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PubMed2006

Simvastatin enhances learning and memory independent of amyloid load in mice.

OBJECTIVE: Normal aging is often associated with a decline in learning and memory functions. This decline is manifested to a much greater extent in Alzheimer's disease. Recent studies have indicated statins, a class of cholesterol-lowering drugs, as a potential therapy for Alzheimer's disease. Our objective was to determine whether administering a statin drug (simvastatin) would protect against the development of behavioral deficits in an established mouse model of Alzheimer's disease. METHODS: Tg2576 mice and their nontransgenic littermates were treated with simvastatin and assessed by behavioral tests and biochemical analyses. RESULTS: Simvastatin treatment not only reversed learning and memory deficits in the Tg2576 mice, but also enhanced learning and memory in the nontransgenic mice. Moreover, levels of amyloid beta protein in the brains of treated mice did not differ from those of untreated mice. Simvastatin treatment was associated with increased expression levels of protein kinase B (Akt) and endothelial nitric oxide synthase in the mouse brain. INTERPRETATION: Our findings demonstrate that the effects of simvastatin on learning and memory are independent of amyloid beta protein levels. The mechanisms by which simvastatin exerts its beneficial effects may be related to modulation of signaling pathways in memory formation.

Alzheimer Disease↗
PubMed2005

Profound but transient deficits in learning and memory after global ischemia using a novel water maze test.

The pyramidal CA1 neurons of the hippocampus are critically involved in spatial learning and memory. These neurons are especially vulnerable to cerebral ischemia, but in spite of this, it has been consistently difficult to show any learning and memory deficits in two-vessel occlusion models of global ischemia. Transient global ischemia was induced in adult male rats under general anaesthesia administered by artificial respiration to prevent respiratory arrest. Systemic blood pressure was reduced to below 50 mmHg by instant adjustments of the halothane concentration, before and during bilateral occlusion of the carotid arteries. Cerebral blood flow was monitored by laser-Doppler flowmetry. Dying neurons were detected by TUNEL at 14 days after ischemia and surviving neurons by NeuN at 14 and 125 days after ischemia. Learning and memory was assessed in a novel water maze with three successive left-right choices. Transient global ischemia produced a profound and selective degeneration of CA1 neurons at 14 days after ischemia. This degeneration was associated with severe impairments in learning at 13 days after ischemia and in memory, as tested 24 h afterwards. At 125 days after ischemia, there was no significant learning and memory impairment, whereas the number of CA1 neurons was increased. These results show that transient global ischemia induced by two-vessel occlusion may lead to severe, but transient, impairments in learning and memory using a novel water maze, and that restored learning and memory is associated with an increased number of CA1 neurons.

Analysis of Variance↗
PubMed1996

Metabotropic glutamate receptors in hippocampal long-term potentiation and learning and memory.

Glutamate receptors have been identified as important interfaces in learning and memory paradigms as well as in mechanisms of synaptic plasticity, such as long-term potentiation (LTP) and long-term depression (LTD), which are believed to be the underlying cellular basis of at least some forms of learning. Although investigations of G-protein-coupled receptors have a long history, those depending on ligand-binding of glutamate have only been discovered recently, and this is the reason why our knowledge about metabotropic glutamate receptors (mGluRs) is at present very limited. However, the development of relatively specific antagonists and agonists has enabled the analysis of the role of mGluRs in synaptic plasticity, mostly studied on the models of LTP and LTD. Among others, we have been able to demonstrate that activation of mGluRs is essential for induction and maintenance of long-lasting hippocampal LTP in vitro and in vivo. The work conducted by several groups, including ours, has now provided compelling evidence that mGluR activation is an important step in the cellular cascades leading to memory formation in vertebrates. This led us to assume, given that the hippocampus plays a prominent role in spatial rather than discrimination learning, that mGluRs may participate in the processing of spatial information via hippocampal mechanisms, and may thus be similarly important as N-methyl-D-aspartate receptors. This article surveys the literature dealing with mGluRs in hippocampal LTP and learning and memory. We will demonstrate that, although the understanding of cellular mechanisms of neuronal plasticity and of the pharmacology of learning and memory has advanced, the missing link to prove that LTP is a substrate for some form forms of learning still remains unsolved. Nevertheless, it appears reasonable to argue that mGluRs in LTP and learning may share some, but not all features, and it will be an interesting approach for further analysis to address the unresolved issues.

Animals↗
PubMed2001

Effect of irradiation at the early foetal stage on adult brain function of mouse: learning and memory.

PURPOSE: To study the long-term effect of early foetal irradiation on the learning and memory in the adult mouse. MATERIALS AND METHODS: The abdominal area of pregnant Swiss albino mice was exposed to a single dose of 0.25-1.5Gy gamma-radiation on the 14th day of gestation and the mice were left to deliver their offspring. At 6 months of age, the learning and memory functions of the F(1) mice were tested by hole-board activity, conditioned avoidance response and radial arm maze performance. The animals were again subjected to the radial arm maze test at 12 and 18 months of age. RESULTS: There was a significant dose-dependent decrease in the learning ability and memory retention of 6-month-old mice at doses > 0.25Gy. The significant changes persisted to 18 months of age in mice exposed to >or= 0.5Gy. All changes showed a linear dose-response at doses < 1Gy. CONCLUSIONS: The gestational day 14 of Swiss albino mice is a sensitive stage in brain development to gamma-ray-induced impairment of learning and memory during the adult life. Permanent deficits in these functions can be induced by a dose of approximately 0.5Gy at this stage, when the developmental activity of the cerebral cortex is at its peak.

Age Factors↗
PubMed1987

Learning and memory impairment with benzhexol.

A double-blind trial to determine the effects of a single dose of 2 mg benzhexol on cognitive functioning was undertaken using normal volunteers. Ninety minutes after the drug or placebo was taken, subjects completed a battery of psychological tests designed to measure learning, memory and motor skills. Benzhexol ingestion was associated with significant impairment of short-term memory and slowing of the rate of new learning.

Adult↗
PubMed2005

Memory and verbal learning functions in twins with bipolar-I disorder, and the role of information-processing speed.

BACKGROUND: Euthymic bipolar-I disorder (BP I) patients and their siblings have shown impairments in verbal learning and memory functions compared with controls, suggesting that these impairments may be genetic in origin. Reduced information-processing speed has been associated with impaired memory in the elderly, and recently in schizophrenia. The authors compared verbal learning and memory functioning in twins with BP I and co-twins to control twins, and examined whether the observed deficits are related to information-processing speed. METHOD: Finnish Medical and Population Registers and Twin Cohorts were used to identify the BP I and control twins. Neuropsychological tests assessing verbal learning and memory, working memory, facial recognition, visual memory, and information-processing speed were administered to 26 BP I twins, 19 non-bipolar co-twins, and 114 controls. Group differences were analyzed by generalized estimation equation modeling. RESULTS: BP I patients, but not co-twins, showed impairments in all memory tests compared with controls. Female co-twins showed impairment in verbal learning and memory. Information-processing speed had a significant effect on encoding and learning efficiency. CONCLUSIONS: This study showed for the first time that information-processing speed is related to memory functioning and verbal learning in BP I in a population-based, representative and euthymic sample. Furthermore, the data support the view that defects in verbal memory may be related to the genetic factors predisposing to BP I in females.

Adult↗
PubMed1990

Learning and memory deficits in rats following exposure to 3,3'-iminodipropionitrile.

Rats were examined using a learning and memory test battery 4 weeks following exposure to 3,3'-iminodipropionitrile (IDPN). Initial testing revealed deficits in olfactory discrimination and passive avoidance (PA) conditioning. In order to dissociate learning and performance effects, additional tests were conducted. First, to rule out the possibility that IDPN reduced the aversiveness of foot shock, rats were tested in a simple shock sensitivity paradigm. The results indicated no change in shock sensitivity produced by IDPN. Second, to determine if the hyperactivity produced by IDPN was responsible for deficits in conditioning, several additional tests were conducted including (a) repeated-trials active avoidance (AA) and PA conditioning, (b) a PA study which included both a 1- and 24-hr training-testing interval, and (c) long-delay flavor-aversion conditioning. Rats treated with IDPN required more conditioning trials to reach criterion on both AA and PA procedures suggesting that they were capable of performing the required response but acquired those responses at a much slower rate. The deficits in PA conditioning were similar at both the 1- and 24-hr training-testing interval. Finally, the effects of IDPN on flavor-aversion conditioning depended on the delay separating flavor intake and lithium administration during conditioning. Rats treated with IDPN demonstrated robust flavor aversions when trained with a 30-min but not with a 6-hr delay. In summary, the neurotoxic profile of effects produced by IDPN must be expanded to include a prominent cognitive component characterized by protracted deficits in learning and memory capacity. The present experiment illustrates how chemically induced disruption of learning and memory produced by IDPN can be experimentally dissociated from associate neurological symptoms using a simple, routine battery of neurobehavioral tests.

Animals↗
PubMed2005

The effect of intrahippocampal injection of testosterone enanthate (an androgen receptor agonist) and anisomycin (protein synthesis inhibitor) on spatial learning and memory in adult, male rats.

In most mammals, the hippocampus has a well-documented role in spatial memory acquisition. High concentration of androgen receptors in fundamental centers of learning and memory in brain such as hippocampus shows that there may be some relationships between androgen receptors and cognitive aspects of brain. Previous studies, which have shown sex-dependent differences in hippocampal morphology and physiology, suggest a modulatory role for sex steroids in hippocampal function. Androgens have been shown to modulate some hippocampal-mediated behaviors including learning and memory. To study the mechanism of action of androgens in processes underlying learning and memory, anisomycin, a protein synthesis inhibitor was used to prevent the genomic effects of testosterone. Therefore, the effects of anisomycin and testosterone together were assessed on rat's performance in MWM. Rats received anisomycin (2.5 microg/0.5 microl), testosterone (80 microg/0.5 microl) or both anisomycin (2.5 microg/0.5 microl) and testosterone (80 microg/0.5 microl) through the connulas in the CA1 region. Anisomycin was injected 20 min and testosterone was injected 35 min before training each day. The results showed that anisomycin (2.5 microg/0.5 microl) and testosterone (80 microg/0.5 microl) increased latencies to find the invisible platform. But the group that received testosterone and anisomycin together was decrease in latency and traveled distance to find the invisible platform.

Androgen Receptor Antagonists↗
PubMedDate not supplied

Cellular and molecular mechanisms underlying learning and memory impairments produced by cannabinoids.

Why does smoking marijuana impair learning and memory? Behavioral studies suggest that a disruption of normal hippocampal function contributes to these deficits. In vitro experiments find that cannabinoid receptor activation reduces neurotransmitter release below the levels required to trigger long-term changes in synaptic strength in the hippocampus. Cannabinoids reduce glutamate release through a G-protein-mediated inhibition of the calcium channels responsible for neurotransmitter release from hippocampal neurons. These mechanisms likely play a role in the learning and memory impairments produced by cannabinoids and by endogenous cannabinoid receptor ligands.

Animals↗
PubMed1994

Color learning and memory in honey bees are not affected by protein synthesis inhibition.

The role of protein synthesis was tested for memory formation after color learning in honey bees. Free flying bees were trained to a feeding place. Before the color conditioning started, foragers accustomed to flying to the feeding place received an injection of either cycloheximide in bee ringer or bee ringer alone into the brain. Afterward, the animals were trained appetitively to a specific colored target by three training trials. During the test situation, two targets with different colors and no reward were presented. The choice behavior toward the two targets was evaluated. The first test immediately followed the last trial, the second test 24 h later. A comparison between cycloheximide- and ringer-injected bees showed no significant difference in choice behavior in either test. Although the injection of cycloheximide causes the inhibition of protein synthesis (> 95%) for a period of 3 h, the memory for the learned color signal is not affected. These results corroborate those found for the olfactory conditioning of the proboscis extension reflex in bees (Wittstock, Kaatz, & Menzel, 1993, Menzel, Gaio, Gerberding, Nemrava, & Wittstock, 1993).

Animals↗
PubMed2001

Imaging learning and memory: classical conditioning.

The search for the biological basis of learning and memory has, until recently, been constrained by the limits of technology to classic anatomic and electrophysiologic studies. With the advent of functional imaging, we have begun to delve into what, for many, was a "black box." We review several different types of imaging experiments, including steady state animal experiments that image the functional labeling of fixed tissues, and dynamic human studies based on functional imaging of the intact brain during learning. The data suggest that learning and memory involve a surprising conservation of mechanisms and the integrated networking of a number of structures and processes.

Animals↗
PubMed1976

Effect of imidazole, papaverine and histamine on learning and memory in albino rats.

In experiments for learning of albino rats in a maze and testing of the memory 24 hours and 30 days after learning, it was established that: Imidazole introduced i.p. in doses of 10, 30 and 60 mg/kg had no effect on learning, though it improved the memory both after administration 1 to 15 min before learning and when injected immediately after learning. Papaverine in doses of 2, 0.5 and 0.1 mg/rat and histamine in doses of 0.1, 0.01 and 0.001 mg/rat, introduced ventricularly before learning, make learning impossible (the large doses), deteriorate it (the medium doses), or have no effect on it (the small doses). Memory also deteriorates, with the exception of the smallest histamine dose. Introduced immediately after learning, the large dose of papaverine deteriorates memory, while the small dose results in a tendency to improve the memory indices upon testing 24 hours after the administration. The large dose of histamine administered after learning has no effect, the small dose results in a certain tendency to improve memory when tests are made 30 days after learning. The results obtained and their comparison with the results of previous works of ours involving other drugs with a known effect on the system of the cyclic adenosinemonophosphate (cAMP), e.g. haloperidol, lithium, caffeine and theophylline (in the doses tested), do not suggest any essential role of the effect of these drugs on the cAMP system in the mechanism of their effects on learning and memory.

Animals↗
PubMed1995

Chronic phenytoin induced impairment of learning and memory with associated changes in brain acetylcholine esterase activity and monoamine levels.

Groups of adult, male, Wistar rats were administered phenytoin (DPH) at 5, 12.5, 25, 50, or 75 mg/kg i.p. for 21 days. The learning and memory of these rats were assessed using the T-maze and passive avoidance tests. The plasma DPH levels, acetylcholine esterase (AChE) activity in different brain regions, and the levels of monoamines in the hippocampus were measured. The results indicate that DPH below the therapeutic plasma level did not significantly impair learning and memory. Correspondingly, no changes were noted in the brain 5-HT or AChE activity. However, DPH, at therapeutic plasma concentrations (i.e., 10.5 micrograms/ml in the dosage range of 50 and 75 mg/kg, respectively), significantly impaired learning and memory in rats. The impaired learning and memory functions were associated with increased 5-HT levels and decreased AChE activity in the hippocampus. With a dose of 75 mg/kg DPH, there was a reduction in the AChE activity in the striatum, in addition to hippocampus. It is conjectured that the neurochemical changes brought about by DPH at therapeutic plasma levels may account for the impairment of learning, memory, and cognitive functions in epilepsy.

Acetylcholinesterase↗
PubMed2004

Postnatal dexamethasone and long term learning and memory functions in developing rats: Effect of postnatal age and gender.

In this study, we investigated the effect of dexamethasone on the long-term learning and memory functions in developing rats. In Sprague-Dawley rat pups, we administered a daily dose of dexamethasone (0.5 mg/kg/day) for three consecutive days in three groups of animals: the "ultra-early" group received steroids on postnatal days (PND) 1-3; the "early" group received the drug on PNDs 8-10, and the "late" group received the drug on PNDs 28-30. The control group was not given any medication. All animals underwent structured CNS examinations beginning on PND 15, and continued through PND 20. The pups were tested for spatial learning and memory functions using the Morris Water Maze (MWM) on PNDs 31 through 35, 45 through 49, and 59 through 63. They were also tested for reward-based learning and memory functions using Radial Arm Maze (RAM) on PNDs 70 through 72. We analyzed the effect of dexamethasone, postnatal age, and sex on neurological milestones, and learning and memory functions. We found that neurological examination findings were similar in all groups, as were the results of the reward-based learning using RAM. However, in the MWM, the total distance of swimming and the total time to find the hidden platform showed considerable difference among the groups. Although these functions improved with postnatal age, the female pups in all three steroid groups, and the male pups in the late-steroid group lagged significantly in learning and memory functions compared to the controls, and such lags were transient. However, the interaction terms between dexamethasone, age, and sex were also significant in MWM test results. Steroids administered postnatally may have transient, retarding effect on learning and memory functions, and that animal age and sex may modify such effects. Such lags are not global, but specific to the types of memory tests used, implicating different neural circuitries in the pathogenesis of such abnormalities. Although transient, if such adverse effects occur at critical phases during brain maturation, the implications for poor, long-term outcomes may be more significant. The mechanisms underlying such changes need to be explored.

Age Factors↗
PubMed1979

Food delivery as a conditional stimulus: Feature-learning and memory in pigeons.

Three experiments investigated the learning and memory of discriminations based on presence versus absence of a pre-trial food delivery. In Experiment 1 half the illuminations of a response key were followed by food regardless of the subject's behavior. In one group an extra food delivery preceded only reinforced trials (feature-positive condition), whereas in a second group it preceded only nonreinforced trials (feature-negative condition). Key pecks and approaches revealed more rapid and superior discrimination learning in the first group. Experiment 2 replicated the results of Experiment 1 but yielded no evidence that greater "unexpectedness" of pretrial food conditions facilitates discriminative performance. In Experiment 3, individual pigeons trained on a conditional discrimination exhibited a within-subject feature-positive superiority. Delay between pretrial and trial stimuli interacted with feature-positive versus feature-negative training in both the between-group (Experiment 2) and within-subject (Experiment 3) procedures: performance was decremented at both short and long delays in the feature-positive condition but was decremented only at longer delays in the feature-negative condition. The feature-positive superiority obtained here is incompatible with explanations based on either the general concept of "perceptual organization" or on the conditional nature of feature-negative discriminations.

Journal Article↗
PubMed2005

Comparison of the impact of melatonin on chronic ethanol-induced learning and memory impairment between young and aged rats.

Chronic alcohol exposure causes functional and structural changes in nervous system which have all been associated with learning and memory impairments. Furthermore, alcohol consumption has been shown to alter the pattern of neural cell adhesion molecules (NCAM) which are involved in memory processes. In the current work, we investigated the effects of melatonin on learning and memory deficits induced by alcohol exposure in young and aged rats. A group of young rats (3 months old) were administered ethanol for 45 days and half of them were co-treated with melatonin. Similar treatments were performed in the aged (19 months old) rats. Morris water maze test and passive avoidance task were used to assess cognitive performance. Lipid peroxidation (LPO) and glutathione (GSH) levels were determined to characterize the level of oxidative stress in the hippocampus and cortex. NCAM levels were determined by Western blotting in the hippocampal homogenates. There was a significant elevation in LPO levels and a reduction in GSH levels in aged and alcohol-exposed rats. Furthermore, both young and aged rats displayed some cognitive impairment when given with alcohol for 45 days. Co-administration of melatonin with ethanol significantly reduced LPO and elevated GSH levels while improving the learning and memory deficits induced by ethanol; the aged rats exhibited a greater response to melatonin supplementation. Moreover, melatonin modulated NCAM expression in hippocampus. Present findings indicate that exposure to ethanol induces learning and memory deficits probably by generating reactive oxygen species and downregulating NCAM 180 in hippocampus of aged rats. Melatonin improves learning and memory deficits and the behavioral responses of rats to melatonin supplementation are age dependent.

Aging↗
PubMed1990

Hippocampal and prefrontal cortex contributions to learning and memory: analysis of lesion and aging effects on maze learning in rats.

Young adult rats with bilateral lesions to the hippocampus or prefrontal cortex, young operated controls, and normal old rats were tested on two complex mazes in the Hebb-Williams series. Approximately half the animals were previously trained on one of the mazes; the remainder received no previous training. The trained hippocampal rats showed sparing of memory for the general skill of maze learning but poor recall of the specific maze on which they had been previously trained. The opposite pattern was observed in trained prefrontal rats. In contrast, the aged rats' memory for maze-specific and maze-general information was impaired. The results confirmed the importance of the hippocampus for recalling highly specific information and pointed to a possible role for the frontal lobes in learning and remembering nonspecific skill-related information. The generalized deficit of the aged rats indicates that both types of memory were compromised and offers further evidence of frontal lobe and hippocampal dysfunction in normal aging.

Aging↗