment activated NF kappa B in the WT cells as early as 0.5 hr after treatment but did not activate NF kappa B in the Y8 cells. Cycloheximide was neither as potent as anisomycin in arresting WT cells at G1 and inducing apoptosis in Y8 cells, nor as potent in decreasing Rb phosphorylation. The finding that caffeine could override the G1 arrest induced by anisomycin and cycloheximide in the WT cells further supports the idea that the effects of anisomycin or cycloheximide on the cell cycle are at the level of cell cycle regulation, and are likely not mediated exclusively through the inhibition of protein synthesis.

Animals↗

The effects of Cycloheximide and Anisomycin on monoamine synthesis in a brain synaptosome preparation.

Cycloheximide (100 mg/kg) and anisomycin (50 mg/kg) decreased the synthesis of [3H]-dopamine (DA) and [3H]-5-hydroxytryptamine (5-TH) from their labelled amino acid precursors in a brain synaptosomal preparation on hour after drug administration in vivo. Treatment with anisomycin also decreased synthesis of [3H]-norepinephrine (NE). Anisomycin (1mM) decreased the accumulation of newly snythesized monoamines when added to the synaptosomal preparation in vitro, while cycloheximide (1mM) impaired only [3H]-norepinephrine formation. All drug-induced decreases in the accumulation of newly synthesized 5-hydroxytryptamine were associated with concomitant decreases in the accumulation of [3H]-tryptophan (Trp) by the synaptosome fraction, suggesting that the drugs may act in part by decreasing precursor availability. However, the same correlation was not observed between [3H]-catecholamine synthesis and [3H]-tyrosine (try) content of the synaptosomal fraction. Comparison of the results obtained after in vivo and in vitro administration of these drugs indicates that cycloheximide may exert many of its effects on monoamine synthesis via a metabolite, while anisomycin appears to act directly.

Animals↗

Effects of anisomycin and CNS stimulants on brain catecholamine synthesis.

Mice were injected with anisomycin, an inhibitor of cerebral protein synthesis; d-amphetamine, strychnine, or caffeine was administered 30 min later. Fifteen min before sacrifice at 1 or 2 hr after injection of anisomycin, 3H-tyrosine was injected intravenously, and catecholamine synthesis rates were estimated by measurement of the specific activity of 3H-tyrosine and the accumulation of 3H-norepinephrine and 3H-dopamine. Anisomycin decreased synthesis rates of catecholamines, but this effect was not significantly affected by any of the CNS stimulants. These results suggest that the recently reported reversal of anisomycin-induced amnesia by these stimulants is not due to an attenuation of brain catecholamine synthesis inhibition.

Animals↗

Anisomycin superinduces annexin V mRNA expression through the ERK1/2 but not the p38 MAP kinase pathway.

Annexin V is a Ca(2+)-dependent phospholipid-binding protein belonging to the annexin family whose regulation is currently not well understood. In this study, we utilized anisomycin, a protein synthesis inhibitor that activates MAP kinases (MAPKs), to examine the role of MAPKs in annexin V expression in the MCAS ovarian carcinoma cell line. A one-step real-time TaqMan-based reverse transcriptase-PCR method was developed to quantify annexin V mRNA expression. We found that annexin V was induced 13.3-fold by anisomycin and that this superinduction was attenuated by pretreatment with the MEK inhibitors, U0126 and PD98059, but not with the p38 MAPK inhibitor, SB203580. In addition, immunoblotting showed that anisomycin stimulated the phosphorylation of ERK1/2 as well as p38 MAPK and that the phosphorylations were blocked by the three kinase inhibitors. Taken together, these results suggest that anisomycin superinduces annexin V mRNA expression through the ERK1/2 MAPK pathway, but not through the p38 MAPK pathway.

Anisomycin↗

Anisomycin, a protein synthesis inhibitor, disrupts traumatic memory consolidation and attenuates posttraumatic stress response in rats.

BACKGROUND: Paradoxical changes in memory represent a troublesome characteristic of posttraumatic stress disorder (PTSD). Exceptionally vivid intrusive memories of some aspects of the trauma are mingled with patchy amnesia regarding other important aspects. Molecular studies of the memory process suggest that the conversion from labile short-term memory into long-term fixed traces involves protein synthesis. This study assessed the effects of administration of anisomycin, a protein synthesis inhibitor, after initial exposure, after exposure to a cue associated with triggering experience, and after reexposure to the triggering trauma in an animal model of PTSD. METHOD: Magnitude of changes in prevalence of anxiety-like behaviors on the elevated plus-maze and nonhabituated exaggerated startle reaction were compared in rats that were exposed to predator stress, with and without microinjection of anisomycin. RESULTS: Microinjection of anisomycin before and after stress exposure reduced anxiety-like and avoidant behavior, reduced the mean startle amplitude, and reversed the stress-induced habituation deficit 7 days later. The persistent anxiety-like behaviors that were seen after stress exposure do not appear to be sensitive to anisomycin after reexposure to a cue associated with the event or after reexposure to the index experience. CONCLUSIONS: Disruption of the process of traumatic memory consolidation may be useful for mitigating PTSD symptoms.

Analysis of Variance↗

Comparison between ischaemic and anisomycin-induced preconditioning: role of p38 MAPK.

To further evaluate the significance of p38 MAPK as trigger or mediator in ischaemic preconditioning, anisomycin and SB 203580 were used to manipulate its activation status. Special attention was given to the concentration of the drugs and protocols used. The isolated perfused rat heart, subjected to either 25 min global ischaemia or 35 min regional ischaemia, was used as experimental model. This was preceded by anisomycin (2 or 5 muM: 3 x 5 min; 5 muM: 5 min or 10 min; 5 muM: 10 min + 10 min washout or 20 muM: 20 min) or SB 203580 (2 muM: 3 x 5 min; before and during 3 x 5 min or 1 x 5 min ischaemic preconditioning; 10 min). Endpoints were functional recovery during reperfusion and infarct size.Anisomycin, regardless of the protocol, reduced infarct size, but did not improve functional recovery. In a number of experiments activation of JNK by anisomycin was blocked by SP 600125 (10 muM). SP 600125 had no effect on the anisomycin-induced reduction in infarct size. SB 203580 when administered for 10 min before sustained ischaemia, improved functional recovery and reduced infarct size. SB 203580 could not abolish the beneficial effects of a multi-cycle preconditioning protocol, but it significantly reduced the outcome of 1 x 5 min preconditioning. In all hearts improved functional recovery and reduction in infarct size were associated with attenuation of p38 MAPK activation during sustained ischaemia-reperfusion. The results indicate that activation of p38 MAPK acts as a trigger of preconditioning, while attenuation of its activation is a prerequisite for improved recovery and a reduction in infarct size.

Animals↗

Effects of ras transformation on the induction of the IL-1 receptor related T1 gene in response to mitogens, anisomycin, IL-1 and TNFalpha.

The T1 gene gives rise to two transcripts encoding a 62 kDa membrane-bound and a 37 kDa secreted protein with similarity to the type I IL-1 receptor. It is weakly expressed in proliferating but not in resting fibroblasts and is strongly induced during the entry of quiescent cells into the cell cycle. Here we show that the T1 gene is also transcriptionally activated in response to the treatment of fibroblasts with cycloheximide and anisomycin. These protein synthesis inhibitors are known to stimulate the JNK and p38/RK signal transduction pathways. We provide evidence that anisomycin triggers T1 gene induction through the stimulation of the p38/RK MAP kinase. This observation is in line with our finding that physiological activators of the p38/RK pathway, the proinflammatory cytokines IL-1 and TNFalpha, stimulate T1 gene expression efficiently. Growth factor mediated T1 gene induction is a delayed early event, requiring ongoing protein synthesis. In contrast, anisomycin induces T1 gene expression at concentrations which block translation completely. Thus, transcriptional induction of the T1 gene via the p38/RK pathway is an immediate early event not requiring de novo protein synthesis. The T1 gene is strongly induced by various mitogens in quiescent NIH3T3 fibroblasts but not in ras transformed NIH3T3 cells. In contrast, all of the three tested agent which activate the p38/RK pathway, IL-1, TNFalpha, and anisomycin led to strong T1 gene expression in normal and ras transformed NIH3T3 cells alike. Thus, the T1 gene can be induced through the activation of at least two MAP kinase pathways: signaling through the ERK pathway can occcur in normal but not in ras transformed NIH3T3 cells, whereas the signaling through the p38/RK pathway is not affected by ras transformation.

3T3 Cells↗

Anisomycin uses multiple mechanisms to stimulate mitogen-activated protein kinases and gene expression and to inhibit neuronal differentiation in PC12 phaeochromocytoma cells.

Treatment of PC12 cells with nerve growth factor (NGF) stimulates extracellular signal-regulated kinases (ERKs), as well as stress-activated c-Jun N-terminal kinases (JNKs) and p38 kinase, and induces neuronal differentiation. While the pivotal role of ERKs in NGF-induced morphological differentiation is well established, the contribution of JNK- and p38-pathways is less clear. The role of the JNK- and p38-pathway in PC12 cells was analysed by using anisomycin, a protein synthesis inhibitor that activates JNKs and p38. Non-toxic concentrations of anisomycin were found to stimulate these enzyme activities as well as the expression of the early response genes c-jun, c-fos and zif268, and to inhibit NGF-induced neurite formation. These effects of anisomycin appear to be mediated by the generation of reactive oxygen species (ROS), which in turn act through both TrkA/Ras-dependent and -independent signalling pathways. In addition, cross-talk between the p38- and ERK-pathways appears to play a role in the action of anisomycin.

Animals↗