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At least 1,711 records · Page 95Linked to original sources
PubMed2006

Consent for plastic surgical procedures.

The objective of this study was to examine patients' attitudes to providing consent for elective plastic and reconstructive surgical procedures and to identify their priorities in terms of information disclosure. Sixty-three consecutive patients attending the elective plastic and reconstructive surgery preadmission clinics at Sandwell Hospital, West Bromwich were prospectively audited by means of a questionnaire which included both open and closed questions. Seventy-five percent of patients volunteered that 'they ought' to have certain information disclosed prior to giving their consent to a surgical procedure. (It was interesting to note that the information they volunteered as wanting to know was not consistently the information that guidelines suggest they are told.) The provision of information is at the centre of the process of valid consent. This study shows the priorities of a group of elective patients prior to plastic surgery procedures, and highlights to clinicians the importance of tailoring information to individual patients.

Adult↗
PubMed2004

Behaviorally-induced ultrastructural plasticity in the hippocampal region after cerebral ischemia.

Behavioral training has been shown to induce synaptic plasticity in both intact and injured animals. Because of the possibility that the adaptive changes after ischemic damage may make the brain more malleable to behavioral training, we examined the effects of complex environment (EC) housing and exercise (EX) after global cerebral ischemia on synaptic structural alterations. Forty-two adult male Wistar rats were included in the study and assigned to either ischemia or sham group. Following ischemic or sham surgery, rats were randomized to either EC, EX, or social condition (SC, paired housing) group. CA1 was processed for electron microscopy and unbiased stereological techniques were used to evaluate plasticity. Significantly decreased neuron density was seen in anterior and medial CA1 in ischemic animals regardless of behavioral training. Neuron density in anterior CA1 was 31% less than the medial area. Synaptogenesis was influenced by cerebral ischemia and behavioral training in that all ischemic groups and sham EC animals showed greater number of synapses per neuron compared to the sham EX and SC groups. Analysis of synapse configuration showed that the synaptogenesis in ischemia EX and SC rats was formed mainly by synapses with single synaptic boutons, whereas in the ischemia EC and sham EC rats synaptogenesis was formed mainly by synapses with multiple synaptic boutons. Furthermore, housing of sham and ischemia rats in EC resulted in increased number of synapses with perforated postsynaptic density. Together, these data suggest that behavioral experience in EC after insult may be able to enhance synaptic plasticity.

Animals↗
PubMed2004

Homeostatic plasticity in hippocampal slice cultures involves changes in voltage-gated Na+ channel expression.

Neurons preserve stable electrophysiological properties despite ongoing changes in morphology and connectivity throughout their lifetime. This dynamic compensatory adjustment, termed 'homeostatic plasticity', may be a fundamental means by which the brain normalizes its excitability, and is possibly altered in disease states such as epilepsy. Despite this significance, the cellular mechanisms of homeostatic plasticity are incompletely understood. Using field potential analyses, we observed a compensatory enhancement of neural excitability after 48 h of activity deprivation via tetrodotoxin (TTX) in hippocampal slice cultures. Because activity deprivation can enhance voltage-gated sodium channel (VGSC) currents, we used Western blot analyses to probe for these channels in control and activity-deprived slice cultures. A significant upregulation of VGSCs expression was evident after activity deprivation. Furthermore, immunohistochemistry revealed this upregulation to occur along primarily pyramidal cell dendrites. Western blot analyses of cultures after 1 day of recovery from activity deprivation showed that VGSC levels returned to control levels, indicating that multiple molecular mechanisms contribute to enhanced excitability. Because of their longevity and in vivo-like cytoarchitecture, we conclude that slice cultures may be highly useful for investigating homeostatic plasticity. Furthermore, we demonstrate that enhanced excitability involves changes in channel expression with a targeted localization likely profound transform the integrative capacities of hippocampal pyramidal cells and their dendrites.

Anesthetics, Local↗
PubMed2005

Selective modulation of Ca(2+) influx pathways by 5-HT regulates synaptic long-term plasticity in the hippocampus.

Both long-term potentiation (LTP) and long-term depression (LTD) can be induced in the Schaffer collateral-CA1 synapse of the hippocampus either by repetitive stimulation of afferent fibres with the frequency of the stimulation determining the polarity of the response or by associative pairing of pre- and postsynaptic activity. An increase in postsynaptic intracellular Ca(2+) concentration is an important signal for the induction of long-term synaptic plasticity. In patch-clamp experiments on hippocampal brain slices, we tested the modulation of different forms of synaptic plasticity by the neurotransmitter serotonin (5-HT) which is known to inhibit high-voltage activated Ca(2+) channels. 1 microM of 5-HT inhibited homosynaptic LTD induced by low frequency stimulation. This effect of 5-HT could be blocked by the selective 5-HT(1A) antagonist WAY 100635. Low frequency-induced LTD is both dependent on Ca(2+) influx through NMDA receptors and high-voltage activated Ca(2+) channels. It was blocked by the NMDA-receptor antagonist D-AP5 and by the N-type Ca(2+) channel antagonist omega-conotoxin GIVA. Tetanus induced LTP was not affected by low concentrations of 5-HT, whereas depotentiation of LTP by asynchronous pairing of EPSPs and postsynaptic action potentials was completely abolished with 5-HT in the bath solution. We conclude that those forms of plasticity which depend on Ca(2+) influx via high-voltage activated Ca(2+) channels are subject to modulation by 5-HT. This might be a relevant mechanism by which 5-HT modifies basic network properties in the brain.

2-Amino-5-phosphonovalerate↗
PubMed2005

Vulnerability of synaptic plasticity in the complexin II knockout mouse to maternal deprivation stress.

The alterations in brain function and structure seen in schizophrenia are mediated by genetics as well as vulnerability due to environmental factors. Postmortem studies in schizophrenic patients have shown that expression of complexin II, which is involved in neurotransmitter release at central nervous system synapses, is decreased in the brain. We examined the physiological characteristics of complexin II gene-deficient mice subjected to maternal deprivation stress to determine whether psychological stress during the early stage of life affected the development of brain function. We compared the electrophysiological properties of CA1 hippocampal pyramidal neurons and spatial memory in the Morris water maze test in the wild-type mouse and the homozygous mutant. In the non-stressed mouse, no significant differences in transsynaptic responses and synaptic plasticity or spatial memory were seen, suggesting that complexin II does not play a critical role in transmitter release or synaptic plasticity under these conditions. In contrast, under conditions of maternal deprivation stress, the knockout mouse showed a significant decrease in post-tetanic potentiation and LTP induction and a significant impairment in Morris water Maze test compared to the wild-type mouse, suggesting that complexin II plays a significant role in neurotransmitter release and synaptic plasticity under this pathological condition. Taken together, these results show that mice lacking complexin II are vulnerable to maternal deprivation stress, which raises the possibility that the complexin II gene may be a factor in the onset of schizophrenia.

Adaptor Proteins, Vesicular Transport↗
PubMed2005

Effect of ganglioside on synaptic plasticity of hippocampus in lead-exposed rats in vivo.

Synaptic plasticity, including long-term potentiation (LTP), long-term depression (LTD) and depotentiation (DP), is important for learning and memory. Previous studies proved that chronic lead exposure especially during early post-natal development induced impairment on synapse plasticity. The purpose of this study is to evaluate the effect of ganglioside on the lead-induced impairments of LTP and DP in rat dentate gyrus in vivo. The experiments were carried out in three groups of rats (control, lead-exposed, ganglioside-treated lead-exposed, respectively). The input-output (I/O) function, pair pulses reaction, excitatory post-synaptic potential (EPSP) and population spike (PS) amplitude were measured in the dentate gyrus (DG) of adult rats (70-90 days) in response to stimulation applied to the lateral perforant path. The results show that (1) chronic lead exposure impaired LTP/DP measured on both EPSP slope and PS amplitude in DG area of the hippocampus. (2) The amplitudes of LTP/DP of lead-exposed group were significantly increased by supplying ganglioside. These results suggest intraperitoneally injection with ganglioside could reverse the lead-induced impairments of synaptic plasticity in rats and might be effective in attenuating the cognitive deficits induced by lead.

Animals↗
PubMed2006

Cortical influences on rapid brainstem plasticity.

Cortical contributions to brainstem plasticity in the somatosensory system are poorly understood. Tactile receptive fields (RFs) of brainstem dorsal column nuclei (DCN) neurons rapidly enlarge when peripheral inputs are disrupted by local anesthetic blocks with lidocaine (LID). Cortical inputs appear to influence this plasticity because enlargements have been shown to be greater when cortical inputs are disrupted. Like disruptions of peripheral inputs, disruptions of DCN inhibition by DCN administration of the GABAA receptor antagonist bicuculline methiodide (BMI) also cause rapid enlargements of DCN RFs when cortical inputs are intact. These findings leave questions about interactions between cortical inputs, DCN inhibition, and DCN RF plasticity. To study potential interactions, the present experiments evaluated RF sizes of DCN tactilely responsive neurons in anesthetized rats following DCN microinjection of BMI when cortical inputs were acutely disrupted or intact. These tests were also supplemented by subsequent LID tests to directly compare post-BMI and post-LID effects on the same RF. BMI caused DCN RF enlargements when cortical inputs were disrupted or intact; however, enlargements after cortical input disruption were greater than when cortical inputs were intact. Following RF enlargement and retraction after BMI, LID often caused a second enlargement of the same RF, across skin that partially matched skin involved in the enlargement after BMI. This occurred when cortical inputs were disrupted or intact. We hypothesize that cortical inputs are not required for BMI and LID to initiate partially matching enlargements in individual DCN tactile RFs, however, cortical inputs constrain magnitudes of these enlargements.

Action Potentials↗
PubMed2005

Effect of beta-amyloid peptide on behavior and synaptic plasticity in terrestrial snail.

A large body of evidence implicates beta-amyloid peptide (betaAP) and other derivatives of the evolutionarily highly conserved amyloid precursor protein (APP) in the pathogenesis of Alzheimer's disease. However, the functional relationship of APP and its proteolytic derivatives to synaptic plasticity is not well known. We demonstrate that 30 min exposure to the 25-35 fragment of betaAP do not markedly change the dynamics of synaptic responses in identified neurons of terrestrial snail while a significant decrease of long-term sensitization was observed after 180 min betaAP bath application. In the behavioral experiments, a significant reduction of sensitization, and decreased ability to develop food-aversion conditioning was observed after betaAP injection. Our results clearly demonstrate that the neurotoxic 25-35 fragment of betaAP may play a significant role in behavioral plasticity by chronically eliminating certain underlying forms of synaptic plasticity. The study also proposes a novel invertebrate model to Alzheimer's disease.

Amyloid beta-Peptides↗
PubMed2005

Separation of plastic mixtures using liquid-fluidized bed technology.

Separation of heavier-than-water plastic mixtures had been investigated via the fluidization of their packed beds induced by an upward flow of water. The samples examined were resin pellets and crushed plastic products including PVC, PET and PBT. On the onset of a flow, a mixed bed was swelled to the state of fluidization and separated into layers of respective resins depending on their density. The effects of the flow rate, an amount of the samples and their density difference were examined on the separation of resin pellets. Under an appropriate condition, the process was completed within a few minutes, and satisfactory separation was attained when the density difference of the samples exceeded 0.05 g cm-3. By using a column equipped with several sample outlets sorted resins could be recovered with their purity intact by withdrawing each layer successively from above through a suitable outlet. Multi-stage separation was also found to be effective in treating close-density samples. Compared with uniform-sized resin pellets, size distribution of crushed plastic samples deteriorated the separation to some extent.

Models, Theoretical↗
PubMed2005

An integrated environment for plastic surgery support: building virtual patients, simulating interventions, and supporting intraoperative decisions.

In the last decade a number of environments for Computer Supported Plastic Surgery have been presented. Nevertheless, an overall approach for training and intraoperative support is still missing or has not been widely exploited yet. We developed a fully integrated system which allows surgical simulation, planning, and support for computer-guided plastic surgery procedures starting from image acquisition to final intraoperative assistance. The system also provides the user with a radiological workstation able to analyse patient medical images and case studies, with advanced bidimensional and three dimensional image processing functionalities. We intend to demonstrate that such a platform can be built at an affordable cost. The radiological workstation is capable of supporting radiologists and surgeons in real patient case studies and the simulation workstation may be adopted by plastic surgeons in teaching and training of complex surgical planning. Moreover, results of simulation can be used in the operating room with a relatively high benefit in terms of improved accuracy, reduction of surgical risks, and decrease in training costs.

Decision Support Techniques↗
PubMed2004

Synaptic basis for developmental plasticity in somatosensory cortex.

Sensory experience drives plasticity of the body map in developing and adult somatosensory cortex, but the synaptic mechanisms underlying such plasticity are not well understood. Recently, several mechanisms that are likely to contribute to map plasticity have been directly observed in response to altered experience in vivo. These mechanisms include long-term potentiation and long-term depression at specific excitatory synapses, competition between lemniscal (barrel) and non-lemniscal (septal) processing streams, and regulation of the number of inhibitory synapses.

Animals↗
PubMed2006

Novel presynaptic mechanisms for coincidence detection in synaptic plasticity.

Long-term plasticity typically relies on postsynaptic NMDA receptors to detect the coincidence of pre- and postsynaptic activity. Recent studies, however, have revealed forms of plasticity that depend on coincidence detection by presynaptic NMDA receptors. In the amygdala, cortical afferent associative presynaptic long-term potentiation (LTP) requires activation of presynaptic NMDA receptors by simultaneous thalamic and cortical afferents. Surprisingly, both types of afferent can also undergo postsynaptically induced NMDA-receptor-dependent LTP. In the neocortex, spike-timing-dependent long-term depression (LTD) requires simultaneous activation of presynaptic NMDA autoreceptors and retrograde signalling by endocannabinoids. In cerebellar LTD, presynaptic NMDA receptor activation suggests that similar presynaptic mechanisms may exist. Recent studies also indicate the existence of presynaptic coincidence detection that is independent of NMDA receptors, suggesting that such mechanisms have a widespread role in plasticity.

Action Potentials↗
PubMed2006

A neural plasticity perspective on the schizophrenic condition.

Imbalanced plasticity of neural networks in the brain is proposed to underlie deficits in the integration of efferent and afferent processes in schizophrenia. These deficits affect the priming of the behavior implementing systems by prior knowledge, and thus impair both controlled regulation and automatic activation of mental and motor processes. The sense of self as a distinct entity can consequently be undermined. In predominantly reality-distorting patients, hypo-plasticity of neural connectivity may cause the emergence of highly focused but inflexible patterns of activation in their representation and response systems. This may lead to dominance of prepotent patterns of activity in these systems and a relative inability of higher control systems to bias lower level activity towards congruence with the ongoing cognitive and motor context. By contrast, predominantly disorganized patients are characterized by hyper-plastic connectivity. This leads to a weakening of prepotent response tendencies but also, as in reality-distorting patients, to less effective top-down contextual constraining.

Ego↗
PubMed2005

Synaptic plasticity and drug addiction.

Recent studies have suggested that the development of addictive behaviours shares common features with traditional learning models. Synaptic plasticity, a possible substrate for learning, has been demonstrated in neural reward circuits and might contribute to the learning of addictive behaviours. Changes in the strength of synaptic connections have been investigated in dopaminergic cells of the ventral tegmental area in response to several addictive drugs. Rapid and persistent forms of synaptic plasticity (specifically, long-lasting synaptic potentiation) have been demonstrated to accompany some of the behavioural effects of addictive drugs. We hypothesize that drug-induced synaptic plasticity might play a role in reward-related learning and addiction by modifying the fine tuning of dopaminergic cell firing.

Brain↗
PubMed2004

Differential corticostriatal plasticity during fast and slow motor skill learning in mice.

BACKGROUND: Motor skill learning usually comprises "fast" improvement in performance within the initial training session and "slow" improvement that develops across sessions. Previous studies have revealed changes in activity and connectivity in motor cortex and striatum during motor skill learning. However, the nature and dynamics of the plastic changes in each of these brain structures during the different phases of motor learning remain unclear. RESULTS: By using multielectrode arrays, we recorded the simultaneous activity of neuronal ensembles in motor cortex and dorsal striatum of mice during the different phases of skill learning on an accelerating rotarod. Mice exhibited fast improvement in the task during the initial session and also slow improvement across days. Throughout training, a high percentage of striatal (57%) and motor cortex (55%) neurons were task related; i.e., changed their firing rate while mice were running on the rotarod. Improvement in performance was accompanied by substantial plastic changes in both striatum and motor cortex. We observed parallel recruitment of task-related neurons in both structures specifically during the first session. Conversely, during slow learning across sessions we observed differential refinement of the firing patterns in each structure. At the neuronal ensemble level, we observed considerable changes in activity within the first session that became less evident during subsequent sessions. CONCLUSIONS: These data indicate that cortical and striatal circuits exhibit remarkable but dissociable plasticity during fast and slow motor skill learning and suggest that distinct neural processes mediate the different phases of motor skill learning.

Analysis of Variance↗
PubMed2005

Development of a framework for sustainable uses of resources: more paper and less plastics?

Taiwan's EPA has implemented a new guideline called the "Plastic Products Restriction Policy", prohibiting some industries to use plastics as packaging materials for the sake of sustainable use of resources. The significant effect resulting from this policy is the substitution of plastic products with paper products. Is this policy beneficial to achieve future sustainability? I attempt to analyze the resource choice between renewable resources and exhaustible resources for production of final products and services in case of exhaustion of natural resources. In this paper, I develop a framework to examine the dynamic responsiveness of a socio-economical system in facing a continual depletion of natural resources provided by an environmental system. In this framework, the status of an environmental system in terms of carrying capacity is affected by the cumulative impacts caused from human activities, including environmental pollution and resource exploitation. Conversely, it also affects the growth of renewable resources. This framework can serve as a guideline to construct indicators to measure the status of the environmental system and the socio-economical system in order to support a policy planner that formulates an appropriate environmental policy. Based on this framework, I also develop a mathematical model to determine the optimal ratio of resources choice between renewable resources and exhaustible resources.

Conservation of Natural Resources↗
PubMed2005

Calcium chelation improves spatial learning and synaptic plasticity in aged rats.

Impaired regulation of intracellular calcium is thought to adversely affect synaptic plasticity and cognition in the aged brain. Comparing young (2-3 months) and aged (23-26 months) Fisher 344 rats, stratum radiatum-evoked CA1 field EPSPs were smaller and long-term potentiation (LTP) was diminished in aged hippocampal slices. Resting calcium, in presynaptic axonal terminals in the CA1 stratum radiatum area, was elevated in aged slices. Loading the slice with the calcium chelator, BAPTA-AM, depressed LTP in young slices, but enhanced this plasticity in old slices. Forty-five minutes following LTP-inducing high frequency stimulation, resting calcium levels were significantly increased in both young and old presynaptic terminals, and significantly reduced by pretreatment with BAPTA-AM. In vivo, intraperitoneal administration of BAPTA-AM prior to training in the reference memory version of the Morris water maze test, significantly improved the acquisition of spatial learning in aged animals, without a significant effect in young rats. These results support the hypothesis that increasing intracellular neuronal buffering power for calcium in aged rats ameliorates age-related impaired synaptic plasticity and learning.

Aging↗
PubMed2005

Evidence that descending serotonergic systems protect spinal cord plasticity against the disruptive effect of uncontrollable stimulation.

Prior work has demonstrated that spinal cord neurons, isolated from the brain through a spinal transection, can support learning. Spinally transected rats given legshock whenever one hindlimb is extended learn to maintain the shocked leg in a flexed position, minimizing net shock exposure. This capacity for learning is inhibited by prior exposure to an uncontrollable stimulus (e.g., intermittent tailshock). The present experiments examined whether spinal cord neurons are more vulnerable to the adverse effects of uncontrollable stimulation after spinal cord injury. Experiment 1 confirmed that uncontrollable shock inhibits subsequent learning in transected rats. Rats that received uncontrollable stimulation prior to transection did not exhibit this effect, suggesting that brain systems exert a protective effect. Experiment 2 showed that this protective effect was removed if subjects received a dorsolateral funiculus lesion prior to shock exposure. Subsequent experiments were designed to determine the identity of the neurochemical systems that protect spinal plasticity. Intrathecal application of serotonin (5-HT) or a 5-HT 1A/7 agonist (8-OH DPAT) in transected rats had a protective effect that blocked the adverse effect of uncontrollable stimulation (Experiment 3). The alpha-2 noradrenergic agonist, clonidine, also protected plasticity (Experiment 4), but this effect was linked to cross-reactivity at the 5-HT 1A receptor (Experiment 5). Microinjection of a 5HT 1A antagonist (WAY 100635) into the spinal cord before intact rats received uncontrollable stimulation blocked the brain-dependent protection of spinal cord neurons. The findings indicate that serotonergic systems normally protect spinal cord plasticity from the deleterious effects of uncontrollable stimulation.

Adrenergic alpha-Agonists↗