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PubMedDate not supplied

[Prenatal exposure to sodium oxybutyrate prevents a disorder of general behavior, learning and memory in the progeny of rats subjected to chronic hemic hypoxia].

The hemic hypoxia caused by the methemoglobin-inducing agent sodium nitrite (40 mg/kg intraperitoneally at days 10 to 19 of pregnancy) evokes a decrease in the birth and survival rates of pups, delayed disorders of motor coordination. Prenatal hypoxia was demonstrated to be able to disturb the habituation in the open field, learning and memory in passive avoidance paradigm, cognitive ability in the plus-maze extrapolative water escape test. The treatment of pregnant rats with sodium hydroxybutyrate (150 mg/kg orally 1-3 times daily at days 12 to 19 of pregnancy) normalizes offsprings' birth and survival rates, prevents the above-mentioned neuropsychological disturbances and improves learning in the active avoidance test.

Animals↗
PubMed2003

The relationship between changes in learning and memory after right unilateral electroconvulsive therapy.

OBJECTIVE: We investigated whether the ability to learn new information, as opposed to recall information, would change significantly in depressed individuals treated by low- or high-dose right unilateral electroconvulsive therapy and tested whether change in learning explained changes in recall. METHOD: Fifty-four depressed patients randomized to receive right unilateral electroconvulsive therapy (ECT) at approximately 2.25 times their seizure threshold (ST) or at doses greater than 2.25 times ST were evaluated for verbal and figural memory as well as verbal and figural learning both pre- and post-ECT. A subset of scores from the Rey Auditory Visual Learning Test and the Rey Figure Test were analyzed using analysis of variance and linear regression techniques. RESULTS: Scores reflecting verbal learning decreased by a mean of approximately 50% immediately after a completed course of ECT as compared with pre-ECT verbal learning scores. Stratification of effect by dose of electrical charge revealed trends that did not achieve statistical significance. Approximately 8% of the change in delayed verbal recall was predicted by changes in verbal learning. Figural learning was not significantly changed in the aggregate (pre-versus post-treatment) or when the effect was stratified by electrical charge. CONCLUSIONS: Verbal learning scores declined immediately after ECT, but the change in learning scores explained only a minor part of the observed changes in verbal recall. These findings support the notion that the deficits in delayed recall after ECT represent a relatively specific cognitive effect that is not completely explained by changes in other aspects of cognition such as learning.

Aged↗
PubMed1998

Effects of N-[2-(1-azabicyclo[3,3,0]octan-5-yl)ethyl]2-nitroaniline fumarate (SK-946), a novel cognition activator, on learning and memory in rodent models.

We examined the effects of N-[2-(1-azabicyclo[3,3,0]octan-5-yl)ethyl]2-nitroaniline fumarate (SK-946) on cognition in various rodent models. SK-946 slightly suppressed spontaneous motor activity, but had no effect on scopolamine-induced motor facilitation. SK-946 ameliorated scopolamine-, pirenzepine-, cycloheximide- and electric shock-induced passive avoidance deficits in rodents when administered before acquiring the training. In an active avoidance test, SK-946 accelerated avoidance acquisition in the later half of training without a marked increase in lever-pressing. In more reliable models of cognitive disorders, i.e. an AF64A intracerebroventricular infusion model using the step-through passive avoidance test, an aged rat model using the step-down passive avoidance test and methylazoxymethanol (MAM)-induced microencephalic rat model using the Morris water maze test, SK-946 ameliorated impaired learning and memory. These results suggest an ability of SK-946 to enhance cognitive functions.

Aging↗
PubMed2006

Effect of dietary restriction on learning and memory impairment and histologic alterations of brain stem in senescence-accelerated mouse (SAM) P8 strain.

The age-associated spontaneous spongy degeneration in the brain stem of senescence-accelerated mouse (SAM) P8 strain has been suggested to be closely associated with the ability to learn and memorize. In this study, we investigated the effects of dietary restriction (DR) initiated from weaning on learning and memory and histologic changes of the brain stem in P8 and control R1 mice. Although no effect of DR was observed in the retention of the passive-avoidance response in both the P8 and R1 mice, the acquisition of the task was significantly improved by DR in P8 mice. On the other hand, the total area and number of vacuoles in the brain stem was significantly higher in ad libitum-fed (AD)-P8 mice than in AD-R1 mice. However, no significant effect was observed on the vacuole formation in the brain stem of P8 mice by DR. These observations suggest that the improvement of the acquisition of the task by DR in P8 mice is possibly due to changes in neuronal function rather than histologic alteration in brain stem.

Age Factors↗
PubMed2000

Motor cortex rules for learning and memory.

Primary motor cortex has a complex, interconnected anatomical and functional architecture with dynamic properties. Recent evidence suggests that, concomitantly with regulating muscle activity and movements, the motor cortex makes key contributions to learning and remembering motor skills.

Animals↗
PubMed2000

Cholinergic excitation of septohippocampal GABA but not cholinergic neurons: implications for learning and memory.

The medial septum/diagonal band (MSDB), which gives rise to the septohippocampal pathway, is a critical locus for the mnemonic effects of muscarinic drugs. Infusion of muscarinic cholinergic agonists into the MSDB enhance learning and memory processes both in young and aged rats and produce a continuous theta rhythm in the hippocampus. Intraseptal muscarinic agonists also alleviate the amnesic syndrome produced by systemic administration of muscarinic receptor antagonists. It has been presumed, but not proven, that the cellular mechanisms underlying the effects of muscarinic agonists in the MSDB involve an excitation of septohippocampal cholinergic neurons and a subsequent increase in acetylcholine (ACh) release in the hippocampus. Using a novel fluorescent labeling technique to selectively visualize live septohippocampal cholinergic neurons in rat brain slices, we have found that muscarinic agonists do not excite septohippocampal cholinergic neurons, instead they inhibit a subpopulation of cholinergic neurons. In contrast, unlabeled neurons, confirmed to be noncholinergic, septohippocampal GABA-type neurons using retrograde marking and double-labeling techniques, are profoundly excited by muscarine. Thus, the cognition-enhancing effects of muscarinic drugs in the MSDB cannot be attributed to an increase in hippocampal ACh release. Instead, disinhibitory mechanisms, caused by increased impulse flow in the septohippocampal GABAergic pathway, may underlie the cognition-enhancing effects of muscarinic agonists.

Acetylcholine↗
PubMed1991

Effects of the novel NMDA antagonist, NPC 12626, on long-term potentiation, learning and memory.

NPC 12626 (2-amino-4,5-(1,2-cyclohexyl)-7-phosphonoheptanoic acid), a newly developed drug which crosses the blood-brain barrier, is a competitive antagonist of N-methyl-D-aspartate receptors. In Experiment I, the effects of NPC 12626 on perforant path - dentate gyrus LTP were tested. NPC 12626 (100 mg/kg, i.p.), injected 150 min prior to tetanization, prevented potentiation of the EPSP slope and population spike amplitude. EPSP-spike potentiation was also prevented. Post-tetanus administration was ineffective. In Experiment II, mice were injected with NPC 12626 (35 mg/kg, i.p.) or saline 35 min prior to spontaneous alternation testing. NPC 12626 significantly decreased alternation rates, but did not affect turn bias or the mean delay between arm entries. This pattern of results may reflect impaired learning or memory. In Experiment III, mice were tested on an inhibitory avoidance task. NPC 12626 (35 mg/kg, i.p.), administered before but not after training, significantly impaired performance. When the drug was administered before training as well as before testing, performance was similarly impaired, indicating that the observed deficits were not attributable to state-dependent learning. Pre-test injections were ineffective. Overall, these results support the hypothesis that some forms of learning require the participation of NMDA receptors and that this participation is largely limited to acquisition processes. In addition, these results point to the utility of peripherally administered NPC 12626 as a tool with which to examine the involvement of NMDA receptors in LTP and learning.

Amino Acids↗
PubMed2006

Importance of K+-dependent Na+/Ca2+-exchanger 2, NCKX2, in motor learning and memory.

Plasma membrane Na+/Ca2+-exchangers play a predominant role in Ca2+ extrusion in brain. Neurons express several different Na+/Ca2+-exchangers belonging to both the K+-independent NCX family and the K+-dependent NCKX family. The unique contributions of each of these proteins to neuronal Ca2+ homeostasis and/or physiology remain largely unexplored. To address this question, we generated mice in which the gene encoding the abundant neuronal K+ -dependent Na+/Ca2+-exchanger protein, NCKX2, was knocked out. Analysis of these animals revealed a significant reduction in Ca2+ flux in cortical neurons, a profound loss of long term potentiation and an increase in long term depression at hippocampal Schaffer/CA1 synapses, and clear deficits in specific tests of motor learning and spatial working memory. Surprisingly, there was no obvious loss of photoreceptor function in cones, where expression of the NCKX2 protein had been reported previously. These data emphasize the critical and non-redundant role of NCKX2 in the local control of neuronal [Ca2+] that is essential for the development of synaptic plasticity associated with learning and memory.

Animals↗
PubMed1997

Neurobiological principles of learning and memory.

An increasing flow of evidences collected on elementary forms of learning processes in selected animal models evidentiates some mechanisms which can represent the basic cellular principles underlying plastic changes: 1. 5HT and second messengers of nucleotide type (like cAMP) have a pivotal role in the learning process. 2. In almost all short-term learning processes the modifications are subserved by a mechanism of protein phosphorylation. 3. In various animal models the modulation of K+ and Ca2+ channels is the molecular mechanism for learning. Experiments performed in sensory T neuron of the leech indicate that the modulation of Na+/K+ electrogenic pump is one of the fundamental mechanism for learning. 4. In long-term plastic changes, the most important finding is that newly synthesized proteins are formed. 5. In addition to what has been observed in the Aplysia model, where changes in synaptic efficacy represent the basic principles of memory storage, in the leech it has been demonstrated that a molecular machinery present in a single neuron can adapt the activity of the cell to environmental stimuli.

Amnesia↗