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Visual cortical plasticity in infant kittens.

The visual cortex of the cat is characterized by marked modifiability of neuronal responsiveness by visual experience in infancy, and stereotyped pattern of functional architectures in adulthood. The question of how the plasticity of the infant visual cortex is compatible with the regular patterns of the adult visual cortex has been a central problem of the brain neuroscience. This question was answered by quantifying the plasticity in the visual cortical circuitry of the infant kittens as changes in synaptic transmission produced after conditioning stimulation of the visual pathway. The results indicate that the solution of this question is the heterogeneous distribution of the synaptic plasticity in the infant visual cortex: the plasticity is not uniformly present in the visual cortical circuitry, but is limited only to a part of the circuitry (the cortico-cortical synapses in the supragranular layers). Therefore, the visual function (photic responsiveness) may be learned during the postnatal life of the kittens by the supragranular cells with plastic synapses, while the other cortical cells with fewer plastic synapses put prenatally designed constraints on the learning, so that the learning yields the adult cortical circuitry with regular patterns of organization.

Action Potentials↗

[Indications for plastic surgery (author's transl)].

The paper deals with the three main areas of indications for plastic surgery: 1. Reconstructive plastic surgery or treatment of defects resulting from trauma or disease. 2. Constructive plastic surgery or treatment of innate defects. 3. Anaplastic surgery or treatment of disfunction of appearance. By defining these different branches of plastic surgery criteria are elaborated that govern all plastic surgery. Differences between the general surgical approach and the plastic surgical approach are explained and emphasis is put on the patients' subjective situation and possible pressures from outside as well as environmental influences that may have bearing on the indication.

Breast↗

Torque capacity of metal and plastic brackets with reference to materials, application, technology and biomechanics.

AIM: The aim of the present study was to investigate slot deformation and the equivalent torque capacity of plastic brackets in comparison with those of a metal bracket in vitro and to simulate them under clinical conditions. MATERIAL AND METHOD: For this purpose the expansion characteristics of the brackets and their resistance to extraoral mechanical loading were compared in in-vitro activating experiments. In a further investigation, the labial crown torque of an upper central incisor was measured in a simulated intraoral clinical situation, using the Orthodontic Measuring and Simulation System (OMSS). Four types of bracket manufactured by Forstadent, Pforzheim, Germany, were tested: the plastic brackets Aesthetik-Line and Brillant, the latter from a previous series (Brillant-old) and from a modified series (Brillant-new), and the metal bracket MINI-MONO. For testing purposes the brackets were torqued with 0.016" x 0.022" (0.41 x 0.56 mm) and 0.018" x 0.022" (0.46 x 0.56 mm) ideal steel archwires (Remanium, Dentaurum, Ispringen, Germany). RESULTS: In the activating experiments, significantly higher torque losses and lower torquing moments were registered with both rectangular archwires with the plastic brackets than with the metal bracket. In the simulation tests, significantly higher torquing moments were registered with the metal bracket than with the plastic brackets. The OMSS model approximates the clinical situation, with the torque loss being notably higher than in the in-vitro activating experiments. This is due to the adjacent teeth giving the archwire additional play. In addition, the torquing process of the rectangular wire may deform the archwire, resulting in subsidiary forces. CONCLUSION: On the basis of the present results, the Brillant and Aesthetik-Line plastic brackets and the MINI-MONO metal bracket can be recommended for torquing. In view of the high torque losses, however, the torques programmed in the straight wire technique must be seen as questionable. It would be helpful to the practitioner if data were provided by the manufacturer on the flexing to be expected in plastic brackets, which has to be offset by additional torque or the possible renunciation of bracket torque.

Biomechanical Phenomena↗

Plasticity in cat visual cortex restored by electrical stimulation of the locus coeruleus.

It has been proposed that the presence of noradrenaline (NA)-containing terminals and NA-related receptors within the visual cortex is necessary to maintain the high level of neuronal plasticity in the immature visual cortex of kittens. In the present study we wanted to show whether electrical stimulation of the locus coeruleus (LC), which contains the somata of these cortical NA fibers, can restore neuronal plasticity to the normally aplastic visual cortex of juvenile and adult cats. We consistently found a significant loss of binocular cells in the visual cortex of mature animals which had monocular vision for only 12 h dispersed over 6 days (2 h a day, otherwise kept in the dark) in combination with concurrent LC stimulation. This result was interpreted as indicating that endogenous NA released from NA terminals restored susceptibility to monocular vision in the mature visual cortex. We next examined how long the restored plasticity lasts in the same animals after the LC stimulation was ended. The animals revived from the first recording session were either returned to the same daily schedule of brief monocular exposure (light/dark = 2/22 h) as before, or subjected to the usual monocular lid suture and kept in a cat colony environment (light/dark = 16/8 h). The LC electrodes had been removed and no more electrical stimulation was delivered at this stage. In the animals subjected to reiteration of brief monocular exposure, the state of reduced binocularity gradually returned to normal over a period of 2-3 weeks after stopping LC stimulation. We calculated that the revived plasticity disappeared at an average rate of a 22% loss every 7 days. This result sharply contrasted with the result obtained in the animals subjected to usual monocular lid suture. In this test the state of reduced binocularity continued for at least the next 3 weeks, suggesting that the restored plasticity was sustained throughout a period of 3 weeks (longest term tested). The different results obtained in the two paradigms may be explained by the different strength of binocular imbalance in the two tests imposed on the visual cortex in which neuronal plasticity was restored partially.

Animals↗

Calibration of [14C]plastic standards for quantitative autoradiography of [125I]labeled ligands with Amersham Hyperfilm beta-max.

The densitometric response of Hyperfilm beta-max (HFBM) to [14C]plastic standards was calibrated to tissue-equivalent concentrations of [125I]. Plastic sections with standard concentrations of [125I] and [14C] were apposed to HFBM for 1, 3, 5, and 9 days, with liver and muscle slices (20 microns thick) labeled with [125I]insulin. The relative optical densities (ROD = log 10 [1/gray level x 256(-1)] produced by [125I]- and [14C]plastic standards were converted to equivalent tissue [125I] concentrations (dpm/mm2). The response of HFBM to the [125I]- and [14C]plastic standards was similar (P less than 0.001). Standard curves of tissue [125I] (dpm/mm2) vs plastic [14C] (microCi/g) concentrations fit second order polynomials (r2 = 0.995-0.999). The results show that [14C]plastic standards are valid for measuring [125I] radioactivity in tissue slices by autoradiography with HFBM.

Animals↗

Relationship between plasticity, mild cognitive impairment and cognitive decline.

A topic of great interest in gerontology research is the prediction of cognitive deterioration which marks the transition from mild cognitive impairment (MCI) to dementia. In this area the term plasticity is a construct of prime importance. Previous studies have demonstrated the existence of plasticity in healthy older persons, and it is thought that this is what discriminates between healthy individuals and those at risk for dementia. The aim of the present study is to demonstrate that plasticity exists in persons with MCI, and that a lack of plasticity may be one of the risk factors related to cognitive decline. An adapted version of the Auditory Verbal Learning Test-the AVLT of Learning Potential-was used to assess plasticity. Participants in the research were 203 older persons whose cognitive status had previously been determined using a cognitive screening test. The results show that plasticity exists in persons with MCI and that its presence is associated with less marked cognitive decline.

Aged↗

Tinnitus as a plastic phenomenon and its possible neural underpinnings in the dorsal cochlear nucleus.

Tinnitus displays many features suggestive of plastic changes in the nervous system. These can be categorized based on the types of manipulations that induce them. We have categorized the various forms of plasticity that characterize tinnitus and searched for their neural underpinnings in the dorsal cochlear nucleus (DCN). This structure has been implicated as a possible site for the generation of tinnitus-producing signals owing to its tendency to become hyperactive following exposure to tinnitus inducing agents such as intense sound and cisplatin. In this paper, we review the many forms of plasticity that have been uncovered in anatomical, physiological and neurochemical studies of the DCN. Some of these plastic changes have been observed as consequences of peripheral injury or as fluctuations in the behavior and chemical activities of DCN neurons, while others can be induced by stimulation of auditory or even non-auditory structures. We show that many parallels can be drawn between the various forms of plasticity displayed by tinnitus and the various forms of neural plasticity which have been defined in the DCN. These parallels lend further support to the hypothesis that the DCN is an important site for the generation and modulation of tinnitus-producing signals.

Cochlear Nerve↗

Neurodegeneration and plasticity.

Neurofibrillary degeneration, associated with the formation of paired helical filaments (PHF), is one of the critical neuropathological hallmarks of Alzheimer's disease (AD). Although the microtubule-associated protein tau in a hyperphosphorylated form has been established as primary PHF constituent, the process of tau phosphorylation and its potential link to degeneration is not very well understood, mostly because of the lack of a physiological in vivo model of PHF-like tau phosphorylation. PHF formation in AD follows a hierarchical pattern of development throughout different cortical areas, which closely matches the pattern of neuronal plasticity in the adult brain. Those brain areas are most early and most severely affected which are involved in the regulation of memory, learning, perception, self-awareness, consciousness, and higher brain functions that require a life-long re-fitting of connectivity, a process based on a particularly high degree of plasticity. Failures of synaptic plasticity are, thus, assumed to represent early events in the course of AD that eventually lead to alteration of tau phosphorylation. Recently, we have used the hibernation cycle, a physiological model of adaptation associated with an extraordinary high degree of structural neuronal plasticity, to analyze the potential link between synaptic plasticity, synaptic detachment and the regulation of tau phosphorylation. During torpor, a natural state of hypothermia, synaptic contacts between mossy fibers and hippocampal pyramidal neurons undergo dramatic regressive changes that are fully reversible very rapidly during euthermy. This rapid, reversible, and repeated regression of synaptic and dendritic components on CA3 neurons is associated with a reversible PHF-like phosphorylation of tau at a similar time course. The repeated formation and degradation of PHF-tau might, thus, represent a physiological mechanism not necessarily associated with pathological effects. These findings implicate an essential link between neuronal plasticity and PHF-like phosphorylation of tau, potentially involved in neurofibrillary degeneration.

Aging↗

Fast-melting tablets based on highly plastic granules.

Highly plastic granules that can be compressed into tablets at low pressure were developed to make fast-melting tablets (FMTs) by compression method. The highly plastic granules are composed of three components: a plastic material, a material enhancing water penetration, and a wet binder. One of the unique properties of the highly plastic granules is that they maintain a porous structure even after compression into tablets. The porous and plastic nature of the granules allows fast absorption of water into the compressed tablet for fast melting/dissolution of the tablet. The prepared tablets possess tablet strength and friability that are suitable for multi-tablet packages. The three-component highly plastic granules provide an effective way of making FMTs by compression.

Chemistry, Pharmaceutical↗

Temporary restorative resins using non-phthalate ester plasticizers.

OBJECTIVE: This study examined temporary restorative resins that use non-phthalate ester plasticizers. METHODS: Three non-phthalate plasticizers were tested: tri-ethyl citrate (TEC), tri-butyl citrate (TBC), and di-butyl sebacate (DBS). The experimental resins were compared with resins that use a phthalate ester plasticizer (di-butyl phthalate, DBP) and commercial products (Dura Seal, Plast Seal, and Fit Seal). For the experimental resins, the ratio of plasticizer to PMMA/MMA resin was varied from 30 to 60% (wt). The mechanical properties of the experimental resins were evaluated using a modified diametral compressive strength and the resistance to explorer insertion. RESULTS: The strengths of the experimental resins with plasticizer concentrations ranging from 40 to 50% (TEC, TBC, and DBP) or from 30 to 40% (DBS), by weight, were equivalent to the strengths of commercial temporary restorative resins. A similar tendency was seen for the resistance to explorer insertion. CONCLUSIONS: The results suggest that new temporary restorative resins can be prepared by choosing the appropriate proportions of resin monomer and non-phthalate ester plasticizer.

Citrates↗

Brain plasticity and ion channels.

It is generally believed that spatio-temporal configurations of distributed activity in the brain contribute to the coding of neuronal information and that synaptic contacts between nerve cells could play a central role in the formation of privileged pathways of activity. Synaptic plasticity is not the only mode of regulation of information processing in the brain and persistent regulations of ionic conductances in some specialized neuronal areas such as the dendrites, the cell body and the axon could also modulate, in the short- and the long-term, the propagation of information in the brain. Persistent changes in intrinsic excitability have been reported in several brain areas in which activity is modified during a classical conditioning. The role of synaptic activity seems to be determinant in the induction but the learning rules and the underlying mechanisms remain to be defined. This review discusses the role of neuronal activity in the induction of intrinsic plasticity in cortical, hippocampal and cerebellar neurons. Activation and inactivation properties of ionic channels in the axon determine the short-term dynamics of axonal propagation and synaptic transmission. Activation of glutamate receptors initiates a long-term modification in neuronal excitability that may represent the substrate for the mnesic engram and for the stabilization of the epileptic state. Similarly to synaptic plasticity, long-lasting intrinsic plasticity appears to be reversible and to express a certain level of input or cellular specificity. These non-synaptic forms of plasticity affect the signal propagation in the axon, the dendrites and the soma. They not only share common learning rules and induction pathways with the better known synaptic plasticity such as NMDA receptor-dependent LTP and LTD but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram.

Animals↗

Antidepressants and prolonged stress in rats modulate CAM-L1, laminin, and pCREB, implicated in neuronal plasticity.

Previously, we reported an ability of NE to promote processes of plasticity in neuroblastoma cells, as observed by morphological changes such as an elongated granule-rich cell body and neuritegenesis, in addition to a progressive decrease in the pluripotent marker Oct4 and an increase in the growth cone marker GAP-43. This was accompanied by the induction of three plasticity genes forming a functional cluster, the cell adhesion molecule L1 (CAM-L1), laminin, and CREB, all involved in neuronal plasticity and neurite outgrowth. In the present study, we hypothesized that the regulation of CAM-L1, laminin, and CREB/pCREB by NE could mediate processes of plasticity in the mode of action of antidepressants, as well as in the long-term effects of stress, in rats, given the association of both with NE alterations and neuronal plasticity. In the first experiment, rats were chronically administered with antidepressants (21 days). In the second experiment, rats were exposed to chronic stress and examined 4 months later, a model shown to exhibit behavioral indices of stress. We found brain region-specific alterations in mRNA and protein levels of CAM-L1, laminin, and pCREB in rats chronically treated with the noradrenergic antidepressant desipramine and, to a lesser extent, in those treated with fluoxetine. Stressed rats presented a decrease in CAM-L1, laminin, and pCREB, specifically in brain areas implicated in stress. Our findings suggest that noradrenergic-regulated plasticity genes such as CAM-L1, laminin, and CREB play an important role both in stress and in the treatment of depression.

Animals↗

Stress-facilitated LTD induces output plasticity through synchronized-spikes and spontaneous unitary discharges in the CA1 region of the hippocampus.

Long-term potentiation (LTP) and long-term depression (LTD) of the excitatory synaptic inputs plasticity in the hippocampus is believed to underlie certain types of learning and memory. Especially, stressful experiences, well known to produce long-lasting strong memories of the event themselves, enable LTD by low frequency stimulation (LFS, 3 Hz) but block LTP induction by high frequency stimulation (HFS, 200 Hz). However, it is unknown whether stress-affected synaptic plasticity has an impact on the output plasticity. Thus, we have simultaneously studied the effects of stress on synaptic plasticity and neuronal output in the hippocampal CA1 region of anesthetized Wistar rats. Our results revealed that stress increased basal power spectrum of the evoked synchronized-spikes and enabled LTD induction by LFS. The induction of stress-facilitated LTD but not LFS induced persistent decreases of the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges; However, HFS induced LTP in non-stressed animals and increased the power spectrum of the synchronized-spikes, without affecting the frequency of the spontaneous unitary discharges, but HFS failed to induce LTP in stressed animals without affecting the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges. These observations that stress-facilitated LTD induces the output plasticity through the synchronized-spikes and spontaneous unitary discharges suggest that these types of stress-related plasticity may play significant roles in distribution, amplification and integration of encoded information to other brain structures under stressful conditions.

Action Potentials↗

Factors critical for the plasticity of dendritic spines and memory storage.

The structure of dendritic spines is highly plastic and responds to synaptic activity, including activity patterns that induce long-term potentiation (LTP) and depression (LTD). Induction of LTP causes enlargement of spine heads, while LTD causes spine head shrinkage. In addition, spine structure is well associated with synaptic weight and the extent of synaptic plasticity, such that structural changes of the spine may represent forms of memory storage. While the correlation between structural and functional plasticity appears to be simple, the underlying mechanisms of spine plasticity are intricate. Spine plasticity requires multiple molecular interactions, and is affected by the surrounding environment and by cellular metabolic state. Here, I synthesize the latest progress in this field by defining six determinants of spine plasticity, and discuss the role of each factor in memory storage.

Animals↗

Ubiquitin-proteasome-mediated local protein degradation and synaptic plasticity.

A proteolytic pathway in which attachment of a small protein, ubiquitin, marks the substrates for degradation by a multi-subunit complex called the proteasome has been shown to function in synaptic plasticity and in several other physiological processes of the nervous system. Attachment of ubiquitin to protein substrates occurs through a series of highly specific and regulated steps. Degradation by the proteasome is subject to multiple levels of regulation as well. How does the ubiquitin-proteasome pathway contribute to synaptic plasticity? Long-lasting, protein synthesis-dependent, changes in the synaptic strength occur through activation of molecular cascades in the nucleus in coordination with signaling events in specific synapses. Available evidence indicates that ubiquitin-proteasome-mediated degradation has a role in the molecular mechanisms underlying synaptic plasticity that operate in the nucleus as well as at the synapse. Since the ubiquitin-proteasome pathway has been shown to be versatile in having roles in addition to proteolysis in several other cellular processes relevant to synaptic plasticity, such as endocytosis and transcription, this pathway is highly suited for a localized role in the neuron. Because of its numerous roles, malfunctioning of this pathway leads to several diseases and disorders of the nervous system. In this review, I examine the ubiquitin-proteasome pathway in detail and describe the role of regulated proteolysis in long-term synaptic plasticity. Also, using synaptic tagging theory of synapse-specific plasticity, I provide a model on the possible roles and regulation of local protein degradation by the ubiquitin-proteasome pathway.

Animals↗

Carotid chemoafferent plasticity in adult rats following developmental hyperoxia.

Developmental hyperoxia impairs carotid chemoreceptor development and induces long-lasting reduction in carotid sinus nerve (CSN) responses to hypoxia in adult rats. Studies were carried out to determine if CSN responses to acute hypoxia would exhibit hypoxia-induced plasticity in adult 3-5-months-old rats previously treated with postnatal hyperoxia (60% O2, PNH) of 1, 2, or 4 weeks duration. CSN responses to acute hypoxia were assessed in adult rats exposed to 1 week of sustained hypoxia (12% O2, SH). In normal adult rats and adult rats treated with 1 week of PNH, CSN responses to acute hypoxia were significantly increased in urethane-anesthetized rats when studied 3-5 h after SH. Apparent increases in CSN responses to hypoxia were not significant in rats treated with 2 weeks of PNH and were clearly absent after 4 weeks of PNH, but exponential analysis suggests a PNH duration-dependent plasticity of the CSN response to acute hypoxia after SH. In a second study rats exposed to 2 weeks of PNH were treated with SH for 1 week as adults and acute hypoxic responses were tested 4-5 months later. CSN responses in these rats were unaffected by SH suggesting a lack of persistent SH-induced functional plasticity. We conclude that rats treated with 1 week of PNH retain the capacity for hypoxia-induced plasticity of carotid chemoafferent function and some potential for plasticity may be present after 2 weeks of PNH, whereas 4 weeks of PNH impairs the capability of rats to exhibit plasticity following 1 week of SH.

Animals↗

Behaviour of biodegradable plastics in composting facilities.

Composting is a preferred treatment strategy for biodegradable plastics (BDPs). In this sense, the collection of BDPs together with organic household wastes is a highly discussed possibility. Under the aspect of the behaviour of BDPs in composting facilities, a telephone survey was carried out with selected composting facility operators. They were interviewed with respect to treated wastes, content of impurities, processes for impurity separation, experiences with biodegradable plastics and assumptions to the behaviour of biodegradable plastics in their facility. Forty percent of the facilities had some experiences with BDPs due to test runs, and also since the occurrence of BDPs in their waste was known. The majority of the operators expressed apprehension regarding an increase of impurities resulting from a combined collection of biowaste and BDPs. In the facilities, measures for the impurity separation from the biowaste were used in common practice - in 33% of the cases, separation of disturbing plastics was done before composting, in 33% after composting, and in 13% before and after composting. The most important separation processes for conventional plastics were sieving and manual sorting. In two cases air classification was also used. When asked about the separation possibility of the conventional but not of the biodegradable plastics in their facilities, the majority of operators were not in a position to comment or they replied that it was not an option. No problems were seen in most cases if the impurity separation follows composting. If impurity separation takes place before composting it was often assumed that the BDPs are mainly separated by sieving. In conclusion, in more than half of the cases, BDPs would not be composted if delivered to a composting facility. Under the actual conditions regarding the collection and the treatment/disposal possibilities, an application of BDPs seems to only be reasonable for clean (i.e., source separated on their own) fractions of BDPs.

Biodegradation, Environmental↗

Recovery of PET from packaging plastics mixtures by wet shaking table.

Recycling requires the separation of materials appearing in a mass of wastes of heterogeneous composition and characteristics, into single, almost pure, component/material flows. The separation of materials (e.g., some types of plastics) with similar physical properties (e.g., specific gravity) is often accomplished by human sorting. This is the case of the separation of packaging plastics in municipal solid wastes (MSW). The low cost of virgin plastics and low value of recycled plastics necessitate the utilization of low cost techniques and processes in the recycling of packaging plastics. An experimental study was conducted to evaluate the feasibility of production of a PET product, cleaned from PVC and PS, using a wet shaking table. The wet shaking table is an environmentally friendly process, widely used to separate minerals, which has low capital and operational costs. Some operational variables of the equipment, as well as different feed characteristics, were considered. The results show that the separation of these plastics is feasible although, similarly to the mineral field, in somewhat complex flow sheets.

Plastics↗