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At least 1,261 records · Page 70Linked to original sources
PubMed2006

Altered signaling pathways underlying abnormal hippocampal synaptic plasticity in the Ts65Dn mouse model of Down syndrome.

The Ts65Dn mouse model of Down syndrome (DS) has an extra segment of chromosome (Chr.) 16 exhibits abnormal behavior, synaptic plasticity and altered function of several signaling molecules. We have further investigated signaling pathways that may be responsible for the impaired hippocampal plasticity in the Ts65Dn mouse. Here we report that calcium/calmodulin-dependent protein kinase II (CaMKII), phosphatidylinositol 3-kinase (PI3K)/Akt, extracellular signal-regulated kinase (ERK), protein kinase A (PKA) and protein kinase C (PKC), all of which have been shown to be involved in synaptic plasticity, are altered in the Ts65Dn hippocampus. We found that the phosphorylation of CaMKII and protein kinase Akt was increased, whereas ERK was decreased. Activities of PKA and PKC were decreased. Furthermore, abnormal PKC activity and an absence of the increase in Akt phosphorylation were demonstrated in the Ts65Dn hippocampus after high-frequency stimulation that induces long-term potentiation. Our findings suggest that abnormal synaptic plasticity in the Ts65Dn hippocampus is the result of compensatory alterations involving the glutamate receptor subunit GluR1 in either one or more of these signaling cascades caused by the expression of genes located on the extra segment of Chr. 16.

Animals↗
PubMed2006

Cyclin-dependent kinase 5 in synaptic plasticity, learning and memory.

Cyclin-dependent kinase 5 (Cdk5) is a serine/threonine kinase with a multitude of functions. Although Cdk5 is widely expressed, it has been studied most extensively in neurons. Since its initial characterization, the fundamental contribution of Cdk5 to an impressive range of neuronal processes has become clear. These phenomena include neural development, dopaminergic function and neurodegeneration. Data from different fields have recently converged to provide evidence for the participation of Cdk5 in synaptic plasticity, learning and memory. In this review, we consider recent data implicating Cdk5 in molecular and cellular mechanisms underlying synaptic plasticity. We relate these findings to its emerging role in learning and memory. Particular attention is paid to the activation of Cdk5 by p25, which enhances hippocampal synaptic plasticity and memory, and suggests formation of p25 as a physiological process regulating synaptic plasticity and memory.

Animals↗
PubMed2007

Molecular mechanisms mediating pathological plasticity in Huntington's disease and Alzheimer's disease.

Neurodegenerative diseases such as Huntington's disease and Alzheimer's disease, although very different in etiology, share common degenerative processes. These include neuronal dysfunction, decreased neural connectivity, and disruption of cellular plasticity. Understanding the molecular mechanisms underlying the neural plasticity deficits in these devastating conditions may lead the way toward new therapeutic targets, both disease-specific and more generalized, which can ameliorate degenerative cognitive deficits. Furthermore, investigations of 'pathological plasticity' in these diseases lend insight into normal brain function. This review will present evidence for altered plasticity in Huntington's and Alzheimer's diseases, relate these findings to symptomatology, and review possible causes and commonalities.

Alzheimer Disease↗
PubMed1984

Plasticizer migration from blood lines in hemodialysis.

Polyvinylchloride (PVC) is the most commonly used material for tubing in extracorporeal circulation. It is usually plasticized by the addition of di-2-ethylhexylphthalate (DEHP). The plasticizer is physically mixed into the PVC. The potential danger of DEHP migration into blood has been discussed. It has been suggested that the polyurethane (PUR) coating should reduce this transport. Eight different types of PVC tubing sets for hemodialysis were investigated for migration of DEHP. In general, they contained approximately 40% by weight of plasticizer. It was shown that approximately 60 mg plasticizer could be extracted from complete tubing sets during a 6-h period. The release rate of DEHP from the PUR coating compared with PVC was increased. The results show that in contrast to previously published information, PUR coating of PVC tubing is not an effective method for reducing migration.

Plasticizers↗
PubMed1980

Contact urticaria from nickel and plastic additives (butylhydroxytoluene, oleylamide).

In two patients urticaria was elicited by contact with nickel-containing objects. Chamber-prick test with nickel sulfate 2.5% in pet. evoked a strong urticarial reaction in both patients. In one of the patients contact with plastic articles also provoked urticaria. A 20-min patch test with several articles of plastic (polyethylene and PVC) and with butylhydroxytoluene (BHT) 1% in ethanol elicited urticarial reactions. BHT is used as an antioxidant in plastic. Furthermore, open patch test with oleylamide (amide of oleic acid) 0.1% in ethanol elicited a strong urticarial reaction in 20 min. This chemical is used as a slipping agent in plastic.

Adult↗
PubMed1986

Dermatitis and urticaria from rubber and plastic gloves.

The number and nature of allergic occupational glove dermatoses were analysed. 542 cases of allergic contact dermatosis were diagnosed during 1974-1983. Amongst these, 68 (12.5%) were caused by rubber or plastic gloves. 2 patients had contact urticaria due to rubber gloves. Gloves were the main cause of occupational allergic rubber eczema, inducing 63 (58.3%) of 108 rubber eczema cases. 38 of them had positive reactions to rubber chemicals and glove material, 14 to glove material only, and 11 to rubber chemicals. 5 cases of allergic eczema from plastic gloves were diagnosed, all due to polyvinyl chloride (PVC). 2 cases of contact urticaria from natural rubber gloves were diagnosed by a provocation test. Epicutaneous testing with material of natural rubber gloves and rubber chemicals was negative. The present study shows that allergy to rubber gloves is usual, while allergy to plastic gloves is rare. Thus, plastic gloves should be used, when possible. Patch testing with protective gloves should always be used when patients develop prolonged hand dermatitis and where the possibility of glove eczema exists.

Clothing↗
PubMed1986

Plastic blankets and heat shields decrease transmission of phototherapy light.

An in vitro study showed that the use of transparent plastic insulation to decrease heat loss from newborn infants substantially decreases the transmission of phototherapy light. The decrease is proportional to the number of plastic layers between the light source and the baby because of reflection from the surface of the plastic. This increases if the surface is irregular. Thickness and the type of plastic used had no effect.

Bedding and Linens↗
PubMed1992

Neuronal plasticity and ageing processes in the frame of the 'Red Queen Theory'.

On the basis of the morphofunctional evidence obtained in old brains of humans and mammals the present hypothesis has been introduced. This hypothesis states that neuronal plasticity can be used either to compensate for neuronal degeneration or to store new information. Thus, in pathological ageing the marked rate of degeneration has fully exhausted the already reduced plasticity capability of neural networks. In this way marked impairments of memory trace formation take place in pathological ageing conditions such as Alzheimer's disease. The essence of this hypothesis is that a competition for the available plasticity exists between the compensatory responses to ageing-induced degeneration and the processes necessary for memory trace formation. We have called this hypothesis the 'Red Queen Theory', an analogy borrowed from Lewis Carroll's book Through the Looking Glass. Thus, in ageing, processes responsible for plasticity must be forced to run at the highest possible rate to maintain the morphofunctional substrate of the existing networks as well as to allow the formation of new memory traces.

Aging↗
PubMed2003

The amygdala, synaptic plasticity, and fear memory.

The nature and mechanisms of synaptic plasticity in the amygdala and the relation of amygdaloid plasticity to behavior are exciting new areas of study in neuroscience. These issues were at the heart of presentations by Paul Chapman, Michael Fanselow, Patricia Shinnick-Gallagher, and Michael Rogawski in a session entitled "Long-Term Plasticity in Amygdala Synaptic Transmission" that was held at the conference featured in this volume. In this chapter, I briefly summarize these talks and give my perspective on the presentations as the session chair. I argue that we must first understand the role of the amygdala in learning and memory in order to understand the contribution of amygdaloid synaptic plasticity to behavior. Although it is generally agreed that the amygdala is involved in several forms of emotional learning and memory such as pavlovian fear conditioning, a recent debate has emerged concerning the precise role of the amygdala in learning versus performing fear responses. I discuss data from my laboratory that unravel this issue. I argue that the basolateral complex of the amygdala (BLA) normally plays an essential role in associative processes in fear conditioning. Nonetheless, rats with BLA lesions acquire and express conditional fear under some conditions. A neuroanatomical model that accounts for these data is presented.

Amygdala↗
PubMed2002

Cell type dependence and variability in the short-term plasticity of EPSCs in identified mouse hippocampal interneurones.

Synapses exhibit different short-term plasticity patterns and this behaviour influences information processing in neuronal networks. We tested how the short-term plasticity of excitatory postsynaptic currents (EPSCs) depends on the postsynaptic cell type, identified by axonal arborizations and molecular markers in the hippocampal CA1 area. Three distinct types of short-term synaptic behaviour (facilitating, depressing and combined facilitating-depressing) were defined by fitting a dynamic neurotransmission model to the data. Approximately 75 % of the oriens-lacunosum-moleculare (O-LM) interneurones received facilitating EPSCs, but in three of 12 O-LM cells EPSCs also showed significant depression. Over 90 % of the O-LM cells were immunopositive for somatostatin and mGluR1alpha and all tested cells were decorated by strongly mGluR7a positive axon terminals. Responses in eight of 12 basket cells were described well with a model involving only depression, but the other cells displayed combined facilitating-depressing EPSCs. No apparent difference was found between the plasticity of EPSCs in cholecystokinin- or parvalbumin-containing basket cells. In oriens-bistratified cells (O-Bi), two of nine cells showed facilitating EPSCs, another two depressing, and the remaining five cells combined facilitating-depressing EPSCs. Seven of 10 cells tested for somatostatin were immunopositive, but mGluR1alpha was detectable only in two of 11 tested cells. Furthermore, most O-Bi cells projected to the CA3 area and the subiculum, as well as outside the hippocampal formation. Postsynaptic responses to action potentials recorded in vivo from a CA1 place cell were modelled, and revealed great differences between and within cell types. Our results demonstrate that the short-term plasticity of EPSCs is cell type dependent, but with significant heterogeneity within all three interneurone populations.

Animals↗
PubMed2003

PSD-95 regulates synaptic transmission and plasticity in rat cerebral cortex.

PSD-95 is one of the most abundant proteins found in the postsynaptic density of excitatory synapses. However, the precise functional role played by PSD-95 in regulating synaptic transmission and plasticity remains undefined. To address this issue, we have overexpressed PSD-95 in cortical pyramidal neurons in organotypic brain slices using particle-mediated gene transfer and assessed the consequences on synaptic transmission and plasticity. The AMPA receptor/NMDA receptor (AMPAR/NMDAR) ratio of evoked EPSCs recorded at +40 mV was greater in PSD-95-transfected pyramidal neurons than in controls. This difference could not be accounted for by a change in rectification of AMPAR-mediated synaptic currents since the current-voltage curves obtained in controls and in PSD-95-transfected neurons were indistinguishable. However, the amplitude of AMPAR-mediated evoked EPSCs was larger in PSD-95-transfected neurons compared to matched controls. Paired-pulse ratio analysis suggested that overexpression of PSD-95 did not alter presynaptic release probability. Transfection of PSD-95 was further accompanied by an increase in the frequency, but not amplitude, of AMPAR-mediated mEPSCs. Together, these results indicate that transfection of PSD-95 increased AMPAR-mediated synaptic transmission. Furthermore, they suggest that this phenomenon reflects an increased number of synapses expressing AMPARs rather than an increased number or function of these receptors at individual synapses. We tested the consequences of these changes on synaptic plasticity and found that PSD-95 transfection greatly enhanced the probability of observing long-term depression. These results thus identify a physiological role for PSD-95 and demonstrate that this protein can play a decisive role in controlling synaptic strength and activity-dependent synaptic plasticity.

Animals↗
PubMed2003

Spike-dependent intrinsic plasticity increases firing probability in rat striatal neurons in vivo.

The collision of pre- and postsynaptic activity is known to provide a trigger for controlling the gain of synaptic transmission between neurons. Here, using in vivo intracellular recordings of rat striatal output neurons, we analyse the effect of a single action potential, generated by ongoing synaptic activity, on subsequent excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of the cerebral cortex. This pairing induced a short-term increase in the probability that cortically evoked EPSPs caused striatal cells to fire. This enhanced EPSP-spike coupling was associated with a decrease in the voltage firing threshold with no apparent change in the synaptic strength itself. Antidromic action potentials in striatal cells were also able to induce the facilitation while subthreshold EPSPs were ineffective, indicating that the postsynaptic spike was necessary and sufficient for the induction of the plasticity. A prior spontaneous action potential also enhanced the probability with which directly applied current pulses elicited firing, suggesting that the facilitation originated from changes in the intrinsic electrical properties of the postsynaptic cell. Using whole-cell recordings in cortico-striatal slices, we found that the increase in membrane excitability as well as in EPSP-spike coupling was abolished by low concentration of 4-aminopyridine. This suggests that the intrinsic plasticity results from a time-dependent modulation of a striatal voltage-dependent potassium current available close to the firing threshold. Action potentials thus provide a postsynaptic signal, not only for associative synaptic plasticity but also for activity-dependent intrinsic plasticity, which directly controls the efficacy of coupling between pre- and postsynaptic neurons.

4-Aminopyridine↗
PubMed2005

Protein kinase A-dependent enhanced NMDA receptor function in pain-related synaptic plasticity in rat amygdala neurones.

Mechanisms of pain-related plasticity in the amygdala, a key player in emotionality, were studied at the cellular and molecular levels in a model of arthritic pain. The influence of the arthritis pain state induced in vivo on synaptic transmission and N-methyl-d-aspartate (NMDA) receptor function was examined in vitro using whole-cell voltage-clamp recordings of neurones in the latero-capsular part of the central nucleus of the amygdala (CeA), which is now defined as the 'nociceptive amygdala'. Synaptic transmission was evoked by electrical stimulation of afferents from the pontine parabrachial area (part of the spino-parabrachio-amygdaloid pain pathway) in brain slices from control rats and from arthritic rats. This study shows that pain-related synaptic plasticity is accompanied by protein kinase A (PKA)-mediated enhanced NMDA-receptor function and increased phosphorylation of NMDA-receptor 1 (NR1) subunits. Synaptic plasticity in the arthritis pain model, but not normal synaptic transmission in control neurones, was inhibited by a selective NMDA receptor antagonist. Accordingly, an NMDA receptor-mediated synaptic component was recorded in neurones from arthritic animals, but not in control neurones, and was blocked by inhibition of PKA but not protein kinase C (PKC). Exogenous NMDA evoked a larger inward current in neurones from arthritic animals than in control neurones, indicating a postsynaptic effect. Paired-pulse facilitation, a measure of presynaptic mechanisms, was not affected by an NMDA-receptor antagonist. Increased levels of phosphorylated NR1 protein, but not of total NR1, were measured in the CeA of arthritic rats compared to controls. Our results suggest that pain-related synaptic plasticity in the amygdala involves a critical switch of postsynaptic NMDA receptor function through PKA-dependent NR1 phosphorylation.

Amygdala↗
PubMed2006

Nicotine-induced enhancement of synaptic plasticity at CA3-CA1 synapses requires GABAergic interneurons in adult anti-NGF mice.

The hippocampus, a key structure for learning and memory processes, receives an important cholinergic innervation and is densely packed with a variety of nicotinic acetylcholine receptors (nAChRs) localized on principal cells and interneurons. Activation of these receptors by nicotine or endogenously released acetylcholine enhances activity-dependent synaptic plasticity processes. Deficits in the cholinergic system produce impairment of cognitive functions that are particularly relevant during senescence and in age-related neurodegenerative pathologies. In particular, Alzheimer's disease (AD) is characterized by a selective loss of cholinergic neurons in the basal forebrain and nAChRs in particular regions controlling memory processes such as the cortex and the hippocampus. Field excitatory postsynaptic potentials were recorded in order to examine whether nicotine was able to regulate induction of long-term potentiation at CA3-CA1 synapses in hippocampal slices from adult anti-NGF transgenic mice (AD 11), a comprehensive animal model of AD, in which cholinergic deficits due to nerve growth factor depletion are accompanied by progressive Alzheimer-like neurodegeneration. Both AD 11 and wild-type (WT) mice exhibited short- and long-lasting synaptic plasticity processes that were boosted by nicotine. The effects of nicotine on WT and AD 11 mice were mediated by both alpha7- and beta2-containing nAChRs. In the presence of GABA(A) receptor antagonists, nicotine failed to boost synaptic plasticity in AD 11 but not in WT mice, indicating that in anti-NGF transgenic mice GABAergic interneurons are able to compensate for the deficit in cholinergic modulation of glutamatergic transmission. This compensation may occur at different levels and may involve the reorganization of the GABAergic circuit. However, patch-clamp whole-cell recordings from principal cells failed to reveal any change in spontaneous release of GABA following pressure application of nicotine to nearby GABAergic interneurons. Together, these experiments indicate that in AD 11 mice a rearrangement of the GABAergic circuit can 'rescue' nicotine-induced potentiation of synaptic plasticity. This may be relevant for developing proper therapeutic tools useful for the treatment of AD.

Alzheimer Disease↗
PubMed2005

Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor.

Monocular deprivation normally alters ocular dominance in the visual cortex only during a postnatal critical period (20 to 32 days postnatal in mice). We find that mutations in the Nogo-66 receptor (NgR) affect cessation of ocular dominance plasticity. In NgR-/- mice, plasticity during the critical period is normal, but it continues abnormally such that ocular dominance at 45 or 120 days postnatal is subject to the same plasticity as at juvenile ages. Thus, physiological NgR signaling from myelin-derived Nogo, MAG, and OMgp consolidates the neural circuitry established during experience-dependent plasticity. After pathological trauma, similar NgR signaling limits functional recovery and axonal regeneration.

Animals↗
PubMed2005

Map plasticity in somatosensory cortex.

Sensory maps in neocortex are adaptively altered to reflect recent experience and learning. In somatosensory cortex, distinct patterns of sensory use or disuse elicit multiple, functionally distinct forms of map plasticity. Diverse approaches-genetics, synaptic and in vivo physiology, optical imaging, and ultrastructural analysis-suggest a distributed model in which plasticity occurs at multiple sites in the cortical circuit with multiple cellular/synaptic mechanisms and multiple likely learning rules for plasticity. This view contrasts with the classical model in which the map plasticity reflects a single Hebbian process acting at a small set of cortical synapses.

Animals↗
PubMed1972

Plastics on the Sargasso sea surface.

Plastic particles, in concentrations averaging 3500 pieces and 290 grams per square kilometer, are widespread in the western Sargasso Sea. Pieces are brittle, apparently due to the weathering of the plasticizers, and many are in a pellet shape about 0.25 to 0.5 centimeters in diameter. The particles are surfaces for the attachment of diatoms and hydroids. Increasing production of plastics, combined with present waste-disposal practices, will undoubtedly lead to increases in the concentration of these particles. Plastics could be a source of some of the polychlorinated biphenyls recently observed in oceanic organisms.

Bacteria↗
PubMed1984

Neurotransmitter plasticity at the molecular level.

Contrary to long-held assumptions, recent work indicates that neurons may profoundly change transmitter status during development and maturity. For example, sympathetic neurons, classically regarded as exclusively noradrenergic or cholinergic, can also express putative peptide transmitters such as substance P. This neuronal plasticity is directly related to membrane depolarization and sodium ion influx. The same molecular mechanisms and plastic responses occur in mature as well as developing neurons. Further, contrary to traditional teaching, adult primary sensory neurons may express the catecholaminergic phenotype in vivo. Transmitter plasticity is not restricted to the peripheral nervous system: ongoing studies of the brain nucleus locus ceruleus in culture indicate that specific extracellular factors elicit marked transmitter changes. Consequently, neurotransmitter expression and metabolism are dynamic, changing processes, regulated by a variety of defined factors. Transmitter plasticity adds a newly recognized dimension of flexibility to nervous system function.

Adrenal Medulla↗