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At least 775 records · Page 43Linked to original sources

PubMed2005

Early learning failure impairs adult learning in rats.

Early life experiences may affect adult learning ability. In two experiments we tested the effect of early learning failure on adult performance in Wistar rats. In the first experiment 17-day-old rats (PN17), but not 25-day-old rats (PN25), trained in a hidden platform water maze task showed deficits in tone-shock avoidance learning when they were 3-months-old. The second experiment, which included random-platform and non-platform control groups, confirmed the effect of early (PN18) spatial learning failure on adult avoidance learning. However, post-weaning training (PN25) without platform also tended to induce adult learning deficits as long as the adult task difficulty was increased. The older non-platform group did not differ from the impaired group which received early training in a fixed hidden platform task. The results are discussed in terms of the relevance of early learning outcome and developmental stage on adult general learning deficits which may be related to the learned helplessness phenomenon and developmental neural plasticity.

Age Factors↗

PubMedDate not supplied

[The action of neurotropin on the processes of conditioned-reflex avoidance in rats].

Preliminary neurotropin administration improved subsequent conditioned avoidance learning of rats in a shuttle-box: increased the number of conditioned avoidance reactions and decreased their latency in comparison with the control but did not change the number of intertrial responses. "The demolition" (5 series of negative reinforcements applied despite of avoidance occurrence) caused behavioural stress reactions and inhibited the conditioned and unconditioned avoidance learned reactions. Neurotropin injection before the demolition abolished such disturbances, that having been done after the demolition restored conditioned avoidance. The positive effects of neurotropin were suggested to be due to its antistress property and ability to improve the formation of a result of an acceptor of action.

Acoustic Stimulation↗

PubMed2005

The effect of prenatal morphine exposure on memory consolidation in the chick.

The central nervous system exhibits remarkable plasticity in early life and can be altered significantly by prenatal morphine exposure. Previous studies show that prenatal morphine exposure may alter the capacity for learning and memory in post-partum chicks. The one-trial passive avoidance learning paradigm with 1-day-old chicks is an excellent model to study several mechanisms of memory formation, including STM, ITM, and LTM. The following represents our investigation of the effect of prenatal morphine exposure on learning and memory deficits in the chick. In these experiments, morphine was injected into the airspace of eggs (20 mg/kg) and the one-trial passive avoidance learning paradigm was used to test the effect of prenatal morphine exposure on memory consolidation. The data suggest that chicks injected with morphine daily from E12 to E16 had significantly impaired long-term memory at 120 min after training (p<0.001) but not intermediate-term memory at 30 min after training.

Animals↗

PubMedDate not supplied

[The effect of administering corticoliberin into the striatum on the open-field and shuttle-box behaviors of KHA and KLA strain rats].

The effects of corticotropin-releasing hormone (CRH) injected into the dorsal neostriatum on the open-field and shuttle-box behavior were studied in rats with high (Koltushi high avoidance, KHA) and low (Koltushi low avoidance, KLA) capability for avoidance learning. The effects of this hormone on the behavior of these rat strains were different. In KLA rats with passive strategy of behavior the CRH injection led to a rapid locomotor activation in the open field, while the rats with active behavioral strategy (KHA) reacted to the injection by a significant decrease in locomotion and change for the passive mode of behavior. The same CRH effects on locomotion were obtained in the shuttle-box experiments. Moreover, in the KLA rats the neurohormone injection resulted in an improvement of avoidance learning in contrast to the KHA rats, in which CRH substantially impaired avoidance learning. The obtained evidence is discussed in terms of the important role of striatal CRH in the choice of behavioral strategy in stress.

Animals↗

PubMed2002

Cooling lesions of the lateral parabrachial nucleus during LiCl activation block acquisition of conditioned taste avoidance in male rats.

Lesions of the lateral parabrachial nucleus (lPBN) disrupt acquisition of LiCl-induced conditioned taste avoidance. Animals with lesions in this area also fail to exhibit taste neophobia. This raises the possibility that an inability of rats to recognize the taste solution as novel contributes to the deficit in taste avoidance learning. If this is the case, then one would expect conditioned taste avoidance not to be disrupted if the lPBN is functional during taste processing but not during LiCl processing. The first three experiments demonstrated that cooling was a viable method by which to temporarily inactivate the lPBN. Measurement of neural temperature during cooling indicated that the lPBN was cooled to temperatures that have been shown to block synaptic transmission but not axonal transmission. Cooling the lPBN itself induced a conditioned avoidance to a sucrose solution but this avoidance was abolished by exposure to daily cooling for 1 week prior to acquisition. In experiment 4, all animals were preexposed to lPBN cooling for 1 week. Those rats that received cooling lesions during a period that started immediately after sucrose solution consumption and extended through the peak effectiveness of LiCl failed to acquire a taste avoidance. These results fail to support the hypothesis that the deficit in taste avoidance learning after permanent lesions of the lPBN is due to an inability of lesioned animals to recognize the taste as novel. They are consistent with the hypothesis that this neural area processes ascending information about LiCl.

Animals↗

PubMed2003

Herbivore host plant selection: whitefly learns to avoid host plants that harbour predators of her offspring.

Evidence is accumulating that herbivorous arthropods do not simply select host plants based on their quality, but also on the predation risk associated with different host plants. It has been suggested that herbivores exclude plant species with high predation risk from their host range. This assumes a constant, predictable predation risk as well as a rather static behaviour on the part of the herbivore; plants are ignored irrespective of the actual predation risk. We show that adult females of a small herbivore, the whitefly Bemisia tabaci, can learn to avoid plants with predatory mites that attack only juvenile whiteflies, while they accept host plants of the same species without predators. Predatory mites disperse more slowly than whiteflies; they cannot fly and walk from plant to plant. Hence, by avoiding plants with predators, the whiteflies create a temporary refuge for their offspring. We suggest that the experience of arthropod herbivores with risks associated with host plants plays an important role in their host plant selection.

Adaptation, Physiological↗

PubMed2005

Learning under stress in the adult rat is differentially affected by 'juvenile' or 'adolescent' stress.

Epidemiological studies suggest that childhood trauma is associated with a predisposition to develop both mood and anxiety disorders, while trauma during adolescence is associated mainly with anxiety disorders. We studied in the rat the long-term consequences of 'juvenile' stress, namely stress experienced in a period in which substantial remodelling occurs across species in stress-sensitive brain areas involved in emotional and learning processing. In adulthood, 'juvenile' stressed rats exhibited reduced exploration in a novel setting, and poor avoidance learning, with 41% learning mainly to escape while 28% exhibited learned helplessness-like behaviours. In adult rats that underwent 'adolescent' stress, learned helplessness-like behaviours were not evident, although decreased exploration and poor avoidance learning were observed. This suggests that in the prepubertal phase juvenility may constitute a stress-sensitive period. The results suggest that juvenile stress induces lasting impairments in stress-coping responses. The 'juvenile' stress model presented here may be of relevance to individuals' reported predisposition to anxiety and depression following childhood trauma, and their increased susceptibility only to anxiety disorders following adolescent stress.

Adaptation, Psychological↗

PubMed2006

Docosahexaenoic acid-induced protective effect against impaired learning in amyloid beta-infused rats is associated with increased synaptosomal membrane fluidity.

In the present study, we investigated the relationship between the docosahexaenoic acid (DHA)-induced protection of learning deficit of amyloid beta(1-40)-infused Alzheimer's disease (AD) model rats and changes in synaptosomal plasma membrane fluidity of the cerebral cortex. Synaptosomal membrane lateral and rotational fluidity were measured using pyrene excimer spectroscopy and fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene (DPH), respectively. Avoidance learning ability, as assessed by a two-way active avoidance paradigm, decreased significantly in the AD model rats. Pyrene-determined annular/non-annular fluidity ratio and the DPH-determined bulk fluidity of the synaptosomal plasma membrane decreased in the amyloid beta(1-40)-infused rats. Oral pre-administration of DHA (300 mg/kg per day for 12 weeks) significantly increased both lateral and rotational fluidity. The synaptosomal membrane DHA content increased and the cholesterol to phospholipid molar ratio and lipid peroxidation decreased. The annular to non-annular fluidity ratio of the synaptic plasma membrane was positively correlated with total avoidance learning. The present results indicate that DHA-induced alterations in synaptic plasma membrane fluidity may contribute to the synaptic plasma membrane-related functions that constitute avoidance learning-related memory in amyloid beta(1-40)-infused rats.

Alzheimer Disease↗

PubMed1998

Behavioural changes following a four-week inhalation exposure to hemimellitene (1,2,3-trimethylbenzene) in rats.

Trimethylbenzene isomers (TMBs): 1,2,4-TMB (pseudocumene--PS), 1,2,3-TMB (hemimellitene--HM) and 1,3,5-TMB (mesitylene--MES) are important constituents of solvent mixtures. In the US, the adopted TLV-TWA value for TMBs is 125 mg/m3 or 25 ppm (ACGIH 1996). Recent experiments at our laboratory have revealed an impaired learning of passive and active avoidance responses and a longer persistence of an effect of footshock (increase in latency of the paw-lick response to heat) in rats tested several weeks after a four-week inhalation exposure (6h/day, five days/week) to PS at a concentration of 100 or 250 ppm (15). The concentration-effect relationship appeared to be nonlinear; the effect of 100 ppm HM was more pronounced than that of 250 ppm. In the present experiment we investigated the effects of a repeated four-week (6h/day, 5 days/week) inhalation exposure to HM at concentrations of 0, 25, 100 or 250 ppm on radial-maze performance, open-field activity, passive and active avoidance learning, and on the shock-induced changes in latency of the paw-lick response to heat (hot-plate test). The tests were performed between days 14 and 61 after the last exposure. No significant effects on radial-maze performance and open-field activity were noted in any of the dose groups. In the remaining tests effects of exposure were noted but, similarly as in the case of PS exposure, the concentration-effect relationship was not linear. In rats exposed to HM at 25 or 100 ppm, but not 250 ppm, learning of the passive avoidance, i.e. refraining from performance of a punished response (stepping off an elevated platform) was significantly impaired. Moreover, in rats exposed to 100, but not 250 ppm of HM, acquisition of the two-way active avoidance in the shuttle-box was slower and the footshock-induced increase in latency of the paw-lick response to heat persisted longer than in the unexposed animals. The results suggest that a low-level inhalation exposure to HM, just like low-level exposure to PS, may lead to long-lasting disturbances in the CNS functions. The nonlinear concentration-effect relationship observed in the case of both TMB-s requires clarification in further studies.

Administration, Inhalation↗

PubMed2002

Docosahexaenoic acid provides protection from impairment of learning ability in Alzheimer's disease model rats.

Docosahexaenoic acid (C22:6, n-3), a major n-3 fatty acid of the brain, has been implicated in restoration and enhancement of memory-related functions. Because Alzheimer's disease impairs memory, and infusion of amyloid-beta (Abeta) peptide (1-40) into the rat cerebral ventricle reduces learning ability, we investigated the effect of dietary pre-administration of docosahexaenoic acid on avoidance learning ability in Abeta peptide-produced Alzheimer's disease model rats. After a mini-osmotic pump filled with Abeta peptide or vehicle was implanted in docosahexaenoic acid-fed and control rats, they were subjected to an active avoidance task in a shuttle avoidance system apparatus. Pre-administration of docosahexaenoic acid had a profoundly beneficial effect on the decline in avoidance learning ability in the Alzheimer's disease model rats, associated with an increase in the cortico-hippocampal docosahexaenoic acid/arachidonic acid molar ratio, and a decrease in neuronal apoptotic products. Docosahexaenoic acid pre-administration furthermore increased cortico-hippocampal reduced glutathione levels and glutathione reductase activity, and suppressed the increase in lipid peroxide and reactive oxygen species levels in the cerebral cortex and hippocampus of the Alzheimer's disease model rats, suggesting an increase in antioxidative defence. Docosahexaenoic acid is thus a possible prophylactic means for preventing the learning deficiencies of Alzheimer's disease.

Administration, Oral↗

PubMed1993

Involvement of amyloid precursor protein in memory formation in the rat: an indirect antibody approach.

The potential role of different isoforms of amyloid precursor proteins (APPs) in memory and learning processes was investigated in rats using antibodies differentiating between APP isoforms containing or lacking the Kunitz protease inhibitor (KPI) domain. Rats received intracerebroventricular injection of control immunoglobulins (IgGs), anti-KPI-APP (= anti-P3) or anti-N-terminus-APP (= anti-P4). No immediate effects on learning of a passive avoidance task were observed; however, performance evaluated 1 day later was somewhat impaired by the anti-P3 antibody (reacting with APPKPI) and even more markedly impaired by the anti-P4 antibody (reacting with both APP695 and APPKPI) relative to control antibody. The antibodies did not affect performance of an active avoidance task acquired prior to the experimental treatment or active avoidance learning 8 days post-treatment. These results suggest that blockade of APP by an antibody injected intracerebroventricularly impairs the consolidation and/or retrieval of memory in rats.

Amyloid beta-Protein Precursor↗

PubMedDate not supplied

Comparative studies of somatostatin-14 and some of its fragments on passive avoidance behavior, open field activity and on barrel rotation phenomenon in rats.

Behavioral effects of somatostatin-14, and some of its fragments [somatostatin(3-8), somatostatin(9-14), somatostatin(7-10)] after intracerebroventricular (ICV) administration have been investigated in male rats. In a passive avoidance learning test, somatostatin-14 (0.6 nM) given immediately after the learning session increased the avoidance latency at 24 hr after the injection, when compared to a somatostatin(3-8) (0.6 nM)-treated group. However, compared to a saline-treated group, the peptides did not significantly influence the avoidance latency. Somatostatin-14 administered in higher dose (6.0 nM) decreased the avoidance latency compared to the saline-treated group, while its fragments did not influence it. In an open field behavioral test, immediately after the 24-hr passive avoidance test, 6 nM of somatostatin-14 decreased the rearing activity, while the fragments did not influence this behavior. Somatostatin-14 produced barrel rotation in a dose-related manner, but after the injection of a high dose of the peptide (12 nM) all of the animals died in cardiorespiratory failure (apnea, pulmonary oedema). The fragments did not produce barrel rotation.

Amino Acid Sequence↗

PubMed2004

Peripheral vasopressin accelerates extinction of conditioned taste avoidance.

Both peripheral and central administration of vasopressin improves retention and delays extinction when given before or after acquisition of shock avoidance learning. For conditioned taste avoidance, however, vasopressin prolongs extinction when injected peripherally before acquisition tests and accelerates extinction when infused intracerebroventricularly after acquisition. The following experiments were designed to determine whether this inconsistency is based on the route of administration or timing of vasopressin treatment. Because acquisition of conditioned taste avoidance is strengthened when an agent that is capable of inducing avoidance is administered after LiCl injection, it was determined in experiment 1 that a 6 microg/kg dose of vasopressin did not induce conditioned taste avoidance when administered 50 min after consumption of a sucrose solution. In experiment 2, it was determined that this dose of vasopressin accelerated extinction of a LiCl-induced conditioned taste avoidance when given 50 min after LiCl injection. These results suggest that the inconsistency is not based on route of administration. In experiment 3, it was determined that there was a tendency for animals to show prolonged extinction when vasopressin was administered 20 min before access to a sucrose solution. All of the results taken together suggest that the differential effects of vasopressin on extinction are due to the timing of administration. It was suggested that vasopressin accelerates extinction when given after acquisition by reducing the effectiveness of LiCl and it prolongs extinction when given before acquisition by altering neural responsiveness in areas mediating conditioned taste avoidance.

Analysis of Variance↗

PubMed1990

Effects of exposure to a pyrethroid insecticide during lactation on the behavior of infant and adult rats.

Cyhalothrin, a pyrethroid insecticide, was administered to female Wistar rats as a 0.02% solution plus 0.04% sucrose (w/v) in drinking water from whelping to pup weaning after 21 days of lactation. The pesticide did not change the maternal behavior of the dams as measured by the scoring system of Soderstein and Eneroth. The body weight of pups exposed to the pesticide and at age 90 days was not different from that of controls, and the motor activity of the pups measured in a simple photocell activity cage was not affected by pesticide treatment. Furthermore, no overt signs of neural toxicity were observed in the offspring. However, the treatment disrupted rat behavior in adulthood when assessed by using an inhibitory avoidance learning task. Thus, inhibitory avoidance tests carried out on rats at 90 days of age were capable of demonstrating neural toxicity of Cyhalothrin (0.02%) present only in the drinking water of dams during 21 days of lactation.

Animals↗

PubMed1977

The effect of cycloheximide on mouse learning.

Mice were trained in an avoidance learning task. The incorporation of 3H-leucine into the hippocampal regions of trained mice was higher than that of control mice. When mice were injected with cycloheximide, a strong inhibitor of protein synthesis, impairment was evident in acquisition of learning. Cycloheximide produced morphological changes in mitochondria and microtubules of some brain axons. It is suggested that the cycloheximide-induced learning impairment may be due to the blocking of the synthesis of the specific protein necessary of neutral conductivity.

Animals↗

PubMed1984

Behavioral changes in the rat after low doses of cholinesterase inhibitors.

In rats the acute effects of low doses of five cholinesterase (ChE) inhibitors were investigated in six behavioral tests. Considerable differences were found between the inhibitors studied. TEPP and sarin at doses up to 30% LD50 were without effects. In contrast, soman, physostigmine, and pyridostigmine caused effects at dose levels which did not produce overt symptoms and did not affect running speed and simple coordinated locomotion. Soman (less than or equal to 3% LD50), physostigmine (less than or equal to 4.5% LD50), and pyridostigmine (less than or equal to 10% LD50) interfered with two-way shuttlebox avoidance learning, open field behavior, and complex coordinated movements ( hurdle -stepping task). Tests of retention in a passive avoidance learning test appeared less sensitive. It is concluded that paradigms that involve higher CNS structures and require motor activity are sensitive to some ChE inhibitors at doses far below those that cause overt symptoms. The individual characteristics of ChE inhibitors play an important role. In contrast to TEPP and sarin, soman has a predominantly central effect. Further, the finding that pyridostigmine was also effective at unexpectedly low dose levels suggests that this compound may have more central actions than hitherto accepted.

Animals↗

PubMed1991

Insular cortex and amygdala lesions differentially affect acquisition on inhibitory avoidance and conditioned taste aversion.

These experiments examined the effects of NMDA-induced lesions of the amygdala and insular (gustatory) cortex (IC) on inhibitory avoidance learning and conditioned taste aversion (CTA) in rats. IC lesions, but not amygdala lesions, disrupted CTA. In contrast, lesions of either brain region disrupted inhibitory avoidance learning. These findings support the view that the IC is strongly involved in the acquisition of external as well as visceral aversively motivated behavior. Despite extensive functional interconnections, these 2 brain regions appear to have different roles in mediating different forms of aversively based learning.

Amygdala↗

PubMed2004

Activation of phasic pontine-wave generator prevents rapid eye movement sleep deprivation-induced learning impairment in the rat: a mechanism for sleep-dependent plasticity.

Animal and human studies of sleep and learning have demonstrated that training on various tasks increases subsequent rapid eye movement (REM) sleep and phasic pontine-wave (P-wave) activity, followed by improvement in performance on the learned task. It is well documented that REM sleep deprivation after learning trials blocks the expected improvement in performance on subsequent retesting. Our aim was to test whether experimentally induced P-wave generator activation could eliminate the learning impairment produced by post-training REM sleep deprivation. Rats were trained on a two-way active avoidance-learning task. Immediately thereafter, two groups of those rats received a control vehicle (100 nl saline) microinjection and one group received a carbachol (50 ng in 100 nl saline) microinjection into the P-wave generator. The carbachol-injected group and one of the two control saline microinjected groups were selectively deprived of REM sleep during a 6 hr polygraphic recording session. All rats were then tested on the avoidance-learning task. The rats that received both the control saline injection and REM sleep deprivation showed learning deficits compared with the control saline-injected rats that were allowed to sleep normally. In contrast, the rats that received the carbachol microinjection and REM sleep deprivation demonstrated normal learning. These results demonstrate, for the first time, that carbachol-induced activation of the P-wave generator prevents the memory-impairing effects of post-training REM sleep deprivation. This evidence supports our hypothesis that the activation of the P-wave generator during REM sleep deprivation enhances a physiological process of memory, which occurs naturally during post-training REM sleep.

Animals↗