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E L Bennett

Publications and source records attributed to E L Bennett.

At least 37 records · Page 2Linked to original sources
PubMed1988

Time courses of amnesia development in two areas of the chick forebrain.

The roles of different forebrain structures in stages of memory formation were investigated by injecting agents into either the left medial hyperstriatum ventrale (MHV) or right lateral neostriatum (LNS) close to the time of one-trial taste-avoidance training. With L-glutamate injected into either the left MHV or right LNS 5 minutes pretraining, retention was good 1 minute posttraining but significantly impaired at 5 minutes and each subsequent time point. With emetine injected into either area, retention was still good 60 minutes posttraining but significantly impaired at 90 minutes. With ouabain, retention declined more slowly following injection into the right LNS (at 45 minutes) compared to injection in the left MHV (at 30 minutes). A second experiment confirmed the regional difference in amnesia development produced by ouabain. These results indicate that the duration of short-term memory is longer following inhibition of intermediate-term memory (ITM) in the right LNS, compared to inhibition of ITM in the left MHV.

Animals↗
PubMed1987

Investigations into the neuropharmacological basis of temporal stages of memory formation in mice trained in an active avoidance task.

The memorial effects of glutamate, LaCl3, ouabain, or anisomycin injection around the time of active avoidance training in mice were assessed in this study. Based on the Gibbs and Ng hypothesis of memory formation in chicks (Biobehav. Rev., 1 [1977] 113-136), it was predicted that these pharmacological agents would not only induce significant amnesia but, more specifically, short duration memory should be selectively impaired by glutamate and LaCl3, intermediate duration memory should be impaired by ouabain, and anisomycin should affect only long-lasting memories. Results of the experiments described below indicate these drugs are potent inhibitors of memory formation in rodents. In addition, LaCl3-induced amnesia was fully prevented by CaCl2. However, the mechanism by which glutamate and ouabain affected memory may not be exactly as described by Gibbs and Ng: gamma-D-glutamylglycine and diphenylhydantoin did not completely prevent glutamate- and ouabain-induced amnesias, respectively. Finally, all amnestic agents induced amnesia that developed within minutes of training, and the time course of development of amnesia for each drug could not be distinguished from one another. These data are discussed in terms of their implications for the Gibbs and Ng model of memory formation.

Animals↗
PubMed1987

Anisomycin impairs long-term working memory in a delayed alternation task.

A long-term temporal component of working memory of rats trained on the radial maze has been shown to be susceptible to disruption by the protein synthesis inhibitor, anisomycin. It is not clear whether protein synthesis played a role in working memory because accurate performance on the radial maze required the storage of a large amount of information, or because the information was to be held in store for relatively long periods of time. This experiment tested these hypotheses by assessing the effect of anisomycin on choice accuracy in a comparatively simple spatial delayed alternation task. Results indicate that under the present training conditions, protein involvement in working memory is related more to the length of the retention interval than to the amount of information retained.

Animals↗
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↗
PubMed1987

Short- and long-term components of working memory in the rat.

Previous experiments suggested that working memory of rats trained on a radial maze can be discussed in terms of its short- and long-term temporal components. For example, in Mizumori, Channon, Rosenzweig, and Bennett's (1985) study, long-term working memory was found to be susceptible to disruption by the protein synthesis inhibitor anisomycin (ANI). In Experiment 1 of this report, we examined the neuropharmacological nature of short-term working memory of rats trained to retrieve food from all arms of a 12-arm radial maze. Delay intervals of varying length were placed between Choices 6 and 7. Lanthanum (LaCl3) and glutamate (GLU) injected bilaterally into the hippocampus effectively impaired retention over short delay intervals, which suggests a possible role for calcium and/or potassium and for glutamate in working memory. However, another equally likely explanation for the amnesic effects of LaCl3 and GLU is that these drugs impaired reference memory. To test more directly the hypothesis that LaCl3, GLU, or ANI might differentially affect working and reference memory, we tested the effects of these drugs on performance of rats trained to retrieve food from only 8 arms of the 12-arm maze in Experiment 2. The remaining 4 arms were never baited, in order to test reference memory function. We predicted that rats would make errors only in baited arms (i.e., errors of working memory). Instead, results of Experiment 2 showed that LaCl3, GLU, or ANI injection produced errors in unbaited arms even before a 120-min delay. If rats were injected with LaCl3 or GLU, baited-arm errors were observed only after the delay period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Neurochemical and behavioral effects of catecholamine and protein synthesis inhibitors in mice.

A series of biochemical and behavioral experiments tested the hypothesis that anisomycin (ANI), a protein synthesis inhibitor, produced decrements in long-term memory by raising free tyrosine levels and by the accumulation of catecholamines (CAs) rather than by its primary effect on protein synthesis. We compared the effects of ANI and three catecholamine synthesis inhibitors (CAIs)--diethyldithiocarbamic acid, alpha-methyl-p-tyrosine, and tetrabenazine--on cerebral concentrations of tyrosine and CAs and on the rate of accumulation of CAs. ANI had a relatively small effect, whereas the CAIs resulted in large reductions. When ANI and a CAI were used in combination, effects on CA levels were determined mainly by the CAI. The amnestic effects of ANI and the CAIs were also compared across seven experimental paradigms. Pretraining administration of any of the four drugs could result in amnesia for passive avoidance training, but only when training was weak. With an increase in training strength, a series of three injections of ANI (one pre- and two post-training) caused amnesia, but a similar series of CAI injections did not. Substituting one CAI injection for the second of three successive ANI injections did not cause amnesia, but substituting cycloheximide, another protein synthesis inhibitor, resulted in amnesia. With an active avoidance test, ANI caused amnesia while AMPT did not; d-amphetamine blocked the amnestic effect of ANI but caused amnesia in AMPT injected mice. Whereas ANI lengthened the temporal gradient over which electroconvulsive shock produced amnesia, AMPT or DDC did not. DDC caused only transient amnesia for passive avoidance training, while the amnestic effect of ANI remained constant at 24-hr and 1-week retention tests. We conclude that ANI and CAIs have distinctly different abilities to produce amnesia. These experiments provide additional support for the hypothesis that protein synthesis is required for formation of long-term memory.

Amnesia↗
PubMed1986

Memory stages and brain asymmetry in chick learning.

Stages of formation of memory and the roles of different forebrain structures in memory formation were investigated by injecting various agents into the brains of chicks close to the time of peck-avoidance training. With L-glutamate injected bilaterally into the hyperstriatum 5 min pretraining, retention was good 1 min posttraining but significantly impaired at 5 min and each subsequent time point from 10 min to 24 hr. With ouabain, retention declined more slowly, showing significant impairment at 15 min and thereafter. With any of three protein synthesis inhibitors (anisomycin, cycloheximide, or emetine), retention was still good 60 min posttraining but significantly impaired at 90 min. The three time courses of decline of retention are consistent with hypotheses of three sequentially dependent stages of memory formation. Glutamate, ouabain, and emetine were found to affect only a restricted volume of tissue. Any of these three agents induced amnesia when injected into the left (but not the right) medial hyperstriatum ventrale or into the right (but not the left) lateral neostriatum; so it appears that both structures are required for formation of memory. Agents that are specific for a presumed stage of memory formation and whose action is restricted spatially should help reveal the roles of different brain structures in different stages of memory formation.

Animals↗
PubMed1986

Environmental correlates of ranging behaviour in the banded langur, Presbytis melalophos.

Data are presented from a long-term study of banded langurs in three contrasting rain forest habitats in Peninsular Malaysia. Results from different sites and months are used to correlate ranging patterns with food availability and other environmental variables. Day range lengths are correlated with availability of preferred foods; the degree of territoriality is related to the distribution and size of food sources and length of time for which any one of these produces favoured food items.

Animals↗
PubMed1985

Effects of dietary choline on memory and brain chemistry in aged mice.

The purpose of this study was to investigate in more detail the characteristics of the age-related extension of the retrograde amnesia gradient previously demonstrated in a passive avoidance task [6]. In Experiment 1, it was found that while 2-3 month old mice were susceptible to the amnesic effects of anisomycin (ANI) only when given prior to 15 min post-training, memory of 14-16 month old mice was susceptible to disruption when ANI was given as late as 20 min post-training, and retention of 17-20 month old mice was impaired when ANI was injected even as late as 30 min after training. Experiment 2 examined whether the age-related change in susceptibility to the effects of ANI could be ameliorated by chronic pretreatment with a choline-enriched diet. Results showed that ANI injected 20 min after training did not induce amnesia in choline treated mice (14.5 month old), but did induce amnesia when injected 15 min post training. Subsequent assay of choline acetyltransferase (ChAT) and tyrosine hydroxylase (TH) activity showed that choline treatment significantly reduced ChAT activity but did not affect TH activity. It appears that dietary choline treatment can render new long-term memories less susceptible to disruption following training.

Aging↗
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↗
PubMed1984

Behavioral studies with mice exposed to DC and 60-Hz magnetic fields.

Behavioral measures were evaluated in adult CD-1 and LAF-1 mice continuously exposed for 72 h to a 1.5-Tesla (1 T = 10(4) Gauss) homogeneous DC magnetic field, and in LAF-1 mice continuously exposed for 72 h to a sinusoidal 60-Hz, 1.65-mT (rms) homogeneous AC field. Three types of behavioral tests were employed: (1) Memory of an electroshock-motivated passive avoidance task was assessed in animals that had been trained immediately prior to the field exposure. The strength of memory was varied either by altering the strength of the electric footshock during training, or by administering a cerebral protein synthesis inhibitor, anisomycin, at the time of training. (2) General locomotor activity was measured using a quadrant-crossing test immediately after termination of the magnetic field exposure. (3) Sensitivity of the experimental subjects to the seizure-inducing neuropharmacological agent, pentylenetrazole , was assessed immediately after the field exposure on the basis of three criteria: (a) the percentage of subjects exhibiting a generalized seizure, (b) the mean time to seizure, and (c) the mean seizure level. The results of these studies revealed no behavioral alterations in exposed mice relative to controls in any of the experimental tests with the 1.5-T DC field or the 60-Hz, 1.65-mT (rms) AC field.

Animals↗
PubMed1984

Investigation of the reported protective effect of cycloheximide on memory.

Many findings support the hypothesis that formation of long-term memory requires synthesis of proteins in the nervous system close to the time of learning. This hypothesis has been challenged recently by reports that the protein synthesis inhibitor cycloheximide (CYC) injected 2 hr prior to passive avoidance training in mice or rats attenuated the memory impairment induced by a usually amnestic dose of CYC administered 30 min pretraining. To investigate the reports of a "protective" effect of the prior injection, we attempted to replicate them and test their generality. For replication we administered either paired injections of CYC--120 mg/kg 2 hr prior to training and 30 mg/kg 30 min prior to training--or single injections of CYC (either 120 mg/kg or 30 mg/kg) 30 min pretraining and tested for retention of the passive avoidance habit either 1 or 7 days later. No attenuation of amnesia was observed at 1 day tests. Attenuation of amnesia following the double injection of CYC was observed at 7 day tests. When another protein synthesis inhibitor, anisomycin, was used in the same experimental design, there was no "protective" effect; two injections of anisomycin produced greater memory impairment for the passive avoidance habit than did the single low dose. Also, for active avoidance training, two successive injections of CYC caused significantly greater amnesia than did a single dose; this is the opposite of a "protective" effect. We suggest that the reported "protective" effect of CYC on memory is an as yet unexplained phenomenon that does not generalize to other antibiotic drugs and is specific to the passive avoidance task.

Animals↗
PubMed1983

Increased sodium ion conductance through nicotinic acetylcholine receptor channels in PC12 cells exposed to nerve growth factors.

22Na+ uptake in response to cholinergic stimulation was measured in PC12 cells grown in media containing either beta-nerve growth factor (NGF) from mouse submaxillary gland or a component of Bungarus multicinctus venom (fraction 9B) which has nerve growth factor activity. Our results showed that each of these nerve growth factors increased the Na+ conductance capacity of ACh receptor-linked ion channels in PC12 cells. Compared to untreated cells, Na+ uptake was enhanced by about 40% in cells exposed for 24 to 30 hr to either 50 ng/ml of beta-NGF or to 5 micrograms/ml of fraction 9B. This cholinergically stimulated Na+ flux increased with time and reached a level 2- to 3-fold higher than that of untreated cells after 4 to 6 days' exposure to NGFs. The generation of neurites in response to NGFs from either source occurred with the same time course as the increase in Na+ channel conductance. Growth factor-enhanced Na+ uptake remained for several days after NGFs were removed from cells and neurites were lost. Na+ flux into untreated and into 9B- or beta-NGF-treated cells was inhibited to a greater extent by a nicotinic than by a muscarinic antagonist. Dibutyryl cyclic AMP did not cause an increase in Na+ uptake in response to cholinergic agonists at concentrations which stimulated neurite-like process formation, and dibutyryl cyclic AMP did not potentiate the effects of NGFs.

Animals↗
PubMed1981

Radiolabeled alpha-bungarotoxin derivatives: kinetic interaction with nicotinic acetylcholine receptors.

The binding interactions of purified tritiated [3H]-alpha-Bgt and monoiodinated and diiodinated derivatives of alpha-bungarotoxin with membrane-bound nicotinic acetylcholine receptors (nAChR) from Torpedo californica electroplax and rat brain have been characterized by several kinetic and equilibrium techniques. By all criteria, [3H]-alpha-Bgt and 125I-labeled monoiodinated alpha-Bgt ([125I]-alpha-Bgt) exhibited comparable specificities and affinities for nAChR. In contrast, affinity of nAChR for 125I-labeled diiodinated alpha- Bgt ([125I2]-alpha-Bgt) was reduced, and [125I2]-alpha-Bgt-nAChR complexes showed anomalous biphasic dissociation kinetics. [125I]-alpha-Bgt and [125I2]-alpha-Bgt binding was inhibited most potently by native alpha-Bgt as opposed to iodinated toxins. [3H]- alpha-Bgt was the radiotoxin most resistant to inhibitory influences. The use of well-characterized, chemically modified alpha -Bgt derivatives may identify ligand binding microheterogeneities and tissue-specific receptor subclasses.

Animals↗
PubMed1981

Long-term memory: disruption by inhibitors of protein synthesis and cytoplasmic flow.

Colchicine (60 micrograms/kg), an inhibitor of axoplasmic transport, administered subcutaneously to mice had no detectable effect on retention when given shortly after active avoidance training, nor did a pretraining injection of anisomycin (ANI) have an amnesic effect. However, when ANI was administered shortly prior to training and colchicine was administered after training, retention performance was impaired. The amnesic effect was dependent on the time at which colchicine was administered. The amnesic effect was also obtained when ANI was combined with either vinblastine (6 micrograms/kg) or podophyllotoxin (3 micrograms/kg), drugs that inhibit axoplasmic transport. Intracerebral injections of colchicine (60 ng to 60 pg) caused amnesia in subjects pretreated with ANI, but not in subjects pretreated with saline. Lumicolchicine, an isomer of colchicine, which has similar central nervous system effects but has a low binding affinity for microtubule protein, did not impair retention in ANI pretreated mice. It is suggested that axonal transport of recently synthesized protein is required for long-term memory storage.

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