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Biomedical subjects

E L Bennett

Publications and source records attributed to E L Bennett.

At least 19 recordsLinked to original sources
PubMed1992

Kappa opioid receptor activity modulates memory for peck-avoidance training in the 2-day-old chick.

To examine the role of kappa opioid receptors in memory formation, 2-day-old chicks were injected intracerebrally with either the endogenous opioid peptide dynorphin(1-13), the highly kappa selective agonist U-50,488 or the kappa selective antagonist nor-binaltorphimine (nor-BNI), given one-trial peck-avoidance training, and tested 24 h later. Dynorphin(1-13) impaired memory in a dose dependent manner at 24 h test. Injection of U-50,488 caused a biphasic dose-dependent effect on memory; low doses caused a trend toward enhanced memory and high doses caused significant impairment. Conversely, injection of low doses of nor-BNI caused a trend toward memory impairment, and higher doses caused significant memory enhancement. The results indicate that memory formation for one-trial peck-avoidance training may be modulated by kappa opioid receptor activity.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1992

Comparative study of roles of the lobus parolfactorius and intermediate medial hyperstriatum ventrale in memory formation in the chick brain.

Two discrete areas of the chick brain, the intermediate medial hyperstriatum ventrale (IMHV) and lobus parolfactorius (LPO), were found to have different functions during the formation of memory for a 1-trial peck-avoidance paradigm. Glutamate, ouabain, and emetine, known to disrupt short-, intermediate-, and long-term memory when injected into the IMHV, were injected into the cerebellum and LPO. All amnestic agents investigated produced amnesia when injected into the IMHV; only one of these agents produced amnesia when injected into the LPO, and none of the agents produced amnesia when injected into the cerebellum. The chick brain was also found to exhibit hemispheric asymmetries: The left IMHV and LPO were more sensitive to the amnestic agents than their corresponding right structure. From these data, hypotheses for the roles of these structures during memory are proposed.

Animals↗
PubMed1991

Hydrolysis of [Leu]enkephalin by chick brain in vitro.

Using high-performance liquid chromatography with electrochemical detection to measure substrate disappearance and metabolite accumulation following addition of [Leu]enkephalin to samples prepared from chick brain in vitro, the following were found: 1. [Leu]enkephalin hydrolysis by whole forebrain homogenates is almost solely attributable to aminopeptidase MII activity. 2. [Leu]enkephalin hydrolysis by whole forebrain P2 membrane fractions is attributable to both aminopeptidase MII and dipeptidyl carboxypeptidase activity. 3. Differences are apparent in both [Leu]enkephalin disappearance and Tyr-Gly-Gly accumulation in P2 membrane fractions, but not in homogenate fractions, prepared from several regions of the chick brain.

Aminopeptidases↗
PubMed1991

Hydrolysis of [Leu]enkephalin by chick plasma in vitro.

The in vitro hydrolysis of [Leu]enkephalin added to plasma collected from 2-day-old chicks was studied with two different techniques: thin-layer chromatography separation of intact [3H]-[Leu]enkephalin from its [3H]-Tyr-containing metabolites and high-performance liquid chromatography-electrochemical detection assay of [Leu]enkephalin disappearance and Tyr-containing metabolite accumulation. The radiometric assay evaluated enkephalin hydrolysis at close to presumed physiological concentrations of this peptide, whereas the liquid chromatography assay necessitated 100-fold higher peptide concentrations to achieve adequate sensitivity. Similar results were obtained with both techniques. We found that the in vitro hydrolysis of [Leu]enkephalin is more rapid in chick plasma (half-life, 0.7-1 min) than in rat (half-life, 2-2.5 min) or mouse (half-life, 9-14 min) plasma. Comparison of the rate of enkephalin hydrolysis and pattern of metabolite accumulation in the absence vs. the presence of various peptidase inhibitors suggested that a bestatin-sensitive aminopeptidase, probably aminopeptidase M, is the primary enzyme responsible for the hydrolysis of enkephalin by chick plasma, and that less than 1% of the total hydrolysis of [Leu]-enkephalin by chick plasma is attributable to dipeptidyl carboxy-peptidase activity. This pattern of enzyme activities differs from that which we identified previously in rat and mouse plasma.

Aminopeptidases↗
PubMed1990

The timing of an injection procedure affects pharmacological actions on memory.

In a series of experiments examining the effects of the protein synthesis inhibitor anisomycin on memory for a novel active avoidance task in mice, we found that the timing of administering the drug (pretraining or posttraining) affected its amnestic potency. Anisomycin injected after training was more effective than when injected before training. Adding a saline injection, such that all groups received both pre- and posttraining injections, resulted in greater amnesia with anisomycin given before rather than after training. These results indicate that the procedure of drug administration alters the effectiveness of amnestic agents.

Animals↗
PubMed1990

Cholinergic receptor antagonists impair formation of intermediate-term memory in the chick.

Several experiments examined the effects of cholinergic receptor antagonists on formation of memory in the chick. Scopolamine produced amnesia in chicks trained on a one-trial peck avoidance task in a dose-dependent manner. Pretraining injection of scopolamine produced amnesia that developed between 15 and 30 min after training, suggesting that scopolamine interferes with intermediate-term memory (ITM), previously described to be active during this time (Patterson, Alvarado, Warner, Bennett, & Rosenzweig, 1986). Pretraining injection of scopolamine or ouabain, an inhibitor of ATPase activity shown previously to inhibit formation of ITM, produced identical time courses of amnesia development, supporting the hypothesis that scopolamine interferes with ITM. Pirenzepine, an inhibitor of M1 muscarinic receptors, was effective in producing amnesia, whereas gallamine, an M2 receptor inhibitor, did not produce amnesia. These results suggest that M1, but not M2, receptors are involved in memory formation in the chick.

Animals↗
PubMed1989

Is anisomycin-induced amnesia for a passive avoidance task in chicks the result of state-dependent learning?

Many studies suggest that protein synthesis is required for formation of long-term memory. To test whether the protein synthesis inhibitor anisomycin (ANI) actually inhibits long-term memory formation or whether apparent amnesia could be attributed to state-dependency, chicks were both trained and tested under the influence of anisomycin (ANI). Two-day-old cockerels were trained in a 1-trial passive avoidance task. Intracerebral injections (10 microliters per hemisphere) of either saline (SAL) or 11.0 mM ANI were made into the medial hyperstriatum ventrale 5 min pretraining and 5 min pretest. The ANI inhibited cerebral protein synthesis by 70-80%, a level necessary to cause amnesia. Chicks that pecked a small bead dipped in methylanthranilate (MeA) and were injected with SAL both pretraining and pretest avoided pecking at test, showing memory for the bitter substance; chicks given ANI pretraining and SAL pretest pecked at the bead during test, which suggests amnesia. However, those given ANI both pretraining and pretest showed marked avoidance at test. Chicks trained to peck at a small bead dipped in water and given injections of either SAL or ANI pretraining and SAL pretest pecked readily at test. However, water-trained chicks given ANI pretest, regardless of pretraining injection, showed significantly higher avoidance at test. We conclude that peck aversion in the ANI-MeA-ANI group was not due to state-dependency but to generalized avoidance induced by pretest ANI.

Amnesia↗
PubMed1989

Influence of opioid peptides on learning and memory processes in the chick.

Several experiments were conducted to examine the effects of intracranial injection of opioid peptides and antagonists on learning and memory in the chick. Pretraining injection of [leu5]enkephalin and the selective delta receptor agonist [D-Pen2,L-Pen5]enkephalin (DPLPE) into the intermediate medial hyperstriatum ventrale (IMHV) produced impairment. ICI 174,864, a delta-selective antagonist, reversed the impairment produced by either [leu5]enkephalin or DPLE, results indicating that delta receptors may play a role in learning in the chick and suggesting that the impairment produced by [leu5]enkephalin is mediated through delta opioid receptors. beta-endorphin produced a naloxone-reversible impairment in performance, which suggests that this impairment is mediated by opioid receptors. Bilateral injection of beta-endorphin into the IMHV produced impairment, as did unilateral injection into the right, but not left, IMHV. Only bilateral injections into IMHV of [leu5]enkephalin were effective. These results suggest that the effects of beta-endorphin are centrally mediated whereas the effects of [leu5]enkephalin may be localized to other brain regions or are peripherally mediated. These initial results suggest that opioids are associated with learning and memory in the chick.

Animals↗
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↗