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PubMed1972

Effect of corticotropin and desglycinamide 9 -lysine vasopressin on suppression of memory by puromycin.

The puromycin-induced blockade of expression of maze learning in mice can be prevented by subcutaneous administration of "Purified Cortrophin Gel" up to 3 days prior to training. A similar protective effect was not found when highly purified corticotropin was tested, but was observed after administration of desglycinamide(9)-lysine vasopressin. It appears that pressorpeptides are more potent protective agents than corticotropin when administered subcutaneously, and that vasopressin contamination of the commercial preparation was probably responsible for the protective effects previously reported. These experiments suggest that vasopressin and its congeners modify memory consolidation in such a way that the "expression" of memory becomes insensitive to puromycin.

Adrenocorticotropic Hormone↗

PubMed1985

Blockade of beta 1- but not of beta 2-adrenergic receptors replicates propranolol's suppression of the cerebral spread of an engram in mice.

Bitemporal injections of puromycin that primarily affect the hippocampal-entorhinal area induce amnesia of aversive maze-learning in mice for 3 days after training but are ineffective 6 or more days after training. At these later times, additional puromycin sites covering widespread forebrain areas are necessary to induce amnesia, a result that we attribute to the cerebral spread of the engram during the 6-day period. We have reported that blockade of about 60% of cerebral beta-adrenergic receptors by a single, subcutaneous injection of (-)-propranolol, a nonselective beta-receptor antagonist, inhibited engram spread for 60-90 days, at which time engram spread spontaneously occurred. In the present experiments using single doses of antagonists that appeared to block 60% of beta 2- or beta 1-adrenergic receptors, it was found that the selective beta 2 antagonist ICI 118,551 was without effect on engram spread, whereas the selective beta 1 antagonist betaxolol inhibited the spread for at least 3 months. Propranolol's effect consequently appears to be accounted for by its blockade of beta 1 receptors.

Adrenergic beta-Antagonists↗

PubMed1986

Graft-induced behavioral recovery in an animal model of Huntington disease.

Bilateral ibotenic acid lesions of the anteromedial neostriatum produce neuropathological and behavioral changes in rats that are characterized by locomotor hyperactivity and severe maze learning impairments, which can be viewed as analogous to changes seen in Huntington disease. Grafts of fetal striatal neurons, implanted either into the lesioned striatum or into the denervated globus pallidus, reduced both the learning impairments and the locomotor hyperactivity, probably via different mechanisms. The results demonstrate the capacity of neural implants for functional neuronal replacement and promotion of functional recovery after damage to a major telencephalic structure participating in complex cognitive and motoric behaviors.

Animals↗

PubMed1998

Memory and long-term potentiation (LTP) dissociated: normal spatial memory despite CA1 LTP elimination with Kv1.4 antisense.

Long-term potentiation (LTP) in the hippocampal slice preparation has been proposed as an in vitro model for long-term memory. However, correlation of LTP with memory in living animals has been difficult to demonstrate. Furthermore, in the last few years evidence has accumulated that dissociate the two. Because potassium channels might determine the weight of synapses in networks, we studied the role of Kv1.4, a presynaptic A-type voltage-dependent K+ channel, in both memory and LTP. Reverse transcription-PCR and Western blot analysis with specific antibodies showed that antisense oligodeoxyribonucleotide to Kv1.4 microinjected intraventricularly into rat brains obstructed hippocampal Kv1.4 mRNA, "knocking down" the protein in the hippocampus. This antisense knockdown had no effect on rat spatial maze learning, memory, or exploratory behavior, but eliminated both early- and late-phase LTP and reduced paired-pulse facilitation (a presynaptic effect) in CA1 pyramidal neurons without affecting dentate gyrus LTP. This presynaptic Kv1.4 knockdown together with previous postsynaptic Kv1.1 knockdown demonstrates that CA1 LTP is neither necessary nor sufficient for rat spatial memory.

Animals↗

PubMed1981

Effects of essential fatty acid deficiency during late gestation on brain N-acetylneuraminic acid metabolism and behaviour in the progeny.

1. Rat dams given a diet containing 100 g maize oil/kg for approximately two weeks before mating and during the first 14 d of gestation, were given the same diet or one containing 100 g hydrogenated coconut oil/kg (essential fatty acid (EFA)-deficient) in place of maize oil until parturition. After parturition the dams were given the same diets and all progeny were weaned to the maize oil diet at 21 d of age. Brain N-acetylneuraminic acid (NeuNAc) content as well as neuraminidase (sialidase; (EC 3.2.1.18), and cytidine monophosphate N-acetylneuraminic acid synthetase (CMP-NeuNAc synthetase) activities were measured at days, 7, 14, 21 and 168 in the progeny. Y-maze learning was measured at 168 d. 2. Brain weight was independent of dietary fat at all ages. 3. Lack of EFA in the maternal diet during gestation and lactation depressed ganglioside and glycoprotein NeuNAc levels and the activities of sialidase and CMP-NeuNAc synthetase. 4. Maternal dietary deprivation of EFA irreversibly impaired learning behaviour of the progeny. A relationship exists between early exposure to EFA deficiency and learning potential of the progeny.

Animals↗

PubMedDate not supplied

Neonatal exposure to novel environment enhances hippocampal-dependent memory function during infancy and adulthood.

Early life experience affects behavior and brain mechanisms. Handling rats during the first three weeks in life can slow age-related cognitive decline (as measured by a hippocampal-dependent spatial learning task) and reduce age-related hippocampal neuron loss. It is not clear, however, whether this early environmental influence on learning is selective for old age or is more general, affecting cognitive development during infancy and young adulthood as well. We briefly exposed neonatal rats to a novel non-home environment for 3 min daily during the first three weeks of life (as a component of the handling method). We found that this brief early environmental manipulation resulted in enhanced hippocampal-dependent learning immediately after weaning and that this learning enhancement persisted into adulthood. These results suggest that subtle early life events can affect cognitive development in all developmental stages and that changes in neural mechanisms other than neuron number are likely to mediate the learning enhancement at multiple developmental stages.

Animals↗

PubMed2005

Olfactory learning-induced morphological modifications in single dendritic spines of young rats.

Learning-related morphological modifications in single dendritic spines were studied quantitatively in the brains of young Sprague-Dawley rats. We have previously shown that olfactory discrimination rule-learning results in transient physiological and morphological modifications in piriform cortex pyramidal neurons. In particular, spine density along the apical dendrites of neurons from trained rats is increased after learning. The aim of the present study was to identify and describe olfactory learning-induced modifications in the morphology of single spines along apical dendrites of the same type of neurons. By using laser-scanning confocal microscopy, we show that 3 days after training completion spines on neurons from olfactory discrimination trained rats are shorter as compared to spines on neurons from control rats. Further analysis revealed that spine shortening attributed to olfactory discrimination learning derives from shortening of spine head and not from shortening of spine neck. In addition, detailed analysis of spine head volume suggests that spines with large heads are absent after learning. As spine head size may be related to the efficacy of the synapse it bears, we suggest that modifications in spine head dimensions following olfactory rule-learning enhance the cortical network ability to enter into a 'learning mode', in which memories of new odours can be acquired rapidly and efficiently.

Analysis of Variance↗

PubMed2006

Early genomics of learning and memory: a review.

The characterization of the molecular mechanisms whereby our brain codes, stores and retrieves memories remains a fundamental puzzle in neuroscience. Despite the knowledge that memory storage involves gene induction, the identification and characterization of the effector genes has remained elusive. The completion of the Human Genome Project and a variety of new technologies are revolutionizing the way these mechanisms can be explored. This review will examine how a genomic approach can be used to dissect and analyze the complex dynamic interactions involved in gene regulation during learning and memory. This innovative approach is providing information on a new class of genes associated with learning and memory in health and disease and is elucidating new molecular targets and pathways whose pharmacological modulation may allow new therapeutic approaches for improving cognition.

Animals↗

PubMed1991

Ependymin, a brain extracellular glycoprotein, and CNS plasticity.

Ependymin, a glycoprotein of the brain ECF, has been implicated in the neurochemistry of memory and neuronal regeneration. Three behavioral experiments (swimming with a float, avoidance conditioning, and classical conditioning) in the goldfish and one in the mouse (T-maze learning) indicate that ependymin has a role in the synaptic changes that take place in the consolidation step of memory formation and the activity-dependent phase of sharpening of goldfish retinotectal connections during neuronal regeneration. The ECF concentration of the protein was found to decrease after the goldfish learned to associate a light stimulus (CS) with the subsequent arrival of a shock (US): paired CS-US gave changes whereas an unpaired presentation of CS-US gave no changes relative to the unstimulated controls. Ependymin is present in ECF as a mixture of three disulfide-linked dimers of two acidic (alpha and beta) polypeptide chains (37 kDa and 31 kDa). Upon removal of its N-linked glycan fragment by N-glycosidase F, the beta chain yields gamma-ependymin (26 kDa). Determinations of the amino acid sequence of gamma-ependymin indicate that it is a unique protein with no long sequence homologies to any known polypeptide. There are, however, small segments (5-7 amino acids long) with homologies to fibronectin, laminin, and tubulin. Ependymin has the capacity to polymerize into FIP (after activation by phosphorylation) in response to events that deplete ECF calcium. FIP is insoluble in 2% SDS in 6 M urea, 10 mM Ca2+Ac2, 100% acetic acid, chloroform/methanol (2/1), saturated KCNS, and even 100% trifluoroacetic acid. FIP was found to be present in goldfish brain and to be formed as a labeled product in vivo. Ependymin's FIP-forming property was used to propose a molecular hypothesis for generating synaptic changes in response to local extracellular depletions of calcium at sites of "associating inputs." The model assumes that, following NMDA receptor stimulation, the translocated PKC that is generated activates extracellular ependymin by converting it to its phosphorylated form using presynaptically released ATP. The hypothesis was tested in studies of LTP of rat hippocampal slices at CA1. After LTP, new sites that stained with antisera to ependymin, visible at 100x, were obtained in its potentiated radiatum in the CA1 region but not in the unpotentiated CA3. Electron microscopic studies showed that the horseradish peroxidase reaction product obtained was localized at synaptic clefts and postsynaptic regions. The results suggest that FIP may be formed at extracellular and postsynaptic loci where multiple associating inputs interact at CA1.

Animals↗

PubMed1964

PREVENTION OF A MENTAL DEFECT OF PHENYLKETONURIA WITH SEROTONIN CONGENERS SUCH AS MELATONIN OR HYDROXYTRYPTOPHAN.

Mice made phenylketonuric from birth until maturity by continuous administration of phenylalanine plus tyrosine had a subnormal maze-learning ability which was largely prevented when serotonin congeners such as melatonin or 5-hydroxytryptophan were administered continuously from birth to maturity. These results were interpreted to mean that the mental failure of experimental phenylketonuria is attributable to the serotonin deficiency imposed by it in infancy.

5-Hydroxytryptophan↗

PubMed1968

Intracerebral saline: effect on memory of trained mice treated with puromycin.

It was shown that puromycin administered to mice 1 or more days after maze-learning blocks expression of memory; the blockage can be removed by intracerebral injections of saline. We present evidence that intracerebral injections of saline are relatively ineffective in restoring memory when puromycin is administered either before or immediately after training; in these two situations puromycin appears to interfere with consolidation of memory.

Amnesia↗

PubMed1969

Puromycin: effect on memory of mice when injected with various cations.

Puromycin dihydrochloride neutralized with bases of potassium, lithium, calcium, or magnesium fails to block expression of memory of maze learning in mice, unlike puromycin neutralized with NaOH. This failure may be due to cationic binding at anionic membrane sites with a resultant exclusion of sufficient peptidyl-puromycin to make it ineffective in blocking memory.

Animals↗

PubMed1973

Spatial orientation in man: effects of left, right, and bilateral posterior cerebral lesions.

Men with chronic, penetrating missile wounds of the brain were examined with two `spatial' tasks: a visually-guided stylus maze and a locomotor map-reading task. Men whose lesions involved the posterior part of the right cerebral hemisphere were significantly worse than those with left posterior lesions at stylus maze-learning. On the locomotor task, however, a highly significant deficit was found in the group of men with bilateral posterior cerebral lesions, while those with unilateral lesions of either hemisphere and those with bilateral frontal lesions were unimpaired. The contributions of the two cerebral hemispheres to the analysis of spatial information are discussed in the light of these results and it is suggested that, while the right hemisphere has a special role in the perception of space, it does not bear exclusive responsibility for the maintenance of spatial orientation.

Brain Injuries↗

PubMed1985

Antiepileptic and antiamnesic effect of carbamazepine in experimental limbic epilepsy.

Carbamazepine (20 mg/kg, 40 mg/kg or 60 mg/kg) given three times a day, has been demonstrated to have a significant anti-epileptic effect in rats with chronic limbic epilepsy induced by injecting tetanus toxin bilaterally into their hippocampi. This effect involved a reduction in the maximum number of fits occurring on one day, and with the highest dose, a significant reduction in the total number of fits. In a pilot experiment in which continuous EEG records were obtained throughout the syndrome, it appeared that the effect of carbamazepine was to reduce the proportion of EEG seizure discharges which lead to overt motor fits. With the higher drug dose plasma levels of carbamazepine were maintained around 2 micrograms/ml. This experimental epilepsy produces enduring deficits in the rats' memories for a light-discrimination task in a Y-maze learned before induction of epilepsy (8 weeks after initial learning). If the rats are dosed with carbamazepine during their epilepsy this memory deficit is abolished.

Amnesia↗

PubMed2000

Spatial memory impairment in patients after tumour resection: evidence for a double dissociation.

Human spatial memory can be divided into multiple, partly separate cognitive processes. In this study, object location memory was studied using a set of tasks that assessed three different spatial memory aspects: positional memory, object location binding, and a combined process. Also, maze learning and spatial span memory were measured. Ten patients who had undergone intracranial tumour resection participated, and their individual results were compared with control data from 24 healthy subjects. Four patients showed selective spatial memory impairments; two patients were impaired at positional memory, and two other patients were impaired on object location binding and the combined process. This double dissociation provides further evidence for the notion that object location memory is not a unitary system, but consists of at least two separate mechanisms. In addition, spatial memory problems were predominantly present in the patients with lesions in either the right hemisphere or in the parietal lobe. These results are in agreement with previous findings on the involvement of the right hemisphere and the posterior parietal cortices in spatial processing.

Adult↗

PubMed2001

Symbiogenesis in learning classifier systems.

Symbiosis is the phenomenon in which organisms of different species live together in close association, resulting in a raised level of fitness for one or more of the organisms. Symbiogenesis is the name given to the process by which symbiotic partners combine and unify, that is, become genetically linked, giving rise to new morphologies and physiologies evolutionarily more advanced than their constituents. The importance of this process in the evolution of complexity is now well established. Learning classifier systems are a machine learning technique that uses both evolutionary computing techniques and reinforcement learning to develop a population of cooperative rules to solve a given task. In this article we examine the use of symbiogenesis within the classifier system rule base to improve their performance. Results show that incorporating simple rule linkage does not give any benefits. The concept of (temporal) encapsulation is then added to the symbiotic rules and shown to improve performance in ambiguous/non-Markov environments.

Algorithms↗

PubMedDate not supplied

Neurobehavioral alteration in rodents following developmental exposure to aluminum.

Aluminum (Al) is one of the most abundant metals in the earth's crust, and humans can be exposed to it from several sources. It is present in food, water, pharmaceutical compounds, and in the environment, e.g., as a result of acid rain leaching it from the soil. Exposure to Al has recently been implicated in a number of human pathologies, but it has not yet been definitely proved that it plays a major causal role in any of them. In this paper we review the effects of developmental exposure of laboratory animals to Al salts as a model for human pathological conditions. The data presented show behavioral and neurochemical changes in the offspring of AL-exposed mouse dams during gestation, which include alterations in the pattern of ultrasonic vocalizations and a marked reduction in central nervous system (CNS) choline acetyltransferase activity. Prenatal Al also affects CNS cholinergic functions under Nerve Growth Factor (NGF) control, as shown by increased central NGF levels and impaired performances in a maze learning task in young-adult mice. The need for more detailed studies to evaluate the risks for humans associated with developmental exposure to Al, as well as the importance of using more than one strain of laboratory animal in the experimental design, is emphasized.

Administration, Oral↗

PubMed2005

Antihypertensive and neuroprotective effects of astaxanthin in experimental animals.

Astaxanthin is a natural antioxidant carotenoid that occurs in a wide variety of living organisms. We investigated, for the first time, antihypertensive effects of astaxanthin (ASX-O) in spontaneously hypertensive rats (SHR). Oral administration of ASX-O for 14 d induced a significant reduction in the arterial blood pressure (BP) in SHR but not in normotensive Wistar Kyoto (WKY) strain. The long-term administration of ASX-O (50 mg/kg) for 5 weeks in stroke prone SHR (SHR-SP) induced a significant reduction in the BP. It also delayed the incidence of stroke in the SHR-SP. To investigate the action mechanism of ASX-O, the effects on PGF(2alpha)-induced contractions of rat aorta treated with NG-nitro-L-arginine methyl ester (L-NAME) were studied in vitro. ASX-O (1 to 10 microM) induced vasorelaxation mediated by nitric oxide (NO). The results suggest that the antihypertensive effect of ASX-O may be due to a NO-related mechanism. ASX-O also showed significant neuroprotective effects in ischemic mice, presumably due to its antioxidant potential. Pretreatment of the mice with ASX-O significantly shortened the latency of escaping onto the platform in the Morris water maze learning performance test. In conclusion, these results indicate that astaxanthin can exert beneficial effects in protection against hypertension and stroke and in improving memory in vascular dementia.

Animals↗