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PubMed2001

[Effects of selenium on the damage of learning-memory ability of mice induced by fluoride].

Sodium fluoride added with or without sodium selenite in deionized water was administered to male mice for 8 weeks. The influences of fluoride on learning-memory behavior were tested on Y-maze, and the ultrastructure of Gray I synaptic interface in the CA3 area hippocampus was quantitatively analyzed by electron microscopy and computer image processing appliance. The main results showed that the learning capability of mice drinking higher concentration of fluoride presented remarkable deterioration. The thickness of post-synaptic density (PSD) was decreased. The width of the synaptic cleft was remarkably increased. It was found that combined administration of fluoride and proper concentration of selenium could decrease the toxic effect of fluoride. There were synergetic toxicities if the concentration of selenium was too high. The results suggested that selenium might antagonize the neurotoxicity of fluoride on behavior and morphology.

Animals↗
PubMedDate not supplied

Nicotine patches in Alzheimer's disease: pilot study on learning, memory, and safety.

In view of the cholinergic deficits present in patients with Alzheimer's disease (AD), a widely investigated treatment strategy for the cognitive deficits in AD is cholinergic stimulation. Although nicotinic cholinergic receptor binding has been demonstrated to be deficient in the AD brain, the predominant theoretical and therapeutic focus to date has been on muscarinic cholinergic receptors and systems. The purpose of the present study was to evaluate the effects of sustained nicotine administration on behavior, cognition, and physiology. A double-blind placebo-controlled trial was conducted in which six patients with probable AD were exposed to 7, 8, and 7 days of placebo, nicotine, and washout, respectively. Daily sessions evaluating learning, memory, and behavior were conducted. Global cognitive functioning, rest and activity levels, cardiac activity, and blood levels were also measured. Findings included improved learning during the nicotine condition, which persisted throughout washout. Memory, behavior, and global cognition were not significantly affected. Sustained administration of nicotine appeared to be safe, although sleep showed a significant decrease.

Administration, Cutaneous↗
PubMed1997

Long-term consequences of neonatal exposure to diazepam on cerebral glucose utilization, learning, memory and anxiety.

The long-term consequences of neonatal exposure to diazepam (DZP) on behavioral abilities and local cerebral glucose utilization (LCGU) in 12 brain regions involved in the control of memory and anxiety were studied in adult rats. Rat pups received a daily subcutaneous injection of 10 mg/kg DZP or of the dissolution vehicle from postnatal day (P) 2 to 21. Learning and memory were tested in P60-P70 rats over 5 consecutive days in a T maze and an eight-arm maze while anxiety and reaction to novelty were tested in a two-compartment box with a two-step staircase on the enriched side. LCGU was measured in the P60 rat by the quantitative autoradiographic [14C]deoxyglucose method. In the T maze, when performed without delay between the two trials, the rate of alternation was significantly lower in DZP- than in vehicle-exposed rats on the first 2 days of testing and similar in both groups on days 3-5. In the procedure with a 30 s intertrial delay, the rate of alternation was similar in DZP- and vehicle-treated rats on all days of testing. In the eight-arm maze, DZP-treated rats were more active, i.e., entered more arms per minute than control animals. The number of arms entered before the first error was lower on day 1 and higher on day 3 in DZP- compared to vehicle-exposed rats. In the two-compartment box, DZP-treated rats crossed more often and spent more time than controls on the lower step of the staircase while control rats made more rearings and spent more time than DZP-exposed rats in the well protected corner of the box. LCGU were decreased by early DZP exposure in six regions which were mammillary body, septum, visual and prefrontal cortices, dorsomedian caudate nucleus and mediodorsal thalamus. In conclusion, postnatal DZP treatment induced at adulthood an increase in activity, a delay in task acquisition but no learning-memory impairment and reduced the level of anxiety allowing active responding to novelty. These quite subtle behavioral changes were accompanied by discrete metabolic decreases in regions mediating anxiety, reflecting a change in the level of anxiety and emotionality.

Animals↗
PubMed2006

Repeated cocaine effects on learning, memory and extinction in the pond snail Lymnaea stagnalis.

The persistence of drug addiction suggests that drugs of abuse enhance learning and/or impair extinction of the drug memory. We studied the effects of repeated cocaine on learning, memory and reinstatement in the pond snail, Lymnaea stagnalis. Respiratory behavior can be operantly conditioned and extinguished in Lymnaea, and this behavior is dependent on a critical dopamine neuron. We tested the hypothesis that repeated cocaine exposure promotes learning and memory or attenuates the ability to extinguish the memory of respiratory behavior that relies on this dopaminergic neuron. Rotating disk electrode voltammetry revealed a K(m) and V(max) of dopamine uptake in snail brain of 0.9 micromol l(-1) and 558 pmol s(-1) g(-1) respectively, and the IC(50) of cocaine for dopamine was approximately 0.03 micromol l(-1). For operant conditioning, snails were given 5 days of 1 h day(-1) immersion in water (control) or 0.1 micromol l(-1) cocaine, which was the lowest dose that maximally inhibited dopamine uptake, and snails were trained 3 days later. No changes were found between the two groups for learning or memory of the operant behavior. However, snails treated with 0.1 micromol l(-1) cocaine demonstrated impairment of extinction memory during reinstatement of the behavior compared with controls. Our findings suggest that repeated exposure to cocaine modifies the interaction between the original memory trace and active inhibition of this trace through extinction training. An understanding of these basic processes in a simple model system may have important implications for treatment strategies in cocaine addiction.

Animals↗
PubMed1987

Effects of standardized ginseng extract on learning, memory and physical capabilities.

Standardized ginseng extract (G115, Pharmaton, Lugano) was administered orally at doses of 3, 10, 30, 100 and 300 mg/kg for 10 days as ten rats were used with each dose. With the "shuttle-box" method for active avoidance most pronounced effect on learning and memory was obtained by the dose of 10 mg/kg. With the "step-down" method for passive avoidance the dose of 30 mg/kg significantly improved retention. In the staircase maze training with positive (alimentary) reinforcement only the dose of 10 mg/kg significantly improved learning and memory. The dose of 100 mg/kg greatly increased the locomotor activity of mice. The results show that ginseng at appropriate doses improves learning, memory and physical capabilities. Bell-shaped dose-effect curves, reported with other nootropic drugs, were obtained.

Animals↗
PubMed1999

Learning, memory and a respiratory central pattern generator.

In an attempt to elucidate the causal mechanisms underlying learning and memory we have developed a model system, aerial respiration in the pond snail Lymnaea stagnalis. A three-neuron central pattern generator (CPG) whose sufficiency and necessity have been demonstrated mediates this behaviour. Aerial respiration, while an important homeostatic behaviour, is inhibited by the activation of the whole body withdrawal response that the animal uses to protect itself. We found that it was possible to operantly condition snails not to perform aerial respiration in a situation, a hypoxic environment, where aerial respiration should predominate. Operant conditioning was achieved by eliciting the pneumostome withdrawal response, part of the whole body withdrawal response, each time the animal attempted to open its pneumostome to breathe. Yoked control animals did not demonstrate an alteration in breathing behaviour. Subsequently we determined neural correlates of this associative behaviour and found that neuronal changes are distributed throughout the CPG. This preparation may afford us the opportunity to determine the casual neuronal changes that underlie learning and memory of associative conditioning.

Animals↗
PubMed1993

Effects of kindling on subsequent learning, memory, behavior, and seizure susceptibility.

To determine the long-term effects of seizures on the developing brain we kindled 20-, 40-, and 60-day-old rats to stage 5 seizures and then elicited an additional 15 seizures using the same kindling stimulation. At age 80 days, all animals that reached stage 5 kindling, and their respective age-matched controls, underwent behavioral testing using the Morris water maze, open field test, and handling test. Prior to euthanasia the animals had seizure threshold tested using flurothyl inhalation. No differences were noted in time to platform in the water maze or activity level in the open field test between the kindled rats and controls in any of the three age groups. Rats kindled at age 20 and 40 were more emotional than the controls in the handling test. In the flurothyl inhalation test, rats kindled at 40 and 60 days of age had a shorter latency to all seizures stages than the controls. These results demonstrate that while kindling results in no alteration of learning, memory, or activity level, it does result in altered emotionality and activity level in immature animals, as well as reduced seizure threshold in pubescent and mature rats. The animal model used appears to be an important variable in determining the long-term effects of seizures.

Administration, Inhalation↗
PubMed1991

Memory, learning and neuromediators.

We consider a model of a neural network where the individual cells interact only by releasing and absorbing the molecules of a neuromediator. We show that such a system can realize the function of associative memory. A learning mechanism based on the chemotaxis is proposed and numerically investigated.

Association Learning↗
PubMed2003

Learning, memory, and transcription factors.

Cognitive disorders in children have traditionally been described in terms of clinical phenotypes or syndromes, chromosomal lesions, metabolic disorders, or neuropathology. Relatively little is known about how these disorders affect the chemical reactions involved in learning and memory. Experiments in fruit flies, snails, and mice have revealed some highly conserved pathways that are involved in learning, memory, and synaptic plasticity, which is the primary substrate for memory storage. These can be divided into short-term memory storage through local changes in synapses, and long-term storage mediated by activation of transcription to translate new proteins that modify synaptic function. This review summarizes evidence that disruptions in these pathways are involved in human cognitive disorders, including neurofibromatosis type I, Coffin-Lowry syndrome, Rubinstein-Taybi syndrome, Rett syndrome, tuberous sclerosis-2, Down syndrome, X-linked alpha-thalassemia/mental retardation, cretinism, Huntington disease, and lead poisoning.

Animals↗
PubMed1996

Function of metabotropic glutamate receptors in learning and memory.

Learning is the modification of behaviour by experience, and memory is the retention of such modifications. Since learning events might be of short duration, selective neuronal mechanisms must exist to translate transient activity into long-lasting memory. Because metabotropic glutamate (mGlu) receptors are coupled to various second messenger cascades they are ideal candidates for such translations. Their involvement in synaptic plasticity has been demonstrated recently, an important finding given that changes in synaptic efficacy are widely believed to be the physical substrate for information storage. Behavioural investigations using selective drugs have demonstrated that memory formation, especially of hippocampus-dependent tasks, is blocked by pre-training treatment with both mGlu-receptor agonists and antagonists. In contrast, agonists administered post-training might amplify memory formation. The hypothesis put forward here suggests that the primary function of mGlu receptors is to set the signal-to-noise ratio and thereby filter out unimportant or amplify important information.

Animals↗
PubMed2006

Changes of learning, memory and levels of CaMKII, CaM mRNA, CREB mRNA in the hippocampus of chronic multiple-stressed rats.

BACKGROUND: The effect of chronic stress on cognitive functions has been one of the hot topic in neuroscience. But there has been much controversy over its mechanism. Such single stressor applied in the past could not simulate complicated living circumstances that people confronted with. The aim of this study was to investigate the effects of chronic multiple-stress on learning and memory as well as on the levels of calcium/calmodulin-dependent protein kinase II (CaMKII), calmodulin (CaM) mRNA, and cAMP-response element binding protein (CREB) mRNA in the hippocampus of rats. METHODS: The rats were divided randomly into stressed and control groups. The stressed group was given chronic multiple-stress for 6 weeks to set up a chronic multiple-stressed model. The rats' performance of spatial learning and memory was tested using Morris Water Maze (MWM) and Y-maze. Meanwhile, the expressions of CaMKII, CaM mRNA and CREB mRNA of rats' hippocampus were detected by immunohistochemistry, Western blot and reverse transcription-polymerase chain reaction (RT-PCR), respectively. In addition, the width of synaptic cleft and the thickness of post-synaptic densities (PSD) were observed in the hippocampal CA3 region of rats by electron microscopy. RESULTS: After exposure to chronic multiple-stress for 6 weeks, the ability of learning and memory of the stressed group was higher than that of the control group (P < 0.05, P < 0.01). The width of synaptic cleft was smaller and the thickness of PSD was larger in the hippocampal CA3 region of the stressed group than in that of the control group (P < 0.01). The CaMK II immunostaining of the stressed group was stronger than that of the control group in the stratum radiatum and oriens of the hippocampal CA1 and CA3, especially in the stratum oriens. Quantitative analysis indicated that the expression of CaMK II, CaM mRNA, and CREB mRNA in the hippocampus of the stressed group was higher than that of the control group (P < 0.05, P < 0.01). CONCLUSIONS: The capacity of learning and memory can be enhanced after chronic multiple-stress. The increased levels of CaMK II, CaM mRNA, and CREB mRNA may contribute to the enhancing effect of chronic multiple-stress on learning and memory.

Animals↗
PubMed1996

[Correlation between ability of learning-memory and synaptosomal free [Ca2+]i in mice of different age].

In the present investigation, the behavior of learning and memory of 1-month and 6-month-old mice was studied by using Y-maze and one-trial passive avoidance response device. The synaptosomal free [Ca2+]i of four main brain regions (Hippocampus, Cerebral cortex, Cerebellum, Tectum of midbrain) of these mice were measured by fluorescent probe Ca2+ indicator Fura-2 and an AR-CM-MIC cation measurement system. The results showed that, in comparison with 1-month-old mice, the ability of discrimination learning and memory of 6-month-old ones were attenuated, and the synaptosomal free [Ca2+]i of hippocampus was increased.

Age Factors↗
PubMed2005

Cortisol, learning, memory, and attention in relation to smaller hippocampal volume in police officers with posttraumatic stress disorder.

BACKGROUND: A proposed explanation for memory impairments in posttraumatic stress disorder (PTSD) is stress-induced hippocampal damage due to elevated cortisol levels. We have previously reported smaller hippocampi in police officers with PTSD. In this study, we examined changes in and associations between cortisol, learning, memory, attention, and hippocampal volume in PTSD. METHODS: In a case-matched control study, 12 police officers with PTSD and 12 traumatized police officers without lifetime PTSD were examined with magnetic resonance imaging (for hippocampal volume), salivary cortisol tests, and neurocognitive assessments. RESULTS: Significantly smaller hippocampi and higher early morning salivary cortisol levels were found in PTSD. Subjects with PTSD performed worse on a delayed visual memory recall task at trend level, and made more perseverations and intrusions on a verbal memory task. Negative correlations were found between PTSD symptom severity and immediate recall function, and between re-experiencing symptoms and left hippocampal volume. A positive correlation was found between salivary cortisol level in early morning and right hippocampal volume; however, hippocampal volume did not correlate with memory. CONCLUSIONS: Smaller hippocampi, higher cortisol levels, and memory impairments were associated with PTSD but were not directly correlated to one another. Memory impairments in PTSD do not seem to be a direct consequence of hippocampal size.

Adult↗
PubMed1993

Glutamate: its role in learning, memory, and the aging brain.

L-Glutamate is the most abundant of a group of endogenous amino acids in the mammalian central nervous system which presumably function as excitatory neurotransmitters and under abnormal conditions may behave as neurotoxins. As neurotransmitters, these compounds are thought to play an important role in functions of learning and memory. As neurotoxins, they are believed to be involved in the pathogenesis of a variety of neurodegenerative disorders in which cognition is impaired. Moreover, brain structures which are considered anatomical substrata for learning and memory may be particularly vulnerable to the neurotoxic actions of these excitatory amino acids, especially in the elderly who are also the segment of the population most susceptible to impairments of mnemonic function. This paper is a review of data concerning the role of excitatory amino acids in the processes of learning and memory and in the pathogenesis and treatment of disorders thereof.

Aging↗
PubMed2004

Effects of puerarin on learning-memory and amino acid transmitters of brain in ovariectomized mice.

In the present study, the protective effects of puerarin (Pur) on learning and memory in ovariectomized mice were investigated. One week after ovariectomy (Ovx) or sham operation, female mice were given a 4-week treatment of Pur (50 or 100 mg/kg,i.p.) or estradiol benzoate (EB, I or 5 pg/day, i.p.). The results showed that, following treatment with 50 or 100 mg/kg Pur in Ovx mice, the training times for achieved learning criterion in aY-maze declined by 11.8 % and 17.8 % (P > 0.05 and P < 0.05), and that memory retention increased by 23.3 % and 28.3 % (P < 0.05 and P < 0.05), respectively. In addition, the prolonged escape latency of platform finding in a water maze was shortened by 15.5% and 23.8% (P < 0.05 and P < 0.05). After a behavior test,the levels of glutamate (Glu) and GABA in the frontal cortex and hippocampus were assessed using high-performance liquid chromatography (HPLC). The results showed that 100 mg/kg Pur normalized the levels of Glu and GABA in the hippocampus of Ovx mice, while the Glu level was significantly elevated from 24.1+/- 4.5 to 27.9+/- 3.5 mg/g protein (P < 0.05), and GABA was decreased from 5.64+/- 1.06 to 4.73+/- 0.85 mg/g protein (P < 0.05). The results indicated that Pur possessed phytoestrogen activity,and long-term treatment of Pur ameliorated learning and memory deficits of Ovx mice through affecting the activity of the glutamatergic/GABAergic system in the hippocampus.

Animals↗
PubMed1991

Cholinergic mechanisms in learning, memory and dementia: a review of recent evidence.

The discovery in the late 1970s that cholinergic neurons in the basal forebrain degenerate in Alzheimer's disease (AD) greatly accelerated research on the role of cholinergic mechanisms in learning and memory. As is often the case in science, the early enthusiasm for the cholinergic hypothesis has been tempered by the results of subsequent research. Although there is substantial pharmacological evidence that unspecified cholinergic systems in the brain play important roles in some forms of learning and memory, recent findings in humans indicate that antimuscarinic drugs do not model the deficits seen in AD. In addition, the goal of elucidating the functions of these basal forebrain neurons in animals has proved to be difficult and is yet to be achieved. Despite substantial effort, therefore, the cognitive and behavioral consequences of cholinergic pathology in AD remain unknown. Under these circumstances, attempts to develop cholinergic pharmacotherapies for these deficits in AD are based on questionable assumptions.

Animals↗
PubMed2004

Effects of electroacupuncture on learning, memory and formation system of free radicals in brain tissues of vascular dementia model rats.

In order to observe the regulative effect of electro-acupuncture on the formation system of free radicals in the brain tissues and learning and memory in vascular dementia (VD) model rats, the Morris's water labyrinth was used for testing the learning ability and memory in VD model rats made by 4-vessel occlusion method, and the activities or contents of nitric oxide (NO), NO synthase (NOS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) were determined. Results showed that the mean escape latency in the electro-acupuncture group was markedly reduced in place test, and the times swam the place of the plate-form in the original plate-form quadrant were significantly more than those in the rest three quadrants in spatial probe test as compared with the model group. In the electro-acupuncture group and the nimodipine group the contents of NO and MDA and the activity of NOS were decreased, while the activities of SOD and GSH-Px were increased. It is indicated that electro-acupuncture can modulate the production and clearance of free radicals, and improve the ability of learning and memory of the VD model rats.

Animals↗
PubMed2006

Small-conductance Ca2+-activated K+ channel type 2 (SK2) modulates hippocampal learning, memory, and synaptic plasticity.

Apamin-sensitive, small-conductance, Ca2+-activated K+ channels (SK channels) modulate neuronal excitability in CA1 neurons. Blocking all SK channel subtypes with apamin facilitates the induction of hippocampal synaptic plasticity and enhances hippocampal learning. In CA1 dendrites, SK channels are activated by Ca2+ through NMDA receptors and restrict glutamate-mediated EPSPs. Studies of SK channel knock-out mice reveal that of the three apamin-sensitive SK channel subunits (SK1-SK3), only SK2 subunits are necessary for the apamin-sensitive currents in CA1 hippocampal neurons. To determine the specific influence of SK2 channels on hippocampal synaptic plasticity, learning, and memory, we used gene targeting through homologous recombination in embryonic stem cells to generate transgenic mice that overexpress SK2 subunits by 10-fold (SK2+/T). In these mice, the apamin-sensitive current in CA1 neurons was increased by approximately fourfold, relative to wild-type (WT) littermates. In addition, the amplitude of synaptically evoked EPSPs recorded from SK2+/T CA1 neurons increased twice as much in response to SK channel blockade relative to EPSPs recorded from WT CA1 neurons. Consistent with this, SK2 overexpression reduced long-term potentiation after high-frequency stimulation compared with WT littermates and severely impaired learning in both hippocampus- and amygdala-dependent tasks. We conclude that SK2 channels regulate hippocampal synaptic plasticity and play a critical role in modulating mechanisms of learning and memory.

Animals↗