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At least 1,279 records · Page 71Linked to original sources

PubMed2002

Amino acid release from the intermediate medial hyperstriatum ventrale (IMHV) of day-old chicks following a one-trial passive avoidance task.

Indirect evidence has implicated glutamate and gamma-amino butyric acid in memory formation for one-trial passive avoidance learning. We have further examined this by following the time course of glutamate and gamma-amino butyric acid release from slices prepared from the intermediate medial hyperstriatum ventrale of day-old chicks (Ross 1 Chunky) trained to avoid a bead covered in the aversant methylanthranilate. At various times after training, slices of left and right intermediate medial hyperstriatum ventrale were incubated in medium containing 50 mM potassium chloride and amino acid release was determined. Thirty minutes after training there was a bilateral increase in calcium-dependent glutamate release in slices from methylanthranilate-trained chicks compared to those trained to peck water. This increase was sustained until 1 h in the left hyperstriatum when an increase in calcium-dependent gamma-amino butyric acid release was also apparent. Glutamate uptake was also enhanced in left hyperstriatum (30 and 60 min) and in the right at 30 min. In the right intermediate medial hyperstriatum ventrale of methylanthranilate birds glutamate release was increased from 3 to 6.5 h and gamma-amino butyric acid at 6.5 h: a time that corresponded to the mobilization of a late process required if long-term memory was to be formed. These results confirm that the amino acids glutamate and gamma-amino butyric acid are released from the intermediate hyperstriatum ventrale in a calcium-dependent, neurotransmitter-like manner. Furthermore, changes in the release of these two amino acids accompany memory formation for a one-trial learning task in the day-old chick.

Animals↗

PubMed1976

Modulation of cycloheximide-resistant memory by sympathomimetic agents.

Amphetamine overcomes the amnesia caused by cycloheximide (CXM) provided it is administered closely following the learning trial. In day-old chickens with one trial passive avoidance learning, there is a short-term, labile memory existing for 90 min following training under the influence of CXM. Amphetamine has been shown to keep the memory at precisely the level exhibited by the labile, cycloheximide-resistant memory trace at the time of injection. Norepinephrine, methoxamine (an alpha adrenergic stimulant) and isoprenaline (a beta adrenergic stimulant) each mimic the amphetamine effect in CXM-pretreated chickens. That the action of amphetamine could be due to its release of norepinephrine is supported by the finding that it could be blocked by both alpha adrenergic (piperoxane) and beta adrenergic antagonists (propranolol). It has been suggested that this labile memory trace depends on the functioning of a sodium pump. Norepinephrine may be modulating memory formation by an action on the sodium pump since in preliminary biochemical assays norepinephrine stimulated the sodium pump (Na+/K+ ATPase) activity in chicken forebrain total homogenate.

Amphetamine↗

PubMed2004

Post-synaptic GABA(B) receptors--possible controllers of coincidence detection?

Post-synaptic GABA(B) responses (slow, late hyperpolarisations which can be eliminated by perfusion with phaclofen) can be recorded in vitro from many, but not all, neurones in the intermediate medial hyperstriatum ventrale (IMHV). The IMHV is an area of the chick forebrain which is remarkable for its plasticity, and for its essential role in two specific types of early learning-imprinting, and a form of one-trial passive-avoidance learning. Post-synaptic GABA(B) responses are strongly statistically associated with other properties (such as high membrane resistance) which are, themselves, dependent on a bird's past history. There is also evidence that their incidence changes with prior training in vivo and with age. GABA(B) hyperpolarisations are always offset to a varying extent by excitatory NMDA components. These two components follow a very similar time-course, so that the duration and (to a lesser extent), the magnitude of a response is controlled by the balance between the two systems. The evidence suggests that this balance fluctuates, and that its fluctuations determine the extent to which any neurone can function as a coincidence detector.

Action Potentials↗

PubMed1999

Protective effects of idebenone and alpha-tocopherol on beta-amyloid-(1-42)-induced learning and memory deficits in rats: implication of oxidative stress in beta-amyloid-induced neurotoxicity in vivo.

Amyloid beta-peptide (A beta), the major constituent of the senile plaques in the brains of patients with Alzheimer's disease, is cytotoxic to neurons and has a central role in the pathogenesis of the disease. Previous studies have suggested that oxidative stress is involved in the mechanisms of A beta-induced neurotoxicity in vitro. In the present study, we examined whether oxidative stress contributes to learning and memory deficits caused by continuous intracerebroventricular infusion of A beta-(1-42). In the A beta-(1-42)-infused rats, spontaneous alternation behaviour in a Y-maze and spatial memory in a water maze task were significantly impaired, as compared with A beta-(40-1)-infused control rats. The retention of passive avoidance learning was also significantly impaired by treatment with A beta-(1-42). Potent antioxidants idebenone and alpha-tocopherol prevented the behavioural deficits in Y-maze and water maze, but not passive avoidance, tasks in A beta-(1-42)-infused rats when they were repeatedly administered by mouth once a day from 3 days before the start of A beta infusion to the end of behavioural experiments. Lipid peroxide levels in the hippocampus and cerebral cortex of A beta-(1-42)-infused rats did not differ from those in control animals, and neither idebenone nor alpha-tocopherol affected the lipid peroxide levels. These results suggest that treatment with antioxidants such as idebenone and alpha-tocopherol prevents learning and memory deficits caused by A beta.

Alzheimer Disease↗

PubMed1993

Behavioral and histological changes after repeated brief cerebral ischemia by carotid artery occlusion in gerbils.

The effects of repeated brief episodes of cerebral ischemia on passive avoidance learning and hippocampal neuronal degeneration were investigated in gerbils. Latency of step-through was shortened for the entire 7-day period when gerbils were trained at day 3 after 3 episodes of carotid artery occlusion for 2 min each at 60-min intervals. In addition, latency of passive avoidance was shortened for 63 days when gerbils were retrained at 14 days after occlusion. Severe neuronal degeneration in the CA1 regions of the hippocampus was observed 4 and 17 days after occlusion. A close correlation was seen between latency in the passive avoidance response and neurological degeneration of the hippocampal CA1 region. This fact was strongly supported by the results of another experiment that 1 2-min occlusion with almost no neuronal degeneration did not affect learning behavior while 3 1-min occlusions showed neuronal death and impairment of learning behavior of a moderate degree 4 days after occlusion. These results suggest that this gerbil model with carotid artery occlusion is useful for the quantitative measurement of functional changes in the chronic phase of repeated cerebral ischemia.

Animals↗

PubMed2000

Learning and discrimination of colored papers in jumping spiders (Araneae, Salticidae).

Color discrimination in jumping spiders Hasarius adansoni was examined by heat-avoidance learning in association with colored papers. The arena for the experiment was divided into two halves by a pair of colored papers. The colored papers used in this study were blue, green, yellow, red, white, gray and black. In training sessions, one half of the arena was heated from the bottom by a hot plate, and freely walking spiders were individually trained to avoid the heated half. In subsequent memory tests without heat, they consistently avoided the heat-associated colored papers. We found that jumping spiders could learn blue-green, blue-yellow, blue-red, blue-gray, green-yellow, green-red, green-gray, yellow-red, yellow-gray and red-gray patterns. Moreover, spiders trained with a blue-white pattern, a green-white pattern, a yellow-white pattern or a red-white pattern could discriminate the blue, green, yellow or red from black. It seems that jumping spiders can discriminate the blue, green, yellow and red papers by their hue, although brightness may also be used together with the color cue to discriminate colored papers.

Animals↗

PubMedDate not supplied

Effects of single or repeated dermal exposure to methyl parathion on behavior and blood cholinesterase activity in rats.

The effects of a single or repeated dermal administration of methyl parathion on motor function, learning and memory were investigated in adult female rats and correlated with blood cholinesterase activity. Exposure to a single dose of 50 mg/kg methyl parathion (75% of the dermal LD(50)) resulted in an 88% inhibition of blood cholinesterase activity and was associated with severe acute toxicity. Spontaneous locomotor activity and neuromuscular coordination were also depressed. Rats treated with a lower dose of methyl parathion, i.e. 6.25 or 12.5 mg/kg, displayed minimal signs of acute toxicity. Blood cholinesterase activity and motor function, however, were depressed initially but recovered fully within 1-3 weeks. There were no delayed effects of a single dose of methyl parathion on learning acquisition or memory as assessed by a step-down inhibitory avoidance learning task. Repeated treatment with 1 mg/kg/day methyl parathion resulted in a 50% inhibition of blood cholinesterase activity. A decrease in locomotor activity and impairment of memory were also observed after 28 days of repeated treatment. Thus, a single dermal exposure of rats to doses of methyl parathion which are lower than those that elicit acute toxicity can cause decrements in both cholinesterase activity and motor function which are reversible. In contrast, repeated low-dose dermal treatment results in a sustained inhibition of cholinesterase activity and impairment of both motor function and memory.

Administration, Cutaneous↗

PubMed2005

Transient prenatal vitamin D deficiency is associated with subtle alterations in learning and memory functions in adult rats.

Based on clues from epidemiology, low prenatal vitamin D has been proposed as a candidate risk factor for schizophrenia. Recent animal experiments have demonstrated that transient prenatal vitamin D deficiency is associated with persistent alterations in brain morphology and neurotrophin expression. In order to explore the utility of the vitamin D animal model of schizophrenia, we examined different types of learning and memory in adult rats exposed to transient prenatal vitamin D deficiency. Compared to control animals, the prenatally deplete animals had a significant impairment of latent inhibition, a feature often associated with schizophrenia. In addition, the deplete group was (a) significantly impaired on hole board habituation and (b) significantly better at maintaining previously learnt rules of brightness discrimination in a Y-chamber. In contrast, the prenatally deplete animals showed no impairment on the spatial learning task in the radial maze, nor on two-way active avoidance learning in the shuttle-box. The results indicate that transient prenatal vitamin D depletion in the rat is associated with subtle and discrete alterations in learning and memory. The behavioural phenotype associated with this animal model may provide insights into the neurobiological correlates of the cognitive impairments of schizophrenia.

Analysis of Variance↗

PubMed1999

Differences in memory impairment and response to GM1 ganglioside treatment following electrolytic or ibotenic acid lesions of the nucleus basalis magnocellularis.

Alzheimer's disease is a progressive dementia associated with cholinergic cell loss in the nucleus of Meynert that induces deficiencies in cholinergic neurotransmission in the neocortex. The nucleus basalis magnocellularis (NBM) is the rodent homologue to the nucleus of Meynert in humans. In this study, we examined the effects of GM1 ganglioside, a neuroprotective agent, on morphological and functional recovery after electrolytic or ibotenic acid lesions of the NBM. In animals, GM1 ganglioside has been shown to reduce some of the behavioral deficits that follow Central Nervous System lesions. Electrolytic or ibotenic acid lesions produced deficits in passive avoidance learning, as assessed by the number of trails taken to acquire the avoidance response. Only the electrolytic lesions impaired spatial memory in the Morris Water Maze (MWM), and GM1 administration did not improve performance on this task. Facilitation of passive avoidance acquisition was observed in animals receiving GM1 treatment after electrolytic or ibotenate lesions. Both types of injuries induced equivalent amounts of damage to the nucleus basalis but the electrolytic lesions produced greater damage to adjacent structures that could be responsible for the additional deficits observed on the MWM task.

Journal Article↗

PubMedDate not supplied

[The reactivity of the hypophyseal-adrenal system in rats with different forms of adaptive behavioral pathology].

The dexamethasone suppression test (DST) was applied to male Wistar rats with different models of depression: group with the learned helplessness, group with informational neurosis provided by time-deficit conditioned avoidance training, as well as groups of rats of two strains selected for low (KLA)--and high (KHA) avoidance learning. The pre-dexamethasone basal and stress-induced corticosterone levels were similar in intact rats and those exposed to inescapable shock. The dexamethasone administration (5 mkg/kg) failed to decrease the serum corticosterone level in rats with learned helplessness. The informational neurosis increased significantly the basal corticosterone level and decreased the stress response. Serum corticosterone levels were similar in KLA and KHA rats. These results give evidence that two stress-induced rat models of depression with similar behavioural disturbances (reduction of escape/avoidance reactions) exhibit marked differences in the activity of hypothalamo-pituitary-adrenal (HPA) axis.

Acoustic Stimulation↗

PubMed1995

Administration of glutamate following a reminder induces transient memory loss in day-old chicks.

Monosodium glutamate (4.0 mM) administered immediately after a visual reminder presented to day-old chickens between 7.5 min and 24 h following a single trial passive avoidance learning task produced transient losses of memory on retention test, an effect not observed in the absence of a reminder or when the reminder was given 48 h post-learning. The duration of the transient deficit decreased with increasing interval between the training and the reminder trial. The time of onset of memory loss after the reminder trial appeared to increase with increasing interval between the training and the reminder trials. The results suggest that, for a period of at least up to 24 h after passive avoidance training, retrieval of memory may lead to processes which are sensitive to inhibition by glutamate, with the duration of sensitivity post-retrieval decreasing as the period of memory consolidation increases. The results extend previously reported findings with rodents and suggest the possibility that consolidation of a stable memorial representation of a learning experience may take place over several days and may entail the concurrent laying down of a stable retrieval mechanism.

Animals↗

PubMed1997

Administration of DL-2-amino-5-phosphonovaleric acid (AP5) induces transient inhibition of reminder-activated memory retrieval in day-old chicks.

DL-2-Amino-5-phosphonovaleric acid (50 microM) administered immediately after a visual reminder presented to day-old chickens between 7.5 min and 24 h following a single trial passive avoidance learning task produced transient losses of memory on retention test, an effect not observed in the absence of a reminder or when the reminder was given 48 h post learning. The duration of the transient deficits decreased with increasing interval between training and the reminder trial. The time of onset of memory loss after the reminder trial appeared to increase with increasing interval between the training and the reminder trials. The results suggest that, for a period of at least up to 24 h after passive avoidance training, retrieval of memory may lead to processes which are sensitive to inhibition by the NMDA receptor antagonist AP5, with the duration of sensitivity post retrieval decreasing as the period of memory consolidation increases. The results extend previously reported findings and suggest the possibility that consolidation of a stable memorial representation of a learning experience may take over several days and may entail the concurrent laying down of a stable retrieval mechanism.

2-Amino-5-phosphonovalerate↗

PubMedDate not supplied

[The effect of nooglutil and piracetam on different forms of operant learning].

We studied effects of a new drug with nootropic action nooglutil (N-(5-hydroxynicotinoil)-L-glutaminic acid, OHK-10) on initial stages of different forms of operant behaviour in rats, namely avoidance learning in Shuttle box, in Skinner box and on T-maze reflex with water reward. Comparing dates resulted from these three methods permitted evaluation of effects of the drugs on learning. Both drugs had no effects on avoidance response in shuttle box and T-maze reflex with water reward. Nooglutil enhanced escape and avoidance responses meanwhile piracetam improved only escape response.

Animals↗

PubMed2003

LiCl-induced flavor avoidance compared between rats and mice using a nondeprivation protocol.

The present studies examine some parameters involved in flavor avoidance learning, using LiCl to induce malaise, in a novel nondeprivation protocol that allows direct comparison between rats and mice. The procedure involves daily presentation of a gelatin dessert that contains carbohydrate (Polycose) and a distinctive food flavor. Regular chow is additionally available at all times. Both rats and mice showed robust intakes of these gels with little change of gram intake as concentration of Polycose was varied in the range 2-30%; at the highest concentration, the caloric yield was approximately 7% of normal daily intake in both species. Rats that were injected on three occasions with LiCl (0.75 meq/kg) 1 h after consumption of a flavored gel formed a complete and sustained conditioned flavor avoidance (CFA). In a two-flavor discrimination protocol, in which a second flavor was followed by injections of saline, rats showed complete avoidance of the LiCl-paired flavor and partial avoidance of the saline-paired flavor. Mice injected on three occasions with LiCl (6 meq/kg) 1 h after intake of a flavored gel formed a partial CFA; a more complete CFA was formed when there was no delay between removal of the flavor and the injection. Using this no-delay protocol, mice, like rats, showed avoidance of a saline-paired flavor in a two-flavor discrimination protocol, and the CFA was strong when the dose of LiCl was reduced to that used in rats (0.75 meq/kg). In comparable protocols, mice thus are able to form complete CFAs using low doses of LiCl that are comparable to CFAs observed in rats, but the interval between flavor and sickness over which associative learning can occur may be shorter in mice.

Animals↗

PubMedDate not supplied

[The expression of the c-fos gene in the brain of mice in the dynamic acquisition of defensive behavioral habits].

Levels of c-fos mRNA expression in mouse cerebral cortex and hippocampus at different stages of footshock escape and avoidance learning were studied by Northern hydridization. In the first series of experiments a mouse was presented with 30 electric footshock daily in a chamber where it could escape from the floor by jumping on the safe platform attached to the wall. A large increase in c-fos mRNA level in the cerebral cortex and hippocampus was observed during the first day of training. Mice that were trained for 9 consecutive days and acquired a footshock escape reaction showed no elevation of c-fos expression in the brain as compared to the quiet control group. In the second series of experiments the levels of c-fos expression were compared in individual mice trained to avoid the footshock by jumping on the platform in response to an auditory conditioned stimulus. Mice which acquired avoidance behavior more rapidly had lower c-fos mRNA levels than slow learners. There was no such to difference between the corresponding yoked control groups which consisted of animals matched the rapid and slow learners by the number of footshocks received. It is concluded that achievement of adaptive results in the course of learning leads to a suppression of further c-fos induction by motivational excitation.

Adaptation, Physiological↗

PubMed1980

Effect of beta-endorphin and naloxone on acquisition, memory, and retrieval of shuttle avoidance and habituation learning in rats.

Naloxone impairs acquisition of shuttle avoidance behavior (0.8 mg/kg IP) and habituation to a rearing response to a tone (1.6 mg/kg IP) in rats. beta-Endorphin (2 microgram/kg IP) has no effect on acquisition, but, when given prior to test sessions, facilitates retrieval of the two tasks. Naloxone has no effect of its own upon retrieval. In addition to these effects, the pretraining administration of beta-endorphin disrupts, and that of naloxone facilitates retention of the two tasks. The results are consistent with the hypothesis that these two forms of learning are state-dependent on the release of beta-endorphin (and, perhaps, of other opiate peptides as well), that this substance is released during training in a sufficient amount for this purpose, and that, in addition, there is a physiological amnesic mechanism mediated by opiate peptides. Furthermore, the results are also consistent with previous observations that beta-endorphin is released from the rat brain during training, but not during test sessions of the two tasks (Izquierdo et al., 1980b). The possibility is discussed that state-dependency and the amnesic effect comprise one single, rather than two separate mechanisms.

Animals↗

PubMed1987

Effect of excess intracranial amino acids on memory: a behavioural survey.

Nineteen naturally occurring amino acids were administered intracranially to day-old chicks at various times before and after a single trial passive avoidance learning task. The results suggest a consistent and simple difference between essential and non-essential amino acids. Except for arginine, phenylalanine, tryptophan and tyrosine, the essential amino acids had no effect on memory formation when administered 5 min before or immediately after learning. However, arginine, phenylalanine and tryptophan yielded amnesia after 60 min following learning, when given between 5 min before and 2.5 min after learning. In the case of tryptophan, amnesia was only temporary, lasting from 60 min to 240 min post-learning. All non-essential amino acids, when administered between 5 min before and 5 min after learning yielded amnesia by 60 min post-learning, with no evidence of recovery by 24 hr post-learning. Alanine-, asparagine-, cysteine- and glutamate-treated chicks, however, showed signs of generalized avoidance shortly after administration. The retention time courses after injection of glutamine, proline, serine and taurine were similar to that obtained with the non-metabolizable amino acid alpha-amino-isobutyric acid, and amnesia arising from administration of these amino acids was counteracted by diphenylhydantoin, as was amnesia induced by phenylalanine and tyrosine. The retention function obtained with tryptophan was similar to that obtained with 5-hydroxytryptamine, and DPH had no effect on the action of tryptophan or the actions of arginine, alanine or asparagine. The findings were interpreted in the context of a three-stage model of memory formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

PubMed1988

Effects of piracetam on learned helplessness in rats.

In rats, the effects of Piracetam (P), the prototype of nootropic drugs, were studied on a very widely used model of behavioral disturbance: the learned helplessness (LH) phenomenon. In this model, exposure to uncontrollable and unsignalled shocks impairs subsequent escape-avoidance learning. In a first experiment, this deficit was abolished by 200 mg/kg of P, and to a lesser extent, by a 100 mg/kg dose, administered before the training session. In non-stressed animals, no dose of P was able to have a facilitatory effect on escape-avoidance. In a second experiment, the administration of P, not before the training session as in Experiment I, but before the stress, had no effect on the LH phenomenon regardless of the dose.

Animals↗