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At least 991 records · Page 55Linked to original sources
PubMed1998

Estrogen-mediated structural and functional synaptic plasticity in the female rat hippocampus.

Light and electron microscopic studies have shown that ovarian steroids regulate the density and number of excitatory synaptic inputs to hippocampal pyramidal cells in the adult female rat; elevated levels of estradiol are associated with a higher density of dendritic spine synapses on CA1 pyramidal cells. Electrophysiological analyses indicate that these hormone-induced synapses increase hippocampal excitability as well as the potential for synaptic plasticity. Importantly, correlation of dendritic spine density and sensitivity to synaptic input of individual CA1 pyramidal cells from estradiol-treated and control animals suggests that synapses induced by estradiol may be a specialized subpopulation that contains primarily the NMDA subtype of glutamate receptor. The apparent NMDA receptor specificity of these synapses may be key to understanding their functional significance. Currently, the behavioral consequences of additional spine synapses are unknown. Numerous studies have aimed at correlating hormone-induced changes in hippocampal connectivity with differences in hippocampus-dependent spatial learning ability in mazes, but the results of these efforts have been equivocal. Anatomical, electrophysiological, and behavioral studies of estradiol-mediated hippocampal plasticity are reviewed. In conclusion, it is suggested that standard behavioral tests of hippocampal function are not sufficient to reveal the behavioral consequences of hormone-induced hippocampal plasticity. Rather, understanding the behavioral consequences of estradiol and progesterone effects on hippocampal connectivity may require analysis of the hippocampus' cognitive and spatial information processing functions in relation to alternative biologically relevant behaviors. A (nonexclusive) proposal that hormone-induced hippocampal plasticity may facilitate appropriate prepartum/maternal behavior is discussed.

Animals↗
PubMed2000

Imaging brain plasticity: conceptual and methodological issues--a theoretical review.

The neural plasticity associated with learning and development is increasingly being studied using functional neuroimaging methods such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). In this paper I outline a set of conceptual and methodological issues that are particularly relevant for the study of neural plasticity. A number of confounds, related to changes in performance and the inherently temporal nature of learning and development, must be addressed when imaging plasticity. The interpretation of changes in imaging signals is greatly underdetermined, suggesting that hypothesis-driven research approaches may be most fruitful. Finally, I argue that the imaging of learning-related and developmental plasticity can enhance the ability of functional neuroimaging to identify and characterize the underlying neural basis of cognition.

Aging↗
PubMed2001

17beta-estradiol: effect on CA1 hippocampal synaptic plasticity.

An understanding of synaptic plasticity in the mammalian brain has been one of R. F. Thompson's major pursuits throughout his illustrious career. A current series of experiments of significant interest to R. F. Thompson is an examination of the interactions between sex hormones, synaptic plasticity, aging, and stress. This research is contained within a broader project whose aim is to investigate animal models that evaluate estrogen interactions with Alzheimer's disease. This paper reviews the recent results that have led to a better understanding of how the sex hormone estrogen influences synaptic plasticity in an important structure within the mammalian brain responsible for learning and memory: the hippocampus. In this review, a number of experiments have been highlighted that investigate the molecular mechanisms that underlie estrogen's effect on two specific forms of synaptic plasticity commonly studied in neurophysiology and the behavioral neurosciences: long-term potentiation and long-term depression.

Aging↗
PubMedDate not supplied

How a child builds its brain: some lessons from animal studies of neural plasticity.

Although the potential vulnerability of children's brain development is generally recognized, relatively little is known about the timing, resiliency, or mechanisms involved. While animal research should be applied only cautiously to human policy, some findings do have important clinical implications. This paper briefly reviews animal studies demonstrating the effects of experience on brain structure. Contemporary theories emphasize the self-organizing potential of brain structure, particularly regions that seem to have evolved for the purpose of storing information. We emphasize three major findings: (1) many regions of the brain are responsive to experience, but they differ in the types of information stored and in their developmental timing. (2) One type of plasticity is typically embedded in a developmental program, and it requires appropriate timing and quality of the information stored for the animal's development to be normal. (3) Another category of plasticity stores information that is idiosyncratic and unpredictable, but is often useful for species such as humans that learn throughout their life span. We therefore expect that some aspects of human brain development use the first type of plasticity and that abnormal experience or deprivation may cause lasting harm to brain and behavior. However, because the other type of plasticity lasts a lifetime, efforts such as psychotherapy or social interventions may help heal a wounded brain.

Animals↗
PubMed2004

Brain plasticity and remodeling of AMPA receptor properties by calcium-dependent enzymes.

Long-term potentiation (LTP) and long-term depression (LTD) are two experimental models of synaptic plasticity that have been studied extensively in the last 25 years, as they may represent basic mechanisms to store certain types of information in neuronal networks. In several brain regions, these two forms of synaptic plasticity require dendritic depolarization, and the amplitude and duration of the depolarization-induced calcium signal are crucial parameters for the generation of either LTP or LTD. The rise in calcium concentration mediated by activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors has been proposed to stimulate various calcium-dependent processes that could convert the induction signal into long-lasting changes in synaptic structure and function. According to several lines of experimental evidence, alterations in synaptic function observed with LTP and LTD are thought to be the result of modifications of postsynaptic currents mediated by the a-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) subtype of glutamate receptors. The question of which type(s) of receptor changes constitutes the basis for the expression of synaptic plasticity is still very much open. Here, we review data relevant to the issue of selective modulation of AMPA receptor properties occurring after learning and memory, environmental enrichment, and synaptic plasticity. We also discuss potential cellular mechanisms whereby calcium-dependent enzymes might regulate AMPA receptor properties during LTP and LTD, focusing on protein kinases, proteases and lipases.

Brain↗
PubMed1991

Ocular dominance plasticity restored by NA infusion to aplastic visual cortex of anesthetized and paralyzed kittens.

We studied the ocular dominance distribution in visual cortex of kittens which had been monocularly exposed to moving-pattern stimuli under anesthesia and paralysis. 1. We did not obtain any discernible changes in ocular dominance, confirming the previous reports that anesthesia and paralysis prevent ocular dominance plasticity from occurring. 2. The plasticity, however, was restored under the acute experimental condition by a cortical infusion of 1-noradrenaline (1-NA). In the 1-NA-infused visual cortex, the ocular dominance distribution was clearly shifted to the open eye after monocular exposure for about 20-24 h. 3. We also studied how quickly and to what extent the changes were induced when the duration of the combined treatment was varied. The results were: (i) the earliest change was observed in approximately 12 h with disappearance of binocular cells, (ii) the treatment was most effective after 20-24 h in inducing the shift of ocular dominance, and (iii) the treatment longer than 24 h (up to 45 h) did not necessarily enhance the shift, though the state of reduced binocularity was sustained throughout. 4. The effects of the cortical 1-NA infusion combined with monocular exposure became less with increasing the age of experimental animals, suggesting the presence of the "susceptible period" in the acute experiments. 5. The effects seemed to become smaller toward the end of a given recording session, suggesting that the restored plasticity wanes with time. The present results further support the idea that the direct activation of the NA system enhances cortical plasticity, in principle, independent of general conditions of experimental animals.

Aging↗
PubMed1988

Blockade of intracortical inhibition in kitten striate cortex: effects on receptive field properties and associated loss of ocular dominance plasticity.

We have investigated the importance of GABAergic inhibition for the receptive field properties and plasticity of cells in the visual cortex of kittens. Osmotic minipumps were used to continuously infuse the GABA-antagonist, bicuculline methiodide (BIC), into striate cortex. Extracellular recordings were made during BIC infusion to assess neuronal response properties during the blockade of inhibition. Recordings were also made from other kittens after concurrent monocular deprivation and BIC infusion to investigate the importance of response selectivity for ocular dominance plasticity. The minipump delivery technique was used to produce a large volume of cortex presumably free of GABA-ergic inhibition. Compared to recordings in saline-infused control hemispheres, about half of the cells in bicuculline-infused hemispheres had abnormally low orientation selectivity. The low selectivity was generally accompanied by marked anomalies in several other receptive field properties. Particularly striking was the large size of the receptive fields. At eccentricities less than 10 deg many receptive fields subtended from 10 to over 30 deg of arc. The less selective neurons also had abnormal responses to flashed stimuli, giving strong transient responses to the onset and offset of large stationary stimuli which filled their receptive fields. These results imply that intracortical inhibition normally suppresses responses to stimuli within a large excitatory zone beyond the classical receptive field. Inhibition is necessary for the normal orientation selectivity of many cells, although the selectivity may be partially established by the cell's excitatory input. Additionally, intracortical inhibition appears to be necessary for the antagonism and segregation of ON and OFF receptive field subregions. In our study of plasticity, we exploited the fact that BIC treatment greatly increases the range of stimuli that activate cortical neurons. Kittens were monocularly deprived for 7 days concurrently with cortical infusion of BIC. After cessation of the drug treatment, physiological recordings were made. Response properties had returned to normal but neurons in BIC-infused hemispheres had a significantly reduced ocular dominance shift compared to neurons in control hemispheres. This is probably related to the reduced selectivity of cells during BIC infusion. The suggestion here is that there is diminished ocular dominance plasticity in BIC-infused hemispheres because of an increased probability of correlated activity between spontaneous discharge from the closed eye and the cortical activity evoked by the open eye afferents.

Animals↗
PubMed1987

Plasticity and rigidity in the representation of the human visual field.

Neuronal plasticity in the mammalian visual system has been studied with a variety of experimental methods like induction of artificial squint and eye rotation. To investigate neuronal plasticity in the human visual system, we examined a patient with a congenital convergent squint of his left eye, who later suffered a vascular lesion in his left occipital lobe that led to an incomplete hemianopia in his right visual field. The examination revealed that the visual field representation in the striate cortex is rigidly prewired with reference to the anatomical fovea. In contrast, plasticity in the oculomotor system enables the patient to use a functional visual axis that does not correspond to the anatomical fovea. Local alterations of sensitivity within the visual field that indicate interactions among non-corresponding retinal points provide additional evidence of functional plasticity.

Esotropia↗
PubMed1987

Reemergence of ocular dominance plasticity during recovery from the effects of propranolol infused in kitten visual cortex.

We wanted to know whether ocular dominance plasticity can increase under the condition in which the number of available beta adrenoreceptors is expected to increase within kitten visual cortex. We adopted a paradigm in which monocular lid suture was carried out some time after the termination of direct infusion of the cortex with a beta adrenoreceptor antagonist. A significant change in ocular dominance was obtained as shown by a decrease in binocular cortical neurons, when time interval between the end of the d,l-propranolol infusion and the start of monocular deprivation was one week. With a 3-week interval (the longest tested), an even greater change in ocular dominance was evident. This consisted of a marked decrease in binocular neurons and a shift in ocular dominance toward the nondeprived eye. In a control study an inert stereoisomer, d-propranolol, did not block the ocular dominance shift. These results were interpreted as suggesting that the level of ocular dominance plasticity becomes high in parallel to an expected increase in availability of beta adrenoceptors for endogenous noradrenaline (NA). We next asked whether it is possible to accelerate or decelerate the naturally occurring recovery of ocular dominance plasticity. When either NA or tunicamycin (an inhibitor of protein glycosylation) was infused into the same cortical area immediately after the end of the propranolol infusion, opposite effects were observed: exogenous NA accelerated the recovery of the shift in ocular dominance and tunicamycin suppressed it. When tunicamycin infusion was delayed by one week, however, its suppressive effect was negligible. Thus, the restoration of ocular dominance plasticity seems to occur in parallel to an increase in the availability of beta adrenoreceptors for endogenous as well as exogenous NA.

Animals↗
PubMed1988

6-Hydroxydopamine treatment and beta adrenergic receptor binding in kittens. Relation to visual cortical plasticity.

Under some circumstances intraventricular administration of 6-OHDA decreases visual cortical plasticity of kittens; the mechanism for this change is not known, but depletion of norepinephrine (NE) is not the entire explanation. We have examined the effects of 6-OHDA treatment on beta adrenergic receptor binding in kitten visual cortex. Subjects were given vehicle solution alone, a low dose of 6-OHDA which depleted cortical NE without affecting visuocortical plasticity, or a higher dose of 6-OHDA which depleted cortical NE and decreased visuocortical plasticity. Drugs were administered in single daily injections via intraventricular cannulas. Saturation assays were performed on homogenates of visual cortical tissue using 125I-pindolol (30-400 pM) along w/ isoproterenol (237 microM) as a cold competitor. We measured radioactivity bound to tissue and retained on filters and analyzed the data using the EBDA computer program (McPherson 1983, 1985); we determined the affinity constant (Kd) and receptor density (Bmax) in multiple assays for each animal. Despite 75-90% NE depletion in both experimental groups, only the group receiving the lower dose of 6-OHDA showed any evidence of supersensitivity. The Kds did not differ among the groups. The data suggest that the effects of 6-OHDA on visuocortical plasticity are not secondary to beta adrenergic supersensitivity.

Animals↗
PubMed1996

A columnar model of somatosensory reorganizational plasticity based on Hebbian and non-Hebbian learning rules.

Topographical and functional aspects of neuronal plasticity were studied in the primary somatosensory cortex of adult rats in acute electrophysiological experiments. Under these experimental conditions, we observed short-term reversible reorganization induced by intracortical microstimulation or by an associative pairing of peripheral tactile stimulation. Both types of stimulation generate large-scale and reversible changes of the representational topography and of single cell functional properties. We present a model to simulate the spatial and functional reorganizational aspects of this type of short-term and reversible plasticity. The columnar structure of the network architecture is described and discussed from a biological point of view. The simulated architecture contains three main levels of information processing. The first one is a sensor array corresponding to the sensory surface of the hind paw. The second level, a pre-cortical relay cell array, represents the thalamo-cortical projection with different levels of excitatory and inhibitory relay cells and inhibitory nuclei. The array of cortical columns, the third level, represents stellate, double bouquet, basket and pyramidal cell interactions. The dynamics of the network are ruled by two integro-differential equations of the lateral-inhibition type. In order to implement neuronal plasticity, synaptic weight parameters in those equations are variables. The learning rules are motivated by the original concept of Hebb, but include a combination of both Hebbian and non-Hebbian rules, which modifies different intra- and inter-columnar interactions. We discuss the implications of neuronal plasticity from a behavioral point of view in terms of information processing and computational resources.

Animals↗
PubMed1986

Interaction of vinyl chloride with poly(vinyl chloride) by inverse gas chromatography: effect of monomer concentration, plasticizer content and temperature.

The interaction of vinyl chloride (VC) with poly(vinyl)chloride) (PVC) has been studied by inverse gas chromatography (IGC). The present work focusses on the effect of monomer concentration, temperature and plasticizer content. Values for thermodynamic parameters such as free energy (delta GS), excess free energy (delta GSXS), enthalphy (delta HS), entropy (delta SS) and activity coefficient (gamma S) corresponding to sorption of the monomer (VCM) by the polymer, have been calculated using chromatographic data. It was found that retention of VC by PVC is favored at lower monomer concentrations. Increase in temperature resulted in increase of delta GS, delta GSXS, and gamma S values corresponding to a less spontaneous process or a weaker interaction between VC and PVC. An increase in plasticizer content of the polymer resulted in an increase of degree of binding of the monomer. Data support the hypothesis that at significantly low concentrations of residual monomer, low storage temperatures and high concentrations of plasticizer, in the polymer, the probability of migration of VC from a plastics packaging material into a food contacting phase is markedly reduced.

Chromatography, Gas↗
PubMedDate not supplied

The monosynaptic connection: modulating influence of opioid peptides on the plasticity of presynaptic neurons and identified synapses.

An investigation of the effect of opioid peptides (leucine-enkephalin and methionine-enkephalin) on the plastic properties of the system of monosynaptically connected LPa7-LPa3 and RPa3, and LPa8-LPa3 and RPa3, neurons in the brain of the edible snail was carried out. It was demonstrated that all three elements in the system under investigation (the presynaptic neuron, the postsynaptic neuron, and the synapse) display the same type of plasticity, i.e., habituation to rhythmic stimulation. The enkephalins exert a modulating effect on the plastic properties of the presynaptic neuron and synapse: they slow down the habituation of the presynaptic neuron in response to intracellular stimulation and the development of habituation at a level of the synapse as well. However, the changes in the character of the postsynaptic response in the presence of enkephalins are not the direct consequence of their influence on the plastic properties of the presynaptic neuron. In addition, the enkephalins decrease the efficiency of synaptic transmission in this system: they decrease the duration of the EPSP in the postsynaptic neuron.

Animals↗
PubMed1976

Plasticizers as interferences in pollutant analyses.

Airborne compounds from two groups of plasticizers used in air conditioner filters and caulks as well as flexible polyvinyl chloride and related plastics have been identified as major sources of low level laboratory contamination that can cause serious interferences in pollutant analyses especially at the low levels requiring GCEC for quantitation. Two compounds from the phthalic acid ester group (PAE'S) OF PLASTICIZERS THAT ARE ENVIRONMENTAL POLLUTANTS AS WELL WERE FOUND INCORPORATED ON AIR CONDITIONER FILTERS LEADING TO CONTAMINATION OF CLEAN AND OIL FILMED DISHES FROM AIR FALLOUT. Solvents, inorganic reagents and hand-to-glass transfer were found to contribute to sample contamination by PAE's. Several PAE's are easily detectable at 0.1 ng levels under some conditions on GCEC and have retention times on several columns of differing polarities that can interfere with analyses of chlorinated pollutants especially p,p'-DDT. Aroclor 1254, a member of the polychlorinated biphenyl group (PCB's) of plasticizers, was found in a caulk around a laboratory window. On oil filmed, but not clean dishes, the compounds collected from air fallout produced chromatograms on GCEC with a close correspondence to Aroclor 1242.

Air↗
PubMed2001

Developmental disorders of activity dependent neuronal plasticity.

A number of neurodevelopmental disorders are caused by defects in activity dependent neuronal plasticity, the process by which neuronal activity shapes developing neuronal circuits. These disorders are caused by genetic mutations or other factors that disrupt intracellular signaling pathways that link the cell surface with the nuclear machinery for gene expression. The signaling pathways disrupted by these disorders are involved in learning, memory and behavior as well as in the synaptic proliferation and pruning that occurs during normal development. Examples of neurodevelopmental disorders that target plasticity include X-linked disorders such as Rett, Fragile-X and Coffin-Lowry Syndromes as well as acquired disorders such as cretinism. Several other X-linked mental retardation syndromes as well as autosomal disorders including neurofibromatosis type 1 and tuberous sclerosis also involve signaling pathways involved in neuronal plasticity. Disruption of neuronal plasticity is a mechanism that may underlie a diverse group of neurodevelopmental disorders.

Brain Diseases↗
PubMed1998

Hippocampal plasticity involves extensive gene induction and multiple cellular mechanisms.

Long-term plasticity of the central nervous system (CNS) involves induction of a set of genes whose identity is incompletely characterized. To identify candidate plasticity-related genes (CPGs), we conducted an exhaustive screen for genes that undergo induction or downregulation in the hippocampus dentate gyrus (DG) following animal treatment with the potent glutamate analog, kainate. The screen yielded 362 upregulated CPGs and 41 downregulated transcripts (dCPGs). Of these, 66 CPGs and 5 dCPGs are known genes that encode for a variety of signal transduction proteins, transcription factors, and structural proteins. Seven novel CPGs predict the following putative functions: cpg2--a dystrophin-like cytoskeletal protein; cpg4--a heat-shock protein: cpg16--a protein kinase; cpg20--a transcription factor; cpg21--a dual-specificity MAP-kinase phosphatase; and cpg30 and cpg38--two new seven-transmembrane domain receptors. Experiments performed in vitro and with cultured hippocampal cells confirmed the ability of the cpg-21 product to inactivate the MAP-kinase. To test relevance to neural plasticity, 66 CPGs were tested for induction by stimuli producing long-term potentiation (LTP). Approximately one-fourth of the genes examined were upregulated by LTP. These results indicate that an extensive genetic response is induced in mammalian brain after glutamate receptor activation, and imply that a significant proportion of this activity is coinduced by LTP. Based on the identified CPGs, it is conceivable that multiple cellular mechanisms underlie long-term plasticity of the nervous system.

Amino Acid Sequence↗
PubMed1991

Evidence for plasticity of the dopaminergic system in parkinsonism.

A series of compensatory mechanisms within the dopaminergic system have been shown to maintain clinical function in the presence of dopamine loss. Experimental evidence for increased presynaptic dopamine turnover owing to increased dopamine synthesis, release, and reduced reuptake exists. Direct evidence that these mechanisms maintain extracellular dopamine levels is provided by intracerebral microdialysis techniques. Postsynaptic denervation supersensitivity clearly occurs with D2 dopamine receptors, although this is less evident with D1 receptors. Similarly, mechanisms of plasticity have been shown to be relevant in human postmortem and Positron Emission Tomographic studies of patients with Parkinson's disease. However, although presynaptic increases in dopamine turnover are well documented, postsynaptic D1 and D2 receptor changes have been more difficult to establish, mainly because of methodological difficulties. D2, but not D1, receptor increases have been documented in drug naive Parkinsonian patients with PET techniques. In transplantation of adrenal gland to striatum in animal models and patients with Parkinsonism where clinical improvement occurs, plasticity of host response may be as important as plasticity of the graft. Although some elements of the compensatory mechanism of dopamine plasticity may be deleterious, such as dyskinesias owing to dopamine receptor supersensitivity, the overall effect of delay and minimization of the clinical expression of disease is advantageous. An even greater understanding of the mechanisms involved may assist in developing future therapeutic strategies.

Adrenal Glands↗
PubMed2004

Use of water-equivalent plastic scintillator for intravascular brachytherapy dosimetry.

Beta irradiation has recently been investigated as a possible technique for the prevention of restenosis in intravascular brachytherapy after balloon dilatation or stent implantation. Present methods of beta radiation dosimetry are primarily conducted using radiochromic film. These film dosimeters exhibit limited sensitivity and their characteristics differ from those of tissue, therefore the dose measurement readings require correction factors to be applied. In this work a novel, mini-size (2 mm diameter by 5 mm long) dosimeter element fabricated from Organic Plastic Scintillator (OPS) material was employed. Scintillation photon detection is accomplished using a precision photodiode and innovative signal amplification and processing techniques, rather than traditional photomultiplier tube methods. A significant improvement in signal to noise ratio, dynamic range and stability is achieved using this set-up. In addition, use of the non-saturating organic plastic scintillator material as the detector enables the dosimeter to measure beta radiation at very close distances to the source. In this work the plastic scintillators have been used to measure beta radiation dose at distances of less than 1 mm from an Sr-90 cardiovascular brachytherapy source having an activity of about 2.1 GBq beta radiation levels for both depth-distance and longitudinal profile of the source pellet chain, both in air and in liquid water, are measured using this system. The data obtained is compared with results from Monte Carlo simulation technique (MCNP 4B). Plastic scintillator dosimeter elements, when used in conjunction with photodiode detectors may prove to be useful dosimeters for cardiovascular brachytherapy beta sources, or other applications where precise near-source field dosimetry is required. The system described is particularly useful where measurement of actual dose rate in real time, a high level of stability and repeatability, portability, and immediate access to results are prime requirements.

Beta Particles↗