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At least 1,135 records · Page 63Linked to original sources
PubMed2002

Pathophysiology of depression: the concept of synaptic plasticity.

Neuronal plasticity or remodeling is most often discussed with regard to cellular and behavioral models of learning and memory. However, neuronal plasticity is a fundamental process by which the brain acquires information and makes the appropriate adaptive responses in future-related settings. Dysfunction of these fundamental processes could thereby contribute to the pathophysiology of mood disorders, and recovery could occur by induction of the appropriate plasticity or remodeling. These possibilities are supported by preclinical and clinical studies demonstrating that there are structural alterations that occur in response to stress and in patients with mood disorders. Moreover, antidepressant treatment may oppose these effects by regulation of signal transduction and gene expression pathways linked to neuronal plasticity. These findings comprise a novel conceptual framework for future studies of the etiology of mood disorders and for the development of novel therapeutic interventions.

Antidepressive Agents↗
PubMedDate not supplied

Gating of action potential propagation by an axonal A-like potassium conductance in the hippocampus: a new type of non-synaptic plasticity.

Synaptic plasticity is usually considered as the main form of activity-dependent functional plasticity in the mammalian brain. Short- and long-term regulation of synaptic transmission have been shown in various types of excitatory synapses including cortical and hippocampal synapses. In this review, we discuss a novel form of non-synaptic plasticity that involves voltage-gated K+ conductances in CA3 pyramidal cell axons. With experimental and theoretical arguments, we show that axons cannot only be considered as a simple structure that transmit reliably the action potential (AP) from the cell body to the nerve terminals. The axon is also able to express conduction failures in specific axonal pathways. We discuss possible physiological conditions in which these axonal plasticity may occur and its incidence on hippocampal network properties.

Action Potentials↗
PubMed1996

The role of polysialic acid and other carbohydrate polymers in neural structural plasticity.

Polysialic acid (PSA) fulfills several criteria for a molecule involved in structural plasticity, including expression in regions capable of plasticity, re-expression in structures undergoing synaptic rearrangement in the adult, downregulation following innervation, and regulation by activity. In addition, removal of PSA reduces the capacity for structural plasticity. PSA may be paradigmatic for other large polymeric carbohydrates, such as glycosaminoglycans and proteoglycans, which also are highly charged and can be extensively hydrated. These carbohydrates may affect structural plasticity by altering cell-cell and/or cell-matrix interactions by increasing intermolecular spacing through hydration.

Animals↗
PubMed1996

The Drosophila tumor suppressor gene, dlg, is involved in structural plasticity at a glutamatergic synapse.

BACKGROUND: Synaptic contacts between neurons and their targets are dynamic entities that can change depending on developmental and functional states of the pre- and postsynaptic cell. However, the molecular factors involved in this plasticity have remained largely unknown. We have demonstrated previously that the Drosophila tumor suppressor gene, discs-large (dlg), is expressed at neuromuscular synapses, and is required for normal synapse structure. A family of dlg homologues is also expressed at mammalian synapses, where they interact with the N-methyl-D-aspartate receptor and ion channels. Here, we provide the first demonstration of the involvement of dlg in structural synaptic plasticity during postsynaptic target growth. RESULTS: We used a temperature-sensitive dlg allele to demonstrate that there are two stages, late embryogenesis and larval stages, at which dlg is necessary for normal formation of synapses. These stages are coincident with dynamic DLG expression at presynaptic sites in the late embryo, and at postsynaptic regions in the larva. Ultrastructural and confocal analyses reveal that Drosophila neuromuscular junctions undergo a dramatic expansion of the postsynaptic apparatus, which is paralleled by target muscle growth. We show that this process of postsynaptic expansion is partially blocked in dlg mutants. CONCLUSIONS: Our results demonstrate that dlg is required during synapse maturation. We show that dlg is involved in the determination of postsynaptic size during target muscle growth. Because motoneuron targets in the larva are continuously growing, synaptic contacts are structurally plastic, undergoing continuous expansion. We conclude that dlg plays an important role in this form of structural synaptic plasticity.

Animals↗
PubMed2004

Integrated technology for evaluation of brain function and neural plasticity.

The study of neural plasticity has expanded rapidly in the past decades and has shown the remarkable ability of the developing, adult, and aging brain to be shaped by environmental inputs in health and after a lesion. Robust experimental evidence supports the hypothesis that neuronal aggregates adjacent to a lesion in the sensorimotor brain areas can take over progressively the function previously played by the damaged neurons. It definitely is accepted that such a reorganization modifies sensibly the interhemispheric differences in somatotopic organization of the sensorimotor cortices. This reorganization largely subtends clinical recovery of motor performances and sensorimotor integration after a stroke. Brain functional imaging studies show that recovery from hemiplegic strokes is associated with a marked reorganization of the activation patterns of specific brain structures. To regain hand motor control, the recovery process tends over time to bring the bilateral motor network activation toward a more normal intensity/extent, while overrecruiting simultaneously new areas, perhaps to sustain this process. Considerable intersubject variability exists in activation/hyperactivation pattern changes over time. Some patients display late-appearing dorsolateral prefrontal cortex activation, suggesting the development of "executive" strategies to compensate for the lost function. The AH in stroke often undergoes a significant "remodeling" of sensory and motor hand somatotopy outside the "normal" areas, or enlargement of the hand representation. The UH also undergoes reorganization, although to a lesser degree. Although absolute values of the investigated parameters fluctuate across subjects, secondary to individual anatomic variability, variation is minimal with regards to interhemispheric differences, due to the fact that individual morphometric characters are mirrored in the two hemispheres. Excessive interhemispheric asymmetry of the sensorimotor hand areas seems to be the parameter with highest sensitivity in describing brain reorganization after a monohemispheric lesion, and mapping motor and somatosensory cortical areas through focal TMS, fMRI, PET, EEG, and MEG is useful in studying hand representation and interhemispheric asymmetries in normal and pathologic conditions. TMS and MEG allow the detection of sensorimotor areas reshaping, as a result of either neuronal reorganization or recovery of the previously damaged neural network. These techniques have the advantage of high temporal resolution but also have limitations. TMS provides only bidimensional scalp maps, whereas MEG, even if giving three-dimensional mapping of generator sources, does so by means of inverse procedures that rely on the choice of a mathematical model of the head and the sources. These techniques do not test movement execution and sensorimotor integration as used in everyday life. fMRI and PET may provide the ideal means to integrate the findings obtained with the other two techniques. This multitechnology combined approach is at present the best way to test the presence and amount of plasticity phenomena underlying partial or total recovery of several functions, sensorimotor above all. Dynamic patterns of recovery are emerging progressively from the relevant literature. Enhanced recruitment of the affected cortex, be it spared perilesional tissue, as in the case of cortical stroke, or intact but deafferented cortex, as in subcortical strokes, seems to be the rule, a mechanism especially important in early postinsult stages. The transfer over time of preferential activation toward contralesional cortices, as observed in some cases, seems, however, to reflect a less efficient type of plastic reorganization, with some aspects of maladaptive plasticity. Reinforcing the use of the affected side can cause activation to increase again in the affected side with a corresponding enhancement of clinical function. Activation of the UH MI may represent recruitment of direct (uncrossed) corticospinal tracts and relate more to mirror movements, but it more likely reflects activity redistribution within preexisting bilateral, large-scale motor networks. Finally, activation of areas not normally engaged in the dysfunctional tasks, such as the dorsolateral prefrontal cortex or the superior parietal cortex in motor paralysis, might reflect the implication of compensatory cognitive strategies. An integrated approach with technologies able to investigate functional brain imaging is of considerable value in providing information on the excitability, extension, localization, and functional hierarchy of cortical brain areas. Deepening knowledge of the mechanisms regulating the long-term recovery (even if partial), observed for most neurologic sequelae after neural damage, might prompt newer and more efficacious therapeutic and rehabilitative strategies for neurologic diseases.

Animals↗
PubMed2003

Brain plasticity in paediatric neurology.

Plasticity includes the brain's capacity to be shaped or moulded by experience, the capacity to learn and remember, and the ability to reorganize and recover after injury. Mechanisms for plasticity include activity-dependent refinement of neuronal connections and synaptic plasticity as a substrate for learning and memory. The molecular mechanisms for these processes utilize signalling cascades that relay messages from synaptic receptors to the nucleus and the cytoskeleton to control the structure of axons and dendrites. Several paediatric neurological disorders such as neurofibromatosis-1, Fragile X syndrome, Rett syndrome, and other syndromic and non-specific forms of mental retardation involve lesions in these signalling pathways. Acquired disorders such as hypoxic-ischaemic encephalopathy, lead poisoning and epilepsy also involve signalling pathways including excitatory glutamate receptors. Information about these 'plasticity pathways' is useful for understanding their pathophysiology and potential therapy.

Adaptation, Physiological↗
PubMed2003

Microvascular plasticity in aging.

Understanding the bases of aging-related cognitive decline remains a central challenge in neurobiology. Quantitative studies reveal little change in the number of neurons or synapses in most of the brain but their ongoing replacement is reduced, resulting in a significant loss of neuronal plasticity with senescence. Aging also may alter neuronal function and plasticity in ways that are not evident from anatomical studies of neurons and their connections. Since the nervous system is dependent upon a consistent blood supply, any aging-related changes in the microvasculature could affect neuronal function. Several studies suggest that, as the nervous system ages, there is a rarefaction of the microvasculature in some regions of the brain, as well as changes in the structure of the remaining vessels. These changes contribute to a decline in cerebral blood flow (CBF) that reduces metabolic support for neural signaling, particularly when levels of neuronal activity are high. In addition to direct effects on the microvasculature, aging reduces microvascular plasticity and the ability of the vessels to respond appropriately to changes in metabolic demand. This loss of microvascular plasticity has significance beyond metabolic support for neuronal signaling, since neurogenesis in the adult brain is regulated coordinately with capillary growth.

Aging↗
PubMed1999

Cortical plasticity in normal and abnormal cognitive development: evidence and working hypotheses.

In this paper I review evidence and viewpoints on developmental plasticity in the cerebral cortex. Although there is some degree of plasticity in the cortex during early postnatal life in the human infant, this plasticity is constrained by various factors. Three working hypotheses about postnatal cortical specialization of function are advanced, and some specific predictions about the limits and extent of plasticity are assessed through both empirical evidence from infants and simulations on simple cortical network models.

Aging↗
PubMed2006

Estrogenic potency of food-packaging-associated plasticizers and antioxidants as detected in ERalpha and ERbeta reporter gene cell lines.

This study presents the estrogenic potency of 21 food-packaging-associated compounds determined for the first time, using two transfected U2-OS (human osteoblasts devoid of endogenous estrogen receptors) estrogen receptor (ER) alpha and beta cell lines. Six plasticizers and three antioxidants were slightly estrogenic in the ERalpha cells. The model compounds bisphenol A and nonylphenol, one plasticizer [tris(2-ethylhexyl)trimellitate (TEHTM)], and two antioxidants (propyl gallate and butylated hydroxyanisole) were estrogenic in both ERalpha and ERbeta cells. Compared to estradiol (E2), these compounds appeared to be relatively more estrogenic in the ERbeta cells than in the ERalpha cells. Three sorbitol-based plasticizers activated neither ERalpha nor ERbeta and may be good replacements of existing plasticizers. All responses were additive with the response of E2. This indicates that they may contribute to the total effects of the pool of estrogenic compounds humans are exposed to. The estrogenic potencies of these compounds, together with the suggested beneficial effect of ERbeta-mediated responses and adverse ERalpha-mediated effects, support the importance of detecting characteristics for ERalpha and ERbeta response separately in independent models, as done in the present study.

Antioxidants↗
PubMed1999

Tensile properties and water absorption of zein sheets plasticized with oleic and linoleic acids.

Corn zein has been investigated for fabrication of biodegradable packaging materials. Our objective was to investigate the effect of added plasticizers, oleic and linoleic acids, on tensile properties and water absorption of zein sheets. Moldable resins were precipitated from aqueous ethanol dispersions of zein and fatty acids and rolled into sheets of approximately 0.5 mm in thickness. To increase plasticization effects, zein-oleic acid sheets were replasticized by heating them in fatty acid baths. Plasticization resulted in flexible sheets of high clarity, low modulus, and high elongation and toughness, although low tensile strength. Water absorption of zein sheets was lowered by plasticization, attributed in part to reduced mass fraction of zein. Polymerization of linoleic acid may have sealed off pores on sheet surfaces, thus slowing water absorption.

Absorption↗
PubMed1998

Performance of a plastic optical fiber stylet for tracheal intubation of a dog.

OBJECTIVE: We set out to establish whether a novel plastic optical fiber incorporated into an endotracheal tube (ETT) stylet could be used for intubation of a dog. A secondary objective examined the need for a direct illumination source from a laryngoscope. Lastly, the fragility of the system was tested. METHODS: An anesthetized dog was repeatedly intubated using a laryngoscope to elevate the tongue and the view of the larynx conducted through the plastic optical fiber stylet (placed within an endotracheal tube) and displayed on a television monitor. Four prototype identical stylets were tested. Repeated intubations were attempted with each stylet and graded as either successful or failed. All four stylets were tested 10 times each using a Miller 4 blade and direct illumination from the laryngoscope. Two of the four stylets were reused during an additional 10 intubation attempts using a Miller 4 blade and laryngoscope (without batteries) with only ambient light. Finally, one stylet was used for intubation after 10, 20, 30, 40 and 50 sharp 90 degree bend-and-straighten cycles using a Miller 4 blade and laryngoscope for direct illumination. RESULTS: All attempted intubations were successful. However, the image quality was dramatically better when direct illumination from a laryngoscope was used than when ambient light was used. One plastic optical fiber stylet was successfully used to intubate after having been used for 20 intubations and 50 sharp 90 degree bend-and-straighten cycles. A partial lens separation occurred between the 41st and 50th bend cycle but the image remained adequate enough to successfully intubate again. CONCLUSIONS: A novel plastic optical fiber incorporated into an ETT stylet can be used with a laryngoscope for intubation of a dog. Direct illumination from a laryngoscope provides a better television monitor image than when only ambient light is used. The system was durable, withstanding over 20 uses and 40 sharp bend-and-straighten cycles before a lens separation failure occurred.

Animals↗
PubMed2003

Isolation and characterization of a bacterium that degrades various polyester-based biodegradable plastics.

Microorganisms isolated from soil samples were screened for their ability to degrade various biodegradable polyester-based plastics. The most active strain, designated as strain TB-13, was selected as the best strain for degrading these plastics. From its phenotypic and genetic characteristics, strain TB-13 was closely related to Paenibacillus amyloyticus. It could degrade poly(lactic acid), poly(butylene succinate), poly(butylene succinate-co-adipate), poly(caprolactone) and poly(ethylene succinate) but not poly(hydroxybutylate-co-valerate). However, it could not utilize these plastics as sole carbon sources. Both protease and esterase activities, which may be involved in the degradation of plastic, were constitutively detected in the culture broth.

Adipates↗
PubMed1998

Factors governing activity-dependent structural plasticity of the hypothalamoneurohypophysial system.

1. The adult hypothalamoneurohypophysial system (HNS) undergoes reversible morphological changes in response to physiological stimulation. 2. In the hypothalamus, stimulation of neurohormone secretion results in reduced astrocytic coverage of oxytocinergic somata and dendrites so that their surfaces become directly juxtaposed. Concurrently, there is a significant increase in the number of GABAergic, glutamatergic. and noradrenergic synapses impinging on the neurons. 3. In the neurohypophysis, stimulation induces retraction of pituicyte processes from the perivascular area and enlargement and multiplication of neurosecretory terminals. 4. These neuronal-glial and synaptic changes are reversible with cessation of stimulation, thus rendering the HNS an excellent model to study physiologically linked structural neuronal plasticity in the adult CNS. 5. We still do not know the cellular mechanisms and factors underlying such plasticity. Recent studies indicate, however, that the adult HNS expresses molecular characteristics normally associated with histogenesis and/or tissue reorganization in developing or regenerating neural systems. They include expression of cell adhesion molecules such as the highly sialylated isoform of the neural cell adhesion molecule, PSA-NCAM, and the glycoproteins, F3 and tenascin-C. 6. The expression of PSA-NCAM and tenascin-C does not show striking differences in terms of age, sex or physiological condition but that of F3 varies considerably with neurohypophysial stimulation. 7. We postulate that such molecular features allow magnocellular neurons and their glia to undergo neuronal-glial and synaptic plasticity throughout life, provided the proper stimulus intervenes. 8. Thus, in the hypothalamic nuclei, centrally released oxytocin acting in synergy with steroids can induce such plasticity, while adrenaline, acting through beta-adrenergic mechanisms, does so in the neurohypophysis.

Animals↗
PubMed2003

Motor enrichment and the induction of plasticity before or after brain injury.

Voluntary exercise, treadmill activity, skills training, and forced limb use have been utilized in animal studies to promote brain plasticity and functional change. Motor enrichment may prime the brain to respond more adaptively to injury, in part by upregulating trophic factors such as GDNF, FGF-2, or BDNF. Discontinuation of exercise in advance of brain injury may cause levels of trophic factor expression to plummet below baseline, which may leave the brain more vulnerable to degeneration. Underfeeding and motor enrichment induce remarkably similar molecular and cellular changes that could underlie their beneficial effects in the aged or injured brain. Exercise begun before focal ischemic injury increases BDNF and other defenses against cell death and can maintain or expand motor representations defined by cortical microstimulation. Interfering with BDNF synthesis causes the motor representations to recede or disappear. Injury to the brain, even in sedentary rats, causes a small, gradual increase in astrocytic expression of neurotrophic factors in both local and remote brain regions. The neurotrophic factors may inoculate those areas against further damage and enable brain repair and use-dependent synaptogenesis associated with recovery of function or compensatory motor learning. Plasticity mechanisms are particularly active during time-windows early after focal cortical damage or exposure to dopamine neurotoxins. Motor and cognitive impairments may contribute to self-imposed behavioral impoverishment, leading to a reduced plasticity. For slow degenerative models, early forced forelimb use or exercise has been shown to halt cell loss, whereas delayed rehabilitation training is ineffective and disuse is prodegenerative. However, it is possible that, in the chronic stages after brain injury, a regimen of exercise would reactivate mechanisms of plasticity and thus enhance rehabilitation targeting residual functional deficits.

Animals↗
PubMed1997

Cholinergic neurotransmission and synaptic plasticity concerning memory processing.

The brain is able to change the synaptic strength in response to stimuli that leave a memory trace. Long-term potentiation (LTP) and long-term depression (LTD) are forms of activity-dependent synaptic plasticity proposed to underlie memory. The induction of LTP appears mediated by glutamate acting on AMPA and then on NMDA receptors. Cholinergic muscarinic agonists facilitate learning and memory. Acetylcholine depolarizes pyramidal neurons, reduces inhibition, upregulates NMDA channels and activates the phosphoinositide cascade. Postsynaptic Ca2+ rises and stimulates Ca-dependent PK, promoting synaptic changes. Electroencephalographic desynchronization and hippocampal theta rhythm are related to learning and memory, are inducible by cholinergic agonists and elicited by hippocampal cholinergic terminals. Their loss results in memory deficits. Hence, cholinergic pathways may act synergically with glutamatergic transmission, regulating and leading to synaptic plasticity. The stimulation that induces plasticity in vivo has not been established. The patterns for LTP/LTD induction in vitro may be due to the loss of ascending cholinergic inputs. As a rat explores pyramidal cells fire bursts that could be relevant to plasticity.

Animals↗
PubMed1989

Role of context in the expression of learning-induced plasticity of single neurons in auditory cortex.

Classical conditioning produces frequency-specific plasticity of receptive fields (RFs) of single neurons in cat auditory cortex (Diamond & Weinberger, 1986). In this article we show that although plasticity may be observed during both training trials and determination of RFs, it is usually expressed in a qualitatively different form (e.g., decreased response during conditioning vs. increased response to this same conditioned stimulus in the postconditioning RF). This differential expression of learning-induced plasticity provides evidence for a role of context in neurophysiological mechanisms of learning in auditory cortex. A model of cortical neurons functioning within a mosaic of influences is presented. The Functional Mosaic model views the induction and expression of plasticity as separate processes.

Animals↗
PubMed1998

Induction of long-term receptive field plasticity in the auditory cortex of the waking guinea pig by stimulation of the nucleus basalis.

Learning induces neuronal receptive field (RF) plasticity in primary auditory cortex. This plasticity constitutes physiological memory as it is associative, highly specific, discriminative, develops rapidly, and is retained indefinitely. This study examined whether pairing a tone with activation of the nucleus basalis could induce RF plasticity in the waking guinea pig and, if so, whether it could be retained for 24 hr. Subjects received 40 trials of a single frequency paired with electrical stimulation of the nucleus basalis (NB) at tone offset. The physiological effectiveness of NB stimulation was assessed later while subjects were anesthetized with urethane by noting whether stimulation produced cortical desynchronization. Subjects in which NB stimulation was effective did develop RF plasticity and this was retained for 24 hr. Thus, activation of the NB during normal learning may be sufficient to induce enduring physiological memory in auditory cortex.

Acoustic Stimulation↗
PubMed1999

Neuromodulation, development and synaptic plasticity.

We discuss parallels in the mechanisms underlying use-dependent synaptic plasticity during development and long-term potentiation (LTP) and long-term depression (LTD) in neocortical synapses. Neuromodulators, such as norepinephrine, serotonin, and acetylcholine have also been implicated in regulating both developmental plasticity and LTP/LTD. There are many potential levels of interaction between neuromodulators and plasticity. Ion channels are substrates for modulation in many cell types. We discuss examples of modulation of voltage-gated Ca2+ channels and Ca(2+)-dependent K+ channels and the consequences for neocortical pyramidal cell firing behaviour. At the time when developmental plasticity is most evident in rat cortex, the substrate for modulation is changing as the densities and relative proportions of various ion channels types are altered during ontogeny. We discuss examples of changes in K+ and Ca2+ channels and the consequence for modulation of neuronal activity.

Age Factors↗