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E L Bennett

Publications and source records attributed to E L Bennett.

At least 19 recordsLinked to original sources
PubMed1997

Evidence for localized and discrete roles for enkephalins during memory formation in the chick.

This study examined effects on memory formation produced by [Leu]enkephalin and [Met]enkephalin administration in 2 regions of the 2-day-old chick brain involved in memory formation: the intermediate medial hyperstriatum ventrale (IMHV) and the lobus parolfactorius (LPO). Basal concentrations of endogenous [Leu]enkephalin and [Met]enkephalin were determined for 5 brain regions, and effects of 1-trial peck-avoidance training on enkephalin concentrations were examined in the IMHV and LPO. [Leu]enkephalin was amnestic when administered in the IMHV but not in the LPO. In contrast, [Met]enkephalin may be amnestic when administered in the LPO but not in the IMHV. Training decreased [Met]enkephalin concentration in the LPO but not in the IMHV. Training had no effect on [Leu]enkephalin concentration in either the IMHV or the LPO. Thus, amnestic effects of [Leu]- or [Met]enkephalin administration are brain-region specific. Regional activity of endogenous [Met]enkephalin during memory formation is consistent with localized amnestic effects produced by [Met]enkephalin administration.

Age Factors↗
PubMed1996

Psychobiology of plasticity: effects of training and experience on brain and behavior.

Supporting Hebb's 1949 hypothesis of use-induced plasticity of the nervous system, our group found in the 1960s that training or differential experience induced neurochemical changes in cerebral cortex of the rat and regional changes in weight of cortex. Further studies revealed changes in cortical thickness, size of synaptic contacts, number of dendritic spines, and dendritic branching. Similar effects were found whether rats were assigned to differential experience at weaning (25 days of age), as young adults (105 days) or as adults (285 days). Enriched early experience improved performance on several tests of learning. Cerebral results of experience in an enriched environment are similar to results of formal training. Enriched experience and training appear to evoke the same cascade of neurochemical events in causing plastic changes in brain. Sufficiently rich experience may be necessary for full growth of species-specific brain characteristics and behavioral potential. Clayton and Krebs found in 1994 that birds that normally store food have larger hippocampi than related species that do not store. This difference develops only in birds given the opportunity to store and recover food. Research on use-induced plasticity is being applied to promote child development, successful aging, and recovery from brain damage; it is also being applied to benefit animals in laboratories, zoos and farms.

Animals↗
PubMed1995

Norepinephrine and neural plasticity: the effects of xylamine on experience-induced changes in brain weight, memory, and behavior.

The hypothesis that norepinephrine (NE) is critically involved in neural plasticity was tested by administering xylamine, (N-2-chloroethyl-2-methylbenzylamine, 50 mg/kg ip) a noradrenergic neurotoxin, to young rats prior to maze training or environmentally enriched housing. In saline-treated rats, exposure to enriched conditions significantly increased the weight of occipital, dorsal, and ventral cortices and the remaining brain compared to individually housed rats. In xylamine-treated rats, only the weight of dorsal cortex increased with exposure to enriched conditions. Maze training increased the weight of dorsal and ventral cortices of saline-treated animals compared to rats without training. However, maze training did not increase brain weights of xylamine-treated rats compared to those of xylamine-treated controls. Xylamine treatment did not reduce brain weights of individually housed animals. Behavior was assessed with spatial learning on a holeboard maze and with investigatory measures of locomotion and hole investigation in a multicompartmented arena. Spatial working memory on the holeboard maze was not impaired by xylamine treatment. Arena measures were affected mainly by the housing condition, testing condition, and strain of rat (Long-Evans vs Wistar), with only subtle changes in behavior induced by NE depletion. Thus, an intact NE projection was required for environmentally dependent changes in cortical morphology. In contrast, measures of memory and investigatory behavior were not dependent on an intact noradrenergic projection. These results support the hypothesis that NE facilitates selective neuronal changes, and that the impairment in cortical weight gain does not results from a general impairment of growth or a secondary response to reduced exploration and activity.

Animals↗
PubMed1995

Protein kinase inhibitors disrupt memory formation in two chick brain regions.

The amnesic effects of protein kinase inhibitors (H-7, HA-156, TFP, W-9, and W-13) on memory formation for a one trial peck-avoidance task in chicks were investigated with bilateral and unilateral injections into either the left or the right intermediate medial hyperstriatum ventrale (IMHV) or the left or right lobus parolfactorius (LPO). All five inhibitors injected bilaterally 5 min pretraining into either the IMHV or LPO or unilaterally into the left IMHV produced amnesia. Unilateral injections into the right IMHV did not produce amnesia. Unilateral injections of W-9 or W-13 into the left but not the right LPO produced amnesia, H-7, HA-156, or TFP did not produce amnesia when injected unilaterally into either the left or right LPO. The time of onset of amnesia produced by injecting TFP and W-13 into the LPO occurred 45 min after training, whereas H-7 produced amnesia significantly later (90 min after training). Amnesia induced by TFP, W-13, and H-7 injected into the LPO occurred significantly later than amnesia produced when these agents were injected into the IMHV. Together these data suggest that the IMHV and LPO process memory sequentially using various protein kinase activities.

Animals↗
PubMed1995

Protein kinase C inhibitor chelerythrine disrupts memory formation in chicks.

Chelerythrine (CHELE), a specific, potent protein kinase C (PKC) inhibitor, disrupts memory formation for a one-trial peck-avoidance task. Three predictions were made about how CHELE, injected into chick brain near the time of training, would affect memory formation, based on previous work with two classes of protein kinase inhibitors (M. R. Rosenzweig et al., 1992; P. A. Serrano et al., 1994) and the in vitro inhibition of PKC by CHELE: (a) CHELE, injected into the intermediate medial hyperstriatum ventrale, would significantly impair memory formation; (b) the amnestic dose would be approximately 10 nmol; (c) CHELE would not produce amnesia for about 45 min after training, but significantly impair memory by 60 min. Experimental tests confirmed each prediction. This study adds to evidence that PKC activity is part of a cascade of neurochemical events initiated by learning and that PKC activity shortly after training is necessary for long-term memory.

Alkaloids↗
PubMed1994

Differential effects of protein kinase inhibitors and activators on memory formation in the 2-day-old chick.

Thirteen protein kinase inhibitors (PKIs) were investigated in chicks for their in vitro effects on PKC activity and for their in vivo effects on memory formation for a peak-avoidance task. Amnesia occurred by 15-30 min post-training when agents that inhibit primarily Ca2+/calmodulin were injected into brain. Amnesia occurred by 60 min post-training when agents that inhibit PKC-, PKA-, and/or PKG-dependent protein kinases, but not Ca2+/calmodulin, were injected. Enhancement of memory formation was accomplished by injecting bradykinin, but not forskolin. Both of these agents, however, attenuated the amnesia produced by H-7. These results are discussed as relevant neural processes involved in memory and synaptic plasticity.

Amnesia↗
PubMed1993

Short-term, intermediate-term, and long-term memories.

This paper focuses on the temporal dimension of memory formation and storage. Is the usual two-fold separation between short-term memory (STM) and long-term memory (LTM) sufficient to encompass all the phenomena of memory? The traditional view is that STM grades into LTM. Evidence for an intermediate-term memory (ITM) has been proposed by some investigators. We have used both rats and chicks to investigate the stages of memory formation. In this paper, the advantages of chicks for this type of research are briefly discussed. Using a paradigm that produces weak training, the retention function for control chicks appears to be made up of four successive components which we have interpreted as representing the memory buffer, STM, ITM, and LTM. In experiments using a variety of kinase inhibitors, we have obtained evidence that ITM and LTM depend on different classes of protein kinase activities. Agents that act on calcium/calmodulin kinase cause amnesia in the ITM range--15 to 30 min post-training. Another class of inhibitors act on one or more of the kinases PKA, PKC, or PKG and cause amnesia by 60 min post-training, so we interpret this group of inhibitors as inhibiting the formation of LTM. However, the three-stage model of memory may be over-simple. For example some agents including [Leu]enkephalin and MK801 cause amnesia 4 or more h after training.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
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↗