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PubMedDate not supplied

Effects of normal aging on visuo-motor plasticity.

Normal aging is associated with declines in neurologic function. Uncompensated visual and vestibular problems may have dire consequences including dangerous falls. Visuo-motor plasticity is a form of behavioral neural plasticity, which is important in the process of adapting to visual or vestibular alteration, including those changes due to pathology, pharmacotherapy, surgery or even entry into microgravity or an underwater environment. To determine the effects of aging on visuo-motor plasticity, we chose the simple and easily measured paradigm of visual-motor rearrangement created by using visual displacement prisms while throwing small balls at a target. Subjects threw balls before, during and after wearing a set of prisms which displace the visual scene by twenty degrees to the right. Data obtained during adaptation were modeled using multilevel modeling techniques for 73 subjects, aged 20 to 80 years. We found no statistically significant difference in measures of visuo-motor plasticity with advancing age. Further studies are underway examining variable practice training as a potential mechanism for enhancing this form of behavioral neural plasticity.

Adult↗
PubMed2001

Experience-dependent plasticity of mouse visual cortex in the absence of the neuronal activity-dependent marker egr1/zif268.

Neuronal activity elicits a rapid increase in the expression of several immediate early genes (IEGs). To clarify a role for IEG response in activity-dependent development, we examined the contribution of the egr1/zif268 gene during visual cortical processing and plasticity in mice. We first analyzed the expression of egr1 mRNA in wild-type (WT) mice using Northern blot hybridization. In the visual cortex, expression of egr1 mRNA increased dramatically after eye opening, systemic injection of kainate, or 30 min of photostimulation after a brief (5 d) period of dark adaptation. Thus, the expression of egr1 is regulated by synaptic activity in the mouse visual cortex, as it is in other species (e.g., monkeys, cats, and rats). To evaluate whether this transcription factor is directly involved in activity-dependent plasticity, mice lacking Egr1 were deprived of the use of one eye during the developmental critical period [postnatal day 24 (P24)-P34]. Extracellular in vivo single-unit recordings from the binocular zone of the visual cortex revealed that visual responses developed normally in egr1 knock-out (KO) mice. Moreover, a similarly significant shift of responsiveness in favor of the open eye was produced in both KO and WT mice by either brief (4 d) or long-term (>2 weeks) occlusion of one eye. There was no apparent compensation among egr2, egr3, or c-fos mRNA and protein expression in the visual cortex of egr1 KO mice. Taken together, these results indicate that egr1 is a useful marker of sensory input in mice but is not intrinsically necessary for the experience-dependent plasticity of the visual cortex. Our findings underscore a mechanistic distinction between sensory plasticity and long-lasting forms of synaptic potentiation in the hippocampus, for which egr1/zif268 was recently found to be essential.

Aging↗
PubMed1997

Targeting of ultrasound contrast material. An in vitro feasibility study.

PURPOSE: It would be beneficial to design a targetable microbubble ultrasound contrast agent that would selectively bind to the areas of interest in the body and enhance the target organ in the ultrasound examination. MATERIAL AND METHODS: We have studied the feasibility of targeting in a model system. We used avidin and biotin as a model ligand-receptor pair. Avidin was adsorbed on the surface of polystyrene, and biotin derivative was attached to microbubble shells. After removal of unincorporated biotin from the microbubbles, they were allowed to come in contact with avidin-coated or albumin-coated plastic. Unbound bubbles were washed by a stream of water. RESULTS: Binding of microbubbles to the surface occurred selectively in the areas where avidin layer was deposited. Binding of microbubbles to avidin layer was dependent on the amount of biotin incorporated in the microbubble shell. Presence of free biotin blocked targeting completely. Acoustic studies were performed using a custom-built ultrasound measurement apparatus and an ultrasound medical imaging system. Microbubble-coated areas of the plastic dish were clearly visualized with ultrasound imaging. A strong backscattered signal was obtained for microbubble surface densities as low as 3%. CONCLUSION: Microbubbles have been selectively targeted via a ligand-receptor system in vitro. Firm binding of microbubbles to avidin-coated surface has been achieved. Microbubbles deposited on the target were visualized with ultrasound imaging systems.

Animals↗
PubMed2005

Distributed neural plasticity for shape learning in the human visual cortex.

Expertise in recognizing objects in cluttered scenes is a critical skill for our interactions in complex environments and is thought to develop with learning. However, the neural implementation of object learning across stages of visual analysis in the human brain remains largely unknown. Using combined psychophysics and functional magnetic resonance imaging (fMRI), we show a link between shape-specific learning in cluttered scenes and distributed neuronal plasticity in the human visual cortex. We report stronger fMRI responses for trained than untrained shapes across early and higher visual areas when observers learned to detect low-salience shapes in noisy backgrounds. However, training with high-salience pop-out targets resulted in lower fMRI responses for trained than untrained shapes in higher occipitotemporal areas. These findings suggest that learning of camouflaged shapes is mediated by increasing neural sensitivity across visual areas to bolster target segmentation and feature integration. In contrast, learning of prominent pop-out shapes is mediated by associations at higher occipitotemporal areas that support sparser coding of the critical features for target recognition. We propose that the human brain learns novel objects in complex scenes by reorganizing shape processing across visual areas, while taking advantage of natural image correlations that determine the distinctiveness of target shapes.

Form Perception↗
PubMed2003

How necessary is the activation of the immediate early gene zif268 in synaptic plasticity and learning?

The immediate early genes (IEGs) are activated rapidly and transiently in response to a multitude of stimuli. The zif268 belongs to a category of regulatory IEGs that activate downstream target genes and is considered to be a triggering mechanism to activate the genomic response in neurons. Several studies have shown that zif268 mRNA is upregulated during different forms of associative learning, and following tetanic stimulation that induces long-lasting LTP. To date, there is a general consensus that zif268 activation may constitute a critical mechanism for the encoding of long-lasting memories, however this is based on relatively few studies. Given the fact that zif268 can be activated by a number of different types of stimuli, it becomes important to determine exactly how it may be implicated in memory. Examination of the current literature suggests that zif268 is necessary in the processing of several types of memory, however, it is not entirely clear what aspects of memory zif268 may be implicated in. Here, we review the existing literature and emphasise that understanding the signalling pathways that lead to activation of the IEGs and the downstream targets of these genes will advance our understanding of how functional activation of zif268 may be implicated in processing long-term memories.

Animals↗
PubMed1993

Laser applications in plastic and reconstructive surgery.

Very shortly after the laser's first successful firing in 1960, applications were found in the medical field in the specialities of ophthalmology and dermatology and have since expanded to include indications in plastic and reconstructive surgery. In the photodestructive mode, laser energy is used selectively to vaporize, incise, excise, ablade and coagulate target tissue; the surgical laser can also degrade or denature protein in the target tissue, and the latter photoreaction now forms the basis for laser tissue welding in a variety of tissue types. The author refers to these photodestructive applications as high reactive-level laser treatment, or HLLT. In laser therapeutic applications, the temperature of the cells may rise only very slightly or not at all, and there is no immediate irreversible change in the target tissue architecture. The level of reaction is thus lower than the cell survival threshold, giving a direct photoactivative effect. The author refers to this as low reactive-level laser therapy, or LLLT: LLLT applications include pain attenuation, wound healing acceleration; enhanced remodeling in accelerated bone and tendon repair; restoration of normal neural function; normalization of abnormal hormonal function; modulation of the autoimmune system; control of hyper- and hypotension and so on. HLLT and LLLT are contrasted and compared, and applications of both HLLT and LLLT in PRS are discussed in brief.

Humans↗
PubMed1998

A model of activity-dependent anatomical inhibitory plasticity applied to the mammalian auditory system.

We construct a model of activity-dependent, anatomical inhibitory plasticity. We apply the model to the mammalian auditory system. Specifically, we model the activity-dependent topographic refinement of inhibitory projections in the auditory brain stem, and we construct an anatomically abstract model of binaural band formation in the primary auditory cortex involving the segregation of different populations of inhibitory and excitatory afferents. Issues raised and predictions made include the nature of interactions between excitatory and inhibitory afferents innervating the same population of target cells, and the possibility that pharmacological manipulations of the developing primary auditory cortex might induce a shift in the periodicity of binaural bands. Any model of inhibitory plasticity must confront the issue of postulating mechanisms underlying such plasticity. In order to attempt to understand, at least theoretically, what the mechanisms underlying inhibitory plasticity might be, we propose the existence of a new class of neurotrophic factors that promote neurite outgrowth from and mediate competitive interactions between inhibitory afferents. We suppose that such factors are up-regulated by hyperpolarisation and down-regulated by depolarisation. Furthermore, we suppose that their activity-dependent release from target cells depends on Cl- influx. Such factors are therefore assumed to be the physiological inverse of such factors as nerve growth factor and brain-derived neurotrophic factor, which are up-regulated by depolarisation and down-regulated by hyperpolarisation, with their activity-dependent release depending on Na+, and not Ca2+, influx.

Animals↗
PubMed1998

Plasticity of synapses in the rat neostriatum after unilateral lesion of the nigrostriatal dopaminergic pathway.

In the 6-hydroxydopamine model of Parkinson's disease in the rat, there is a significant reduction in the number of dendritic spines on the principal projection neurons in the neostriatum, presumably attributable to loss of the nigrostriatal dopamine input. These spines invariably receive input from terminals forming asymmetric synapses that originate mainly from the cortex. The object of the present study was to determine the fate of those terminals after the loss of dendritic spines. Unbiased estimates of synaptic density and absolute numbers of synapses in a defined volume of the neostriatum were made using the "disector" and Cavalieri techniques. Numerical synaptic density of asymmetric synaptic contacts was 17% lower in the neostriatum deprived of dopamine innervation and, in absolute terms, there were 3 billion (19%) fewer contacts. The numerical density of a subpopulation of asymmetric contacts on dendritic spines that have complex or perforated synaptic specializations and normally make up 9% of the asymmetric population was 44% higher on the experimental side. Asymmetric synapses were found to be enriched in glutamate using postembedding immunogold labeling. The present observations demonstrate that the loss of spines previously reported after 6-hydroxydopamine lesions is accompanied by a loss of asymmetric synapses rather than by the movement of synapses from spines to other postsynaptic targets. The study also demonstrates that there is an increase in complex synaptic interactions that have been implicated in synaptic plasticity in other regions of the CNS after experimental manipulations.

Animals↗
PubMedDate not supplied

Role of afferents in the development and cell survival of the vertebrate nervous system.

1. During normal development of the vertebrate central nervous system, a considerable number of neurons die. The factors controlling which neurons die and which survive are not fully understood. 2. Target populations are known to maintain their innervating neurons. However, the role of afferents in maintaining their targets is still under review. 3. In the developing nervous system, deafferentation of a neuron population is difficult to achieve because plasticity (structural re-organization) can cause re-innervation of the area. Re-innervation alters, rather than removes, the afferent supply. 4. Afferent input is important for neuronal survival during development because deafferentation increases neuronal death by 20-30% and increasing input diminishes neuronal death. 5. Deafferented neurons die at the normal time for cell death for any given population. This occurs after the arrival of afferent axons but before the completion of connectivity and the onset of function. 6. Neuronal survival is maintained by any input, such as reinnervation by inappropriate fibres, but for optimal survival, morphological maturation and the acquisition of normal physiology, the correct input is required. 7. Afferents maintain their target neurons via a combination of electrical activity and delivery of trophic agents, which adjust intracellular calcium, thereby facilitating protein synthesis, mitochondrial function and suppressing apoptosis. 8. Evidence from animal and in vitro experiments indicates that afferents play an extremely important role in the survival of developing neurons in the immature vertebrate nervous system.

Animals↗
PubMed1999

Volatile anesthetics block actin-based motility in dendritic spines.

Dendritic spines form the postsynaptic contact sites for most excitatory synapses in the brain. Spines occur in a wide range of different shapes that can vary depending on an animal's experience or behavioral status. Recently we showed that spines on living neurons can change shape within seconds in a process that depends on actin polymerization. We have now found that this morphological plasticity is blocked by inhalational anesthetics at concentrations at which they are clinically effective. These volatile compounds also block actin-based motility in fibroblasts, indicating that their action is independent of neuron-specific components and thus identifying the actin cytoskeleton as a general cellular target of anesthetic action. These observations imply that inhibition of actin dynamics at brain synapses occurs during general anesthesia and that inhalational anesthetics are capable of influencing the morphological plasticity of excitatory synapses in the brain.

Actins↗
PubMed1983

Local regulation of compensatory noradrenergic hyperactivity in the partially denervated hippocampus.

Functional recovery after denervating lesions in the central nervous system (CNS) is particularly prominent if part of the lesioned projection is spared. Several plasticity mechanisms, such as collateral sprouting, hyperactivity of remaining axons and development of receptor supersensitivity, probably contribute to efficient recovery after subtotal lesions. Although denervation-induced collateral sprouting and presynaptic compensatory hyperactivity in spared axons have been described in various systems, any possible interaction or cooperation between the two mechanisms in restoring synaptic transmission in a partially denervated target has so far not been demonstrated. We have shown previously that partial adrenergic denervation of the hippocampus in adult rats is followed by a slow and protracted reinnervation by collateral sprouting from the spared adrenergic afferents. We now report that the partial adrenergic deafferentation is accompanied by a transient increase in turnover of the transmitter in remaining axons which subsides when the denervated region becomes reinnervated, and that the development of this compensatory hyperactivity is confined to the area of maximal denervation. The topographical specificity of the compensatory noradrenergic hyperactivity response, and the interaction between this hyperactivity and the collateral reinnervation process, strongly suggest that the changes in transmitter turnover in spared afferents after denervating lesions can be regulated by local mechanisms operating within the denervated target area.

Animals↗
PubMed2002

Synaptic tagging during synapse-specific long-term facilitation of Aplysia sensory-motor neurons.

Like memory, long-lasting forms of synaptic plasticity have been shown to require mRNA and protein synthesis. Since each neuron has a single nucleus, but can form thousands of synaptic connections, the requirement for transcription raises the question of whether long-lasting forms of plasticity can occur in a synapse-specific manner and, if so, how the products of gene expression can be targeted to alter synaptic strength at some but not all synapses made by a given neuron. One hypothesis that has been put forth to address this question is the synaptic tagging hypothesis, which proposes that the products of gene expression are delivered throughout the cell, but function to increase synaptic strength only at synapses that have been "tagged" by previous synaptic activity. In this review, I describe our studies of synapse-specific, transcription-dependent facilitation of cultured Aplysia sensory-motor synapse in the context of the synaptic tagging hypothesis.

Animals↗
PubMed2003

Frequency modulation of synchronized Ca2+ spikes in cultured hippocampal networks through G-protein-coupled receptors.

Synchronized spontaneous Ca2+ spikes in networked neurons represent periodic burst firing of action potentials, which are believed to play a major role in the development and plasticity of neuronal circuitry. How these network activities are shaped and modulated by extrinsic factors during development, however, remains to be studied. Here we report that synchronized Ca2+ spikes among cultured hippocampal neurons can be modulated by two small factors that act on G-protein-coupled receptors (GPCRs): the neuropeptide PACAP (pituitary adenylate cyclase-activating polypeptide) and the chemokine SDF-1 (stromal cell-derived factor-1). PACAP effectively increases the frequency of the synchronized Ca2+ spikes when applied acutely; the PACAP potentiation of Ca2+ spikes requires the activation of the PACAP-specific PAC1 GPCRs and is mediated by the activation of cAMP signaling pathway. SDF-1, on the other hand, significantly reduces the frequency of these Ca2+ spikes through the activation of its specific GPCR CXCR4; the inhibitory action of SDF-1 is mediated by the inhibition of cAMP pathway through the Gi component of GPCRs. Taken together, these results demonstrate that synchronized neuronal network activity can be effectively modulated by physiologically and developmentally relevant small factors that act on GPCRs to target the cAMP pathway. Such modulation of neuronal activity through GPCRs may represent a significant mechanism that underlies the neuronal plasticity during neural development and functioning.

Action Potentials↗
PubMed2004

Exercise in a pill: feasibility of energy expenditure targets.

The possibility of developing a pill to increase energy expenditure is explored by examining the metabolic processes involved. Such a pill should be targeted at organ systems involved in facultative thermogenesis. In rodents, these are brown adipose tissue (BAT) and skeletal muscle. Since BAT-mediated thermogenesis is not available in adult humans, emphasis here is on skeletal muscle. A hypothesis is presented based on three known facts: (1) plasticity of skeletal muscle, with interconversion of fiber types that differ in their fuel efficiency; (2) presence of thyroxine 5'-deiodinase type 2 (TD2) in human skeletal muscle; (3) gradual increase in thermogenesis that occurs during rehabilitation after starvation, probably in muscle. A low capacity thermogenic system, muscle efficiency thermogenesis (MET), is proposed to occur as adipose stores refill during the transition from famine to feasting to obesity. This system involves increased activity of TD2 and a T3-induced increase in proportion of type II fibers, less efficient at rest and during activity. The protective effect of this system is probably overwhelmed by long-term eating in excess of energy needs. Better understanding of the complex remodeling of differentiated muscle fibers in the conversions proposed and of the regulation of TD2 activity in human skeletal muscle may reveal targets for increasing energy expenditure in humans. In addition, the possibility of exploiting the plasticity of the adipose organ, with conversion of white adipocytes in white adipose tissue to atypical brown adipocytes and increasing thermogenesis in them is considered as another potential target for increasing energy expenditure in humans.

Adaptation, Physiological↗
PubMed2004

Genetic modules and networks for behavior: lessons from Drosophila.

Behaviors are quantitative traits determined through actions of multiple genes and subject to genome-environment interactions. Early studies concentrated on analyzing the effects of single genes on behaviors, often generating views of simplified linear genetic pathways. The genome era has generated a profound paradigm shift enabling us to identify all the genes that contribute to expression of a behavioral phenotype, to investigate how they are organized as functional ensembles and to begin to identify polymorphisms that contribute to phenotypic variation and are targets for natural selection. Recent studies show that the genetic architecture of behavior is determined by dynamic and plastic modular networks of pleiotropic genes and that the behavioral phenotype manifests itself as an emergent property of such networks. Such networks are exquisitely sensitive to genetic background and sex effects. This review describes how Drosophila can serve as a model for uncovering fundamental principles of the genetic architecture of behavior.

Animals↗
PubMed2005

Dose and age-dependent axonal responses of embryonic trigeminal neurons to localized NGF via p75NTR receptor.

Nerve growth factor (NGF) and related neurotrophins are target-derived survival factors for sensory neurons. In addition, these peptides modulate neuronal differentiation, axon guidance, and synaptic plasticity. We tested axonal behavior of embryonic trigeminal neurons towards localized sources of NGF in collagen gel assays. Trigeminal axons preferentially grow towards lower doses of localized NGF and grow away from higher concentrations at earlier stages of development, but do not show this response later. Dorsal root ganglion axons also show similar responses to NGF, but NGF-dependent superior cervical ganglion axons do not. Such axonal responses to localized NGF sources were also observed in Bax-/- mice, suggesting that the axonal effects are largely independent of cell survival. Immunocytochemical studies indicated that axons, which grow towards or away from localized NGF are TrkA-positive, and TrkA-/- TG axons do not respond to any dose of NGF. We further show that axonal responses to NGF are absent in TG derived from mice that lack the p75 neurotrophin receptor (p75NTR). Collectively, our results suggest that localized sources of NGF can direct axon outgrowth from trigeminal ganglion in a dose- and age-dependent fashion, mediated by p75NTR signaling through TrkA expressing axons.

Age Factors↗
PubMed2006

Assessment of image guided accuracy in a skull model: comparison of frameless stereotaxy techniques vs. frame-based localization.

INTRODUCTION: The use of image-guided systems (IGS) for brain biopsy has increased in neurosurgical practice. We sought to evaluate the accuracy of a plastic, disposable burr hole mounted guide for stereotactic biopsy using an IGS and compare the results of different targeting methods with those of frame based localization. METHODS: MRIs were performed on a skull model with mounted fiducials with a stereotactic frame in place and data was loaded onto the Stealth IGS. The model was placed in a Mayfield head holder and fixed to the OR table. Registration of imaging to physical space was carried out. Using three different targeting methods on the Stealth IGS, the distance between the target and the predicted position of the target, the offset error, was measured in three dimensions and confirmed by 2 observers. A sum of squares for the 3 offset errors in all planes was used to calculate the summed vector error. The same MRI dataset used with the Cosman-Roberts-Wells (CRW) stereotactic frame for comparison. The summed vector error was calculated in the same manner to compare the accuracy of targeting with these guides to the frame-based CRW system. RESULTS: For frameless stereotaxy using the "Straight- guide 4 2D" targeting method the mean error was 2.58 +/- 0.51 mm (n=12). The vector error was 5.23 +/- 0.54 (n=4). For the registration set and target using the "Offset- guide 4 2D" targeting method the mean error was 1.66 +/- 0.36 mm (n=12). The vector error was 3.32 +/- 0.72 (n=4). The best localization was obtained with the "probe's eye" planning and targeting. The mean error was 0.33 +/- 0.16 mm (n=12). The vector error was 1.0 +/- 0.28 (n=4). We found a statistical difference between the different techniques (P<0.001) (Kruskal-Wallis One Way Analysis of Variance on Ranks). An all pairwise multiple comparison procedure (Holm-Sidak method) found an overall significance level = 0.05. For the frame-based CRW the mean error from the target was 1.03 +/- 0.19 mm (n=18) and the mean target localization error vector was 2.23 +/- 0.14 (n=6). We found a statistically significant difference between NDT guide "Probes Eye" vs. the MR-CRW (P=0.003, Mann-Whitney Rank Sum Test). CONCLUSIONS: These results indicate that using MR imaging, surgical planning software and the skull mounted Navigus-DT with the probe's eye view option for targeting, localization accuracy appears to fall within acceptable ranges compared with frame-based methods which have been the standards for stereotactic brain biopsy and functional neurosurgery. Furthermore, there may be considerable differences in accuracy between different targeting methods.

Biopsy↗
PubMed2004

Opioid abuse and brain gene expression.

Opiate addiction is a central nervous system disorder of unknown mechanism. Neuronal basis of positive reinforcement, which is essential to the action of opioids, relies on activation of dopaminergic neurons resulting in an increased dopamine release in the mesolimbic brain structures. Certain aspects of opioid dependence and withdrawal syndrome are also related to the activity of noradrenergic and serotonergic systems, as well as to both excitatory and inhibitory amino acid and peptidergic systems. The latter pathways have been recently proven to be involved both in the development of dependence and in counteracting the states related to relapse. An important role in neurochemical mechanisms of opioid reward, dependence and vulnerability to addiction has been ascribed to endogenous opioid peptides, particularly those acting via the mu- and kappa-opioid receptors. Opiate abuse leads to adaptive reactions in the nervous system which occur at the cellular and molecular levels. Recent research indicates that intracellular mechanisms of signal transmission-from the receptor, through G proteins, cyclic AMP, MAP kinases to transcription factors--also play an important role in opioid tolerance and dependence. The latter link in this chain of reactions may modify synthesis of target genes and in this manner, it may be responsible for opiate-induced long-lasting neural plasticity.

Animals↗