Effects of air ions on some aspects of learning and memory of rats and mice.
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Investigations were performed on 13 cats with epileptogenic focus developed after sectioning the optic chiasm and corpus callosum. Learning was begun 3 months after producing the epileptogenic focus by the aluminium method when it was bioelectrically active. Additionally in 6 cats DPH in daily doses of 10--15 mg/kg was given 3 months after development of the focus. Learning of these animals was begun 1--2 months after the beginning of DPH administration which was continued throughout the whole period of learning during a 3-month pause in learning, as well as at the time of memory testing. In all animals the time of conditioned reflex development and differentiation was delayed. Learning was more difficult in animals with epileptogenic focus receiving DPH than in the animals with the epileptogenic focus not receiving DPH. Learning was slightly worse in the hemisphere with the focus than in that without the focus. Presence of clinical epileptic seizures was without any significant effect on the time of learning with the exception of days on which clinical seizures occurred (the percent of responses was then lower). Disturbances of memory of acquired conditioned reflexes were found only in animals with clinical seizures.
Investigations of the neural basis of mammalian memory have focused more often on the medial temporal lobe (MTL) than on any other brain region. In humans, the amnesic syndrome revealed the essential importance of the multiple structures located in the MTL system for declarative memory (the remembrance of events and facts). Other neural systems mediate procedural forms of memory, including delay eyeblink conditioning, which depends on the cerebellum, and cognitive skill learning, which depends on the striatum. We review three functional imaging studies that reveal different patterns of MTL activation associated with declarative and procedural memory tasks. One study shows separate MTL activations during the encoding or retrieval of declarative memories. A second study shows MTL activation that occurs in parallel with cerebellum-dependent delay eyeblink conditioning, but does not appear to influence that form of procedural memory. A third study reveals suppression of the MTL during striatum-dependent cognitive skill learning. These studies provide images of MTL activations that are correlated with, independent from, or antagonistic to memory performance.
Different cholinomimetics are used in conditions of CNS acetylcholine (ACh) deficit. In this study, we examined the effect of the acetylcholinesterase inhibitor galanthamine in a prolonged alcohol intake model of ACh deficit in male Wistar rats. After 16 weeks of alcohol intake and a 2-week pause, rats administered galanthamine (2.5 mg/kg/day i.p.) showed an improved speed of learning and short-term memory in the shuttle box test as compared to the saline-injected alcoholic group (p < 0.05). Four weeks later, significant improvement in the passive avoidance memory of alcoholic galanthamine-treated rats was noted in the eight-arm radial maze (14 day test duration) as compared to the saline-injected alcoholic group (p < 0.05). During the first week in the shuttle box test, the nonalcoholic galanthamine-treated animals exhibited significantly impaired performance as compared to the untreated nonalcoholic control, while four weeks later, in the eight-arm radial maze, both groups did not differ. Our results show that galanthamine improves the speed of learning, short-term memory and spatial orientation of rats in conditions of prolonged alcohol intake.
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The effects of benzodiazepine dependence on the ability to learn and remember new material (determined with the Auditory-Verbal Learning Test) were studied in 20 detoxified, benzodiazepine-dependent patients who were 55 years of age or older and in a drug-dependence rehabilitation program. The patients were matched approximately for age, sex, and IQ with 20 detoxified, alcohol-dependent patients in the same rehabilitation program and 22 control subjects from a community sample. Neuropsychologic testing was performed a mean of 6 to 10 days after the patients had been completely detoxified from the addicting substance. The benzodiazepine-dependent patients had more difficulty with tests of learning and short-term and delayed recall than did the alcohol-dependent or control group. The difference between the benzodiazepine-dependent patients and the control group was statistically significant. The results suggest that benzodiazepine dependence in older people can cause memory impairment that persists into the early drug-free period.
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The possibility of a functional interaction between the amygdala and the ventral hippocampus during learning of a conditioned avoidance response when both brain structures are chemically stimulated with glutamic acid and/or histamine receptor antagonists (pyrilamine, H1-histamine antagonist and ranitidine, H2-histamine receptor antagonist) was studied in rats. Adult male rats were stereotaxically implanted with guide cannulae into the basolateral amygdala (A) and the ventral hippocampus (H). Seventy-two hours after the implant, rats were microinjected with 1 microl of saline solution, 10 nmol glutamic acid or 45 nmol of histamine receptor antagonists in several brain structures combinations. These combinations were: HsalAsal; HmsgAmsg; HmsgAsal; HsalAmsg; HpyrAmsg; HmsgApyr; HranAmsg and HmsgAran. Five minutes after the injection, rats were subjected to a learning task which consisted to avoid an electric shock applied to the animal's feet when an ultrasonic tone of 40 kHz is on for 30 s. Results showed that the simultaneous application of glutamic acid into hippocampus and amygdala interfered with the latency to escape and memory consolidation process. Stimulation with glutamic acid alone into the hippocampus or into the amygdala (HsalAmsg and HmsgAsal groups) interfered slightly with latency but impaired the consolidation process. Blocking the H1-histamine receptors of the amygdala affected slightly latency and efficiency of learning, meanwhile the blocking of H2-histamine receptors interfered with both parameters. Blocking H1- and H2-histamine receptors of the hippocampus significantly impaired latency and efficiency of learning of rats stimulated with glutamic acid into the amygdala. In conclusion, the experimental evidence suggests that hippocampal glutamic acid-neurons functionally interact with histamine-neurons in the basolateral amygdala to modulate memory and learning process.
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In two experiments the authors failed to detect an effect of inducing bilateral, long-lasting synaptic potentiation at perforant path dentate synapses on spatial learning by rats in the Morris place navigation task. Daily sessions of high-frequency stimulation of perforant path axons produced large increases to an asymptotic level in population spike and field excitatory postsynaptic potential recorded in ipsilateral dentate gyrus. Place learning proceeded normally 24 hours after the last of 14 high-frequency stimulation sessions in rats that had previously mastered the procedural aspects of place navigation (Experiment 1) and in rats that were naive (Experiment 2).
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We used fetal habituation to repeated vibroacoustic stimulation to assess fetal memory. After the initial stimulus, we assessed the fetuses 10 min later and again after 24 h. 16 of 19 fetuses habituated rapidly to the stimuli at 10 min (p=0.004) and 24 h (p=0.042) after the initial test. We conclude, therefore, that fetuses are able to learn: they have a short-term memory of at least 10 min, and a long-term memory of at least 24 h.
The neural cell adhesion molecule (NCAM) has been implicated in regulating synaptic plasticity mechanisms as well as memory consolidation processes. Attachment of polysialic acid to NCAM (PSA-NCAM) has been reported to down-regulate its adhesive forces, a process hypothesized to be implicated in synapse selection after learning experiences. PSA-NCAM has been critically implicated in hippocampus-related synaptic plasticity and memory storage, but information about its functional role in other brain areas remains scarce. Here, we studied mice deficient for polysialyltransferase-1 (ST8SialV/PST-1), an enzyme which attaches PSA to NCAM during postnatal development and adulthood, and whose deficiency results in a drastic reduction of PSA-NCAM expression throughout the brain in adulthood. Mice were tested for their performance in the water maze and auditory fear conditioning (AFC). We report that ST8SiaIV knockout mice were impaired in spatial as well as reversal learning in the water maze. On the other hand, AFC was intact and ST8SiaIV mice exhibited no impairments in the acquisition or retention of cued fear memories. Spatial orientation learning and reversal learning require complex integration of spatial information and response selection involving the hippocampus and prefrontal cortex, whereas cued fear conditioning is an associative type of emotional memory that highly depends on amygdala function. Therefore, our results indicate that PSA-NCAM contributes differentially to learning processes that differ in the nature of the neural computations involved, which probably reflects a differential role of this molecule in different brain regions.
OBJECTIVE: To study the influences of the mutants of human apolipoprotein E on the function of cerebral cortex. METHODS: The Southern blot hybridization and ELISA techniques were used for identification of integration and expression of human apoE4 and apoE7 genes at the mice chromosome and in the serum of F1 transgenic mice. Then the active avoidance response test was performed to determine the alteration of learning and short term and long term memory of the transgenic mice. The serum total cholesterol (TC) and triglyceride (TG) were determined simultaneously with enzymatic procedure. RESULTS: (1) In F1 transgenic mice the human apoE genes integrated at the chromosome and expressed in their serum stably. (2) In apoE4 mice the learning and short term memorizing abilities were decreased, and in apoE7 mice the short term memorizing abilities were decreased as well. In addition, the TC and TG increased statistically. CONCLUSIONS: The overexpression of human apoE4 and apoE7 genes in transgenic mice could damage the function of cerebral cortex. It denoted that the mutations of apoE might correlate the pathogenesis of Alzheimer's disease.
The ability to reproduce from memory a short list of verbal items immediately following presentation is known to improve over successive trials on that list, even if these trials are embedded in a sequence of trials on other lists of the same sort (Hebb, 1961). Less clear is whether this "Hebb effect" arises without the list repetition being noticed. This question has long been pondered and has recently taken on particular theoretical significance, but the available evidence is scant and inconsistent. Two experiments are described in which, in essence, a sequence of immediate reproduction trials was followed by tests that called for list recognition (Experiments 1 and 2) and/or estimates of list presentation frequency (Experiment 1). These tests provided quantitative measures of repetition awareness. Typical Hebb effects were found, but there was no evidence that the effects occurred without the subjects' being aware of the repetition; effect-size analyses indicated that both the recognition and frequency responses were more sensitive to repetition than were the reproduction responses. Therefore, not only could the recognition and frequency responses not have been made solely on the basis of how readily the test lists were reproduced, but the Hebb effect could have required an awareness of repetition.