Spike-timing dependent plasticity is a learning mechanism used extensively within neural modelling. The learning rule has been shown to allow a neuron to find the onset of a spatio-temporal pattern repeated among its afferents. In this thesis, the first question addressed is what does this neuron learn? With a spiking neuron model and linear prediction, evidence is adduced that the neuron learns two components: (1) the level of average background activity and (2) specific spike times of a pattern. Taking advantage of these findings, a network is developed that can train recognisers for longer spatio-temporal input signals using spike-timing dependent plasticity. Using a number of neurons that are mutually connected by plastic synapses and subject to a global winner-takes-all mechanism, chains of neurons can form where each neuron is selective to a different segment of a repeating input pattern, and the neurons are feedforwardly connected in such a way that both the correct stimulus and the ...
Supervisors: Ole Paulsen, Tanja Fuchsberger. Spike timing-dependent plasticity (STDP) is a physiologically relevant form of Hebbian learning, in which near coincident pre- and postsynaptic firing induces synaptic plasticity: Long term potentiation (LTP) is induced when the presynaptic spike precedes postsynaptic firing, and long term depression (LTD) when postsynaptic firing precedes the presynaptic spike [1]. However, these plasticity rules are profoundly influenced by neuromodulators [2]. Reward, novelty or surprise are correlated with neuromodulatory signals, such as dopamine, acetylcholine or noradrenaline, which modulate memories and behavioural outcome. They regulate STDP through various mechanisms, as they can control the biophysical properties of dendrites, including the dynamics of spike backpropagation, and can influence the state of kinases and phosphatases implicated in synaptic plasticity (Seol et al., 2007). In our laboratory we recently demonstrated a retroactive effect of ...
Cortical neurons receive balanced excitatory and inhibitory synaptic currents. Such a balance could be established and maintained in an experience-dependent manner by synaptic plasticity at inhibitory synapses. We show that this mechanism provides an explanation for the sparse firing patterns observed in response to natural stimuli and fits well with a recently observed interaction of excitatory and inhibitory receptive field plasticity. ... Our results suggest an essential role of inhibitory plasticity in the formation and maintenance of functional cortical circuitry ...
Long-term potentiation (LTP) and long-term depression (LTD) are generally assumed to be cellular correlates for learning and memory. Different types of LTP induction protocols differing in severity of stimulation can be distinguished in CA1 of the hippocampus. To better understand signaling mechanisms and involvement of neuromodulators such as dopamine in synaptic plasticity, less severe and more physiological low frequency induction protocols should be used. In the study which is reviewed here, critical determinants of spike timing-dependent plasticity (STDP) at hippocampal CA3-CA1 synapses were investigated. We found that dopamine via D1 receptor signaling, but not adrenergic signaling activated by the -adrenergic agonist isoproterenol, is important for successful expression of STDP at CA3-CA1 synapses. The dopamine effect on STDP is paralleled by changes in spike firing properties, thereby changing intrinsic excitability of postsynaptic CA1 neurons, and gating STDP,. Whereas β-adrenergic
To determine if classical conditioning produces general or specific modification of responses to acoustic conditioned stimuli (CS), frequency receptive fields (RF) of neurons in guinea pig auditory cortex were determined before and up to 24 h after fear conditioning. Highly specific RF plasticity ch …
The mammalian sensory neocortex exhibits experience-dependent plasticity such that neurons modify their response properties according to changes in sensory experience. The synaptic plasticity mechanism of long-term potentiation requiring calcium-calmodulin-dependent kinase type II (CaMKII) could underlie experience-dependent plasticity. Plasticity in adult mice can be induced by changes in the patterns of tactile input to the barrel cortex. This response is strongly depressed in adult mice that lack the gene encoding α-CaMKII, although adolescent animals are unaffected. Thus, α-CaMKII is necessary either for the induction or for the expression of plasticity in adult mice.. ...
Structure-based virtual screening for selecting potential drug candidates is usually challenged by how numerous false positives in a molecule library are excluded when receptor plasticity is considered. In this study, based on the binding energy landscape theory, a hypothesis that a true inhibitor can bind to different conformations of the binding site favorably was put forth, and related strategies to defeat this challenge were devised; reducing false positives when receptor plasticity is considered. The receptor in the study is the influenza A nucleoprotein, whose oligomerization is a requirement for RNA binding. The structural flexibility of influenza A nucleoprotein was explored by molecular dynamics simulations. The resultant distinctive structures and the crystal structure were used as receptor models in docking exercises in which two binding sites, the tail-loop binding pocket and the RNA binding site, were targeted with the Otava PrimScreen1 diversity-molecule library using the GOLD software.
Synaptic plasticity directs development of the nervous system and is thought to underlie memory storage in adult animals. A great deal of our current understanding of the role of AMPA receptors in synaptic plasticity comes from studies on developing cortex and cell cultures. In the present study, we instead focus on plasticity in mature neurons in the neocortex of adult animals. We find that the glutamate receptor 1 (GluR1) subunit of the AMPA receptor is involved in experience-dependent plasticity in adult cortex in vivo and that it acts in addition to neuronal nitric oxide synthase (αNOS1), an enzyme that produces the rapid synaptic signaling molecule nitric oxide (NO). Potentiation of the spared whisker response, following single whisker experience, is ∼33% less in GluR1-null mutants than in wild types. We found that the remaining plasticity depended on αNOS1. Potentiation was reduced by ,42% in the single αNOS1-null mutants and completely abolished in GluR1/αNOS1 double-knock-out mice. ...
Background. Synaptic plasticity is thought to be the cellular correlate for the formation of memory traces in the brain. Recently, spike-timing dependent plasticity has gained increased interest as a plausible physiological mechanism for the activity-dependent modification of synaptic strength. It might be fundamental for circuit refinement, map plasticity and the explanation of higher brain functions. It is not clear if spike-timing dependent plasticity is a universal learning rule based on simple biophysical mechanisms. The molecular signalling pathways involved are quite diverse and apparently use-dependent. The fundamental question is what determines the molecular machinery at a synaptic contact that translates electrical activity into a change in synaptic strength.Specific Aims. (1) The influence of active dendritic properties, which can result in the generation of local dendritic spikes, on changes in synaptic strength will be studied. They will have an important impact on the local ...
The plasticity of inhibitory transmission is expected to play a key role in the modulation of neuronal excitability and network function. Over the last two decades, the investigation of the determinants of inhibitory synaptic plasticity has allowed distinguishing presynaptic and postsynaptic mechanisms. While there has been a remarkable progress in the characterization of presynaptically-expressed plasticity of inhibition, the postsynaptic mechanisms of inhibitory long-term synaptic plasticity only begin to be unraveled. At postsynaptic level, the expression of inhibitory synaptic plasticity involves the rearrangement of the postsynaptic molecular components of the GABAergic synapse, including GABAA receptors, scaffold proteins and structural molecules. This implies a dynamic modulation of receptor intracellular trafficking and receptor surface lateral diffusion, along with regulation of the availability and distribution of scaffold proteins. This Review will focus on the mechanisms of the multifaceted
Neuroplasticity studies examining children with hemiparesis (CH) have focused predominantly on unilateral interventions. CH also have bimanual coordination impairments with bimanual interventions showing benefits. We explored neuroplasticity following hand-Arm bimanual intensive therapy (HABIT) of 60 hours in twelve CH (6 females, mean age 11 ± 3.6 y). Serial behavioral evaluations and MR imaging including diffusion tensor (DTI) and functional (fMRI) imaging were performed before, immediately after, and at 6-week follow-up. Manual skills were assessed repeatedly with the Assisting Hand Assessment, Childrens Hand Experience Questionnaire, and Jebsen-Taylor Test of Hand Function. Beta values, indicating the level of activation, and lateralization index (LI), indicating the pattern of brain activation, were computed from fMRI. White matter integrity of major fibers was assessed using DTI. 11/12 children showed improvement after intervention in at least one measure, with 8/12 improving on two or ...
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TY - JOUR. T1 - Beta-amyloid (25-35) induced impairments of hippocampal synaptic plasticity are dependent on stimulation-protocol, genetic background, and aggregation state. AU - Gengler, Simon. AU - Gault, Victor. AU - Harriott, Peter. AU - Holscher, Christian. PY - 2007. Y1 - 2007. M3 - Article. VL - 179. SP - 621. EP - 632. JO - Experimental Brain Research. JF - Experimental Brain Research. SN - 0014-4819. ER - ...
Bacterial morphological plasticity refers to changes in the shape and size that bacterial cells undergo when they encounter stressful environments. Although bacteria have evolved complex molecular strategies to maintain their shape, many are able to alter their shape as a survival strategy in response to protist predators, antibiotics, the immune response, and other threats. Normally, bacteria have different shapes and sizes which include coccus, rod and helical/spiral (among others less common) and that allow for their classification. For instance, rod shapes may allow bacteria to attach more readily in environments with shear stress (e.g., in flowing water). Cocci may have access to small pores, creating more attachment sites per cell and hiding themselves from external shear forces. Spiral bacteria combine some of the characteristics cocci (small footprints) and of filaments (more surface area on which shear forces can act) and the ability to form an unbroken set of cells to build biofilms. ...
The ability to generate action potentials (spikes) in response to synaptic input determines whether a neuron participates in information processing. How a developing neuron becomes an active participant in a circuit or whether this process is activity dependent is not known, especially as spike-dependent plasticity mechanisms would not be available to non-spiking neurons. Here we use the optic tectum of awake Xenopus laevis tadpoles to determine how a neuron becomes able to generate sensory-driven spikes in vivo. At the onset of vision, many tectal neurons do not exhibit visual spiking behavior, despite being intrinsically excitable and receiving visuotopically organized synaptic inputs. However, a brief period of visual stimulation can drive these neurons to start generating stimulus-driven spikes. This conversion relies upon a selective increase in glutamatergic input and requires depolarizing GABAergic transmission and NMDA receptor activation. This permissive form of experience-dependent plasticity
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Our overarching interest is in the question of how experience and deprivation modify synaptic connections in the brain. Experience-dependent synaptic plasticity is the physical substrate of memory, sculpts connections during postnatal development to determine the capabilities and limitations of brain functions, is responsible for the reorganization of the brain after damage, and is vulnerable in numerous psychiatric and neurological diseases and contributes to their symptoms.. Historically, our major efforts to address this question have been focused on the visual cortex and hippocampus. The visual cortex is a site of robust experience-dependent synaptic plasticity, exemplified by the consequences of temporary monocular deprivation (MD) during childhood. MD sets in motion a stereotyped choreography of synaptic modification whereby the deprived-eye inputs to visual cortex rapidly lose strength and, with a delay, the open-eye inputs undergo a compensatory gain in strength. The behavioral ...
TY - JOUR. T1 - Neurotrophins and synaptic plasticity. AU - Usrey, A Kimberley. AU - Katz, Lawrence C.. AU - Lo, Donald C.. PY - 1999. Y1 - 1999. N2 - Despite considerable evidence that neuronal activity influences the organization and function of circuits in the developing and adult brain, the molecular signals that translate activity into structural and functional changes in connections remain largely obscure. This review discusses the evidence implicating neurotrophins as molecular mediators of synaptic and morphological plasticity. Neurotrophins are attractive candidates for these roles because they and their receptors are expressed in areas of the brain that undergo plasticity, activity can regulate their levels and -secretion, and they regulate both synaptic transmission and neuronal growth. Although numerous experiments show demonstrable effects of neurotrophins on synaptic plasticity, the rules and mechanisms by which they exert their effects remain intriguingly elusive.. AB - Despite ...
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AD patients show after iTBS an impairment of LTP-like cortical plasticity forming a paradoxical LTD in comparison to HS. LTD-like cortical plasticity is similar between AD and HS. LTP-like cortical plasticity is not associated with age, but AD patients presenting with more altered LTP-like cortical plasticity have more-severe cognitive decline at 18 months. SAI is impaired in AD and shows a strong association with the individual age of subjects rather than with disease age of onset.. ...
A major hallmark of brain diseases is neuroinflammation. We are interested in how immune mediators affect synaptic plasticity. Particularly, our work focuses on better understanding how these factors influence intracellular calcium stores, i.e. the spine apparatus organelle, and how these changes alter the ability of neurons to express associative and homeostatic synaptic plasticity. We study the role of coagulation factors in this context and test whether these changes can be modified by rTMS.. Ben Shimon M*, Lenz M*, Ikenberg B, Becker D, Shavit Stein E, Chapmann J, Tanne D, Pick CG, Blatt I, Neufeld M, Vlachos A*, Maggio N*° (2015) Thrombin regulation of synaptic transmission and plasticity: implications for health and disease. Front Cel Neurosci. 9: 151.. Becker D, Deller T, Vlachos A° (2015) Tumor necrosis factor (TNF)-receptor 1 and 2 mediate homeostatic synaptic plasticity of denervated mouse dentate granule cells. Sci Rep. 5: 12726.. Strehl A, Lenz M, Itsekson-Hayosh Z, Becker D, ...
The role of dopamine in plasticity at glutamatergic synapses in the striatum is central to our understanding of basal ganglia functions and dopamine-dependent reward mechanisms. Long-term potentiation (LTP) and long-term depression (LTD) at these synapses are thought to be dependent on D1 and D2 dopamine receptors, respectively. However, the mechanisms of LTP and LTD in the striatum are controversial. Using brain slices from transgenic mice, Shen et al. show that LTP and LTD can occur in both D1- and D2-expressing neurons but with different molecular mechanisms. Dopaminergic modulation of plasticity is receptor and cell-type specific. The findings suggest that the control of bidirectional plasticity is not exerted through a monolithic mechanism, as previously asserted, but by cell-type-specific mechanisms depending on the subtype of dopamine receptor expressed.. W. Shen, M. Flajolet, P. Greengard, D. J. Surmeier, Dichotomous dopaminergic control of striatal synaptic plasticity. Science 321, ...
The Haas Lab has developed specific visual stimulation protocols consisted of different periods of light ON and OFF stimuli to induce plasticity or metaplasticity in the optic tectum of awake Xenopus laevis tadpoles (Dunfield and Haas, 2009, 2010; Chen et al. 2012). Using these experience-driven neuronal plasticity induction stimuli and two-photon time-lapse imaging of mitochondrial movement and dendritic arbor growth, and calcium imaging of neuronal activity of individual neurons in the intact and awake developing brain, we are looking at mitochondria localization and size in LTD and LTP neurons. Other imaging and molecular techniques are also being used to underline the specific mitochondria proteins that regulate synaptic plasticity. ...
Synaptic Plasticity. Synaptic Plasticity. I. Synaptic Plasticity (Excitatory spine synapses) Changes in synaptic strength are important for formation of memory. Short Term Plasticity (paired-pulse facilitation, short-term potentiation, synaptic depression) Slideshow 6690266 by lev-levine
Challenges in the pain field include translation from animal models to identification of novel targets for drug development for humans and developing strategies that lead to improvements in patient care. Toward this goal, the symposium featured presentations that reviewed advances in the basic science and clinical arenas. Timothy Brennan, Ph.D., M.D. (Associate Professor of Anesthesia and Pharmacology, University of Iowa, Iowa City, Iowa), discussed the Peripheral and Central Plasticity in an Animal Model of Incisional Pain and Gary Strichartz, Ph.D. (Professor of Anesthesia, Pharmacology and Biophysics, Harvard Medical School, Brigham and Womens Hospital, Boston, Massachusetts), reviewed Pharmacological Studies on Preventing or Modulating the Plastic Changes in Experimental Models of Incisional Pain. Additional presentations on Clinical Evidence for Neural Plasticity in the Postoperative Period: Its Relevance and Modulation and Persistent Pain following Surgery: Neurobiological ...
The efficacy of synaptic transmission changes depending on the neuronal activity in the central nervous system. Such synaptic plasticity underlies experience-dependent refinement of information proces
The results described above emphasize the importance of ion channels at the AIS, and how their location, biophysical properties, and distribution can be modified by activity. However, how activity directly regulates these AIS properties, and whether the phenomenon of AIS plasticity occurs during normal brain function or only in response to large perturbations in neuronal activity or pathological conditions remains unclear. One strategy to begin to elucidate the mechanisms regulating AIS plasticity is to determine how the AIS is assembled during development and then maintained over an organisms lifetime.. How do ion channels become enriched at the AIS? As described above, the AIS is highly enriched in a variety of ion channels and each interacts with scaffolding proteins that link to the flexible actin/βIV spectrin-based submembranous cytoskeleton (Fig. 1D). Two scaffolding proteins have been identified at the AIS: ankG and PSD-93. PSD-93 binds to the KV1 channels found at the AIS, and ...
Learning is primarily mediated by activity-dependent modifications of synaptic strength within neuronal circuits. We discovered that place fields in hippocampal area CA1 are produced by a synaptic potentiation notably different from Hebbian plasticity. Place fields could be produced in vivo in a single trial by potentiation of input that arrived seconds before and after complex spiking. The potentiated synaptic input was not initially coincident with action potentials or depolarization. This rule, named behavioral time scale synaptic plasticity, abruptly modifies inputs that were neither causal nor close in time to postsynaptic activation. In slices, five pairings of subthreshold presynaptic activity and calcium (Ca(2+)) plateau potentials produced a large potentiation with an asymmetric seconds-long time course. This plasticity efficiently stores entire behavioral sequences within synaptic weights to produce predictive place cell activity.. ...
Spike timing-dependent plasticity (STDP) is a strong candidate for an N-methyl-D-aspartate (NMDA) receptor-dependent form of synaptic plasticity that could underlie the development of receptive field properties in sensory neocortices. Whilst inductio
This lecture 1/15 is part of the Computational Modeling of Neuronal Plasticity Course that aims to teach users how to build a mathematical model of a neuron, its inputs, and its neuronal plasticity mechanisms, by writing your own Python program. This lecture provides users with a brief video introduction to the concepts that serves as a companion to the lecture notes and solution figures.. Authors: Florence I. Kleberg and Prof. Jochen Triesch. ...
Arm-amputation involves two powerful drivers for brain plasticity-sensory deprivation and altered use. However, research has largely focused on sensory deprivation and maladaptive change. Here we show that adaptive patterns of limb usage after amputation drive cortical plasticity. We report that individuals with congenital or acquired limb-absence vary in whether they preferentially use their intact hand or residual arm in daily activities. Using fMRI, we show that the deprived sensorimotor cortex is employed by whichever limb individuals are over-using. Individuals from either group that rely more on their intact hands (and report less frequent residual arm usage) showed increased intact hand representation in the deprived cortex, and increased white matter fractional anisotropy underlying the deprived cortex, irrespective of the age at which deprivation occurred. Our results demonstrate how experience-driven plasticity in the human brain can transcend boundaries that have been thought to limit
Citation: Freire, R., Cheng, H. 2004. Experience-dependent changes in the hippocampus of domestic chicks: a model for spatial memory. European Journal of Neuroscience. 20(4):1065-1068. Interpretive Summary: In the modern broiler industry, chickens housed in large groups do not space themselves evenly but instead crowd in particular areas, which may affect chicken health and increase mortality. One contributing factor may be a deficit in spatial skills arising from the absence of essential environmental factors during routine rearing. The present study was to examine whether chick spatial skills can be improved by experimental training at an early age. Compared to control chicks, experience-induced changes in brain morphology reported here suggest that early experience leads to changes in the hippocampus that appear to be related to the development of spatial memory. Enhanced spatial memory in chickens may result in improving their well-being by increasing their distribution and their skills to ...
Transcription of synaptic plasticity-related genes in patients with somnipathy combined with type 2 diabetes, Yi Zhang, Rui Ma, Shaohong Zou, Gaiyu Tong, Gulibakeranmu Abula, Manna
The long-term goal of our research is to understand the neural circuit basis of learning and memory. In this project, we aim to understand how neural circuits p...
Neural Plasticity: (also known as brain plasticity and neural plasticity) can be defined as the ability of the central nervous system (CNS) to adapt in res
In D2 MSNs (fig. S1), repeated pairing of a synaptic stimulation with a postsynaptic spike 5 ms later resulted in LTP of the synaptic response (Fig. 1D). In contrast, preceding synaptic stimulation (-10 ms) with a short burst of postsynaptic spikes induced LTD (Fig. 1E). There were no lasting alterations in synaptic strength with unpaired presynaptic or postsynaptic activity (fig. S1).. Previous studies of striatal LTD induced by conventional plasticity protocols have underscored the importance of D2 receptors (7, 8, 16). In D2 MSNs, timing-dependent LTD was disrupted by antagonizing D2 receptors with sulpiride (control n = 5; sulpiride n = 5; P , 0.05, Mann-Whitney rank sum test), suggesting a similar involvement of D2 receptors (Fig. 1F). Moreover, LTD was disrupted by antagonizing CB1 endocannabinoid (fig. S2) or mGluR5 glutamate receptors (fig. S3). The combination of presynaptic activity and activation of terminal CB1 receptors leads to a lasting reduction in glutamate release probability ...
Vol 9: A Nonlinear Cable Framework for Bidirectional Synaptic Plasticity.. This article is from PLoS ONE, volume 9.AbstractFinding the rules underlying how axons of cortical neurons form neural c. Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
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A cell-specific regulation of redox state thus balances plasticity and stability of cortical networks. Mistimed developmental trajectories of brain plasticity may underlie, in part, the pathophysiology of mental illness. Such prolonged developmental plasticity may, in turn, offer a therapeutic oppor …
The molecular mechanisms controlling the delivery and subsequent stabilization of AMPARs during synaptic plasticity are still poorly understood. Recent findings have suggested PSD-95 as candidate molecule in these processes (El-Husseini et al., 2000; Schnell et al., 2002; Beique, 2003). However, particularly in the light of findings from PSD-95 mutant mice that exhibit enhanced LTP (Migaud et al., 1998), it remained controversial whether and how PSD-95 participates in synaptic plasticity. Here, we show that PSD-95 controls AMPAR delivery during synaptic strengthening by LTP in vitro and during experience-driven synaptic plasticity in vivo. We use three criteria to establish this: First, expression of wt PSD-95 mimics, and second wt PSD-95 occludes AMPAR delivery during synaptic strengthening; third, dominant negative forms of PSD-95 block the incorporation of AMPAR during plasticity.. Several findings indicate that expression of PSD-95 mimics key aspects of LTP and experience-driven synaptic ...
Network structure determines the flow of electrical activity in every neural network and determines its functional and computational properties. Electrical activation of the neuron goes along with an intracellular increase in calcium which induces morphological alterations of the neuron on a slower time scale. Morphological changes, such as changes in dendritic spine and axonal bouton numbers as well as elongation, retraction and branching of axons and dendrites have direct impact on network connectivity (structural plasticity) even in the adult brain: As a consequence of morphological changes, synapses may break, new synapses can form and axonal branches can be re-routed. Rewired network connectivity, in turn, gives rise to an altered activity dynamic and may hold as a source for long term memory formation. Experimental data further support the notion that structural plasticity is not necessarily Hebbian-like but may serve as a neuronal mechanism to maintain electrical activity at a certain ...
Background and Purpose-This study was designed to compare the effects of high-intensity interval training (HIT) and moderate-intensity continuous training (MOD) on functional recovery and cerebral plasticity during the first 2 weeks following cerebral ischemia. Methods-Rats were randomized as follows: Control (n=15), SHAM (n=9), MCAO (n=13), MCAO-D1 (n=7), MOD (n=13) and HIT (n=13). Incremental tests were performed at day 1 (D1) and 14 (D14) to identify the running speed associated with the lactate threshold (SLT) and the maximal speed (Smax). Functional tests were performed at D1, D7 and D14. Microglia form, cytokines, p75NTR, KCC2 and NKCC1 expression were made at D15. Results-HIT was more effective to improve the endurance performance than MOD and induced a fast recovery of the impaired forelimb grip force. The Iba-1 positive cells with amoeboid form and the pro- and anti-inflammatory cytokine expression were lower in HIT group, mainly in the ipsilesional hemisphere. A p75NTR overexpression ...
They say people don’t change, but author Sean Young’s upcoming book, “Stick With It,” examines the science behind doing just that—and making it stick. Over the past fifteen years, Young has worked with the brightest minds in science to identify the psychological processes that affect behavioral change, and according to his book, his methods have achieved a “300 percent increase in lasting change for both individuals and groups.” In other words, by making use of Young’s techniques, you are three times as likely to be able to make a change in your life and permanently stick with it. Why is this important? Just take a look at the way many people handle their health. Do they stick with their diets? Do they routinely take their needed medications? Do they exercise every week? How about finances? Or their relationship habits? Allowing these important areas of our lives to go unexamined and uncontrolled is the source of a vast amount of pain and loss, but by
Signalling pathways leading to post-synaptic plasticity have been examined in many types of experimental studies, but a unified picture on how multiple biochemical pathways collectively shape neocortical plasticity is missing. We built a biochemically detailed model of post-synaptic plasticity describing CaMKII, PKA, and PKC pathways and their contribution to synaptic potentiation or depression. We developed a statistical AMPA-receptor-tetramer model, which permits the estimation of the AMPA-receptor-mediated maximal synaptic conductance based on numbers of GluR1s and GluR2s predicted by the biochemical signalling model. We show that our model reproduces neuromodulator-gated spike-timing-dependent plasticity as observed in the visual cortex and can be fit to data from many cortical areas, uncovering the biochemical contributions of the pathways pinpointed by the underlying experimental studies. Our model explains the dependence of different forms of plasticity on the availability of different ...
When a cell has to endure lasting changes in its environment that require it to actively transport more molecules than normal through the cell membra...
The long-term goal of this project is to identify thalamocortical network mechanisms involved in consolidating experience-dependent plasticity in the visual sys...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
In the mammalian dentate gyrus (DG) neurogenesis continues throughout life. Accumulating evidence suggests a unique contribution of adult-generated neurons in DG synaptic plasticity and hippocampal-mediated learning and memory functions. However, the precise involvement of adult neurogenesis to disease-related cognitive deficits still remains unclear. Intellectual disabilities are the most striking clinical features of Down Syndrome (DS) and are characterized by learning deficits and memory impairment, particularly in hippocampus-related functions. Accordingly, the Ts65Dn mouse model of DS recapitulate many hippocampal cognitive deficits of the human syndrome, and also show decreased adult neurogenesis and impaired DG synaptic plasticity. To elucidate the contribution of faulty adult neurogenesis to DG synaptic plasticity deficits and memory impairment in DS we have treated adult Ts65Dn mice with lithium, a widely used mood stabilizer that also promotes neurogenesis. Results showed that chronic ...
Activity-dependent long-term changes in synaptic efficacy are thought to be important in learning, memory formation, neuronal development and pathological states of neuronal excitability in the CNS. For the past two decades, numerous studies have investigated long-term changes in synaptic efficacy at excitatory glutamatergic synapses. Although inhibitory synapses are essential for proper functioning of the neuronal network, attention has focused only recently on describing and characterizing plasticity at these types of synapse. Not surprisingly, different forms of plasticity at GABAergic, and the closely related glycinergic, synapses have been reported in several regions of the brain. Here we review these different forms of plasticity and focus on their possible roles in developing and adult neuronal networks.
Research Interests The future aint what it used to be - Yogi Berra It is precisely because the future is unpredictable that the mammalian brain has evolved the capacity to acquire new information through sensory experiences, store this information as memories, and rapidly retrieve this information to modify behavior. But how do novel sensory experiences embed themselves in the fabric of the brain to form memories? This question drives the research in my laboratory, which examines the cellular and synaptic mechanisms of experience-dependent plasticity in the neocortex. Specifically, I am interested in understanding i) where experience-dependent plasticity is initiated in the cortical circuitry; ii) how experience regulates the growth or retraction of synapses; iii) whether plasticity is restricted to only a subset of synaptic connections; iv) what distinguishes critical period plasticity from adult plasticity; v) how synaptic plasticity is altered in the aging and diseased brain. Techniques: To ...
Previous studies have reported primary auditory cortex plasticity following vagus nerve stimulation (VNS) paired with a sound. Does this phenomenon extend to other fields in the auditory pathway? In this podcast, Editor-in-Chief Bill Yates talks with Dr. Michael S. Borland and Dr. Crystal Engineer (both from the University of Texas at Dallas) about their recent study, which is the first to to document both cortical and subcortical plasticity following VNS-sound pairing. Listen to learn about auditory plasticity, potential therapies for auditory processing disorders, and more! Listen Now. August 14, 2019. ...
The molecular basis for the decline in experience-dependent neural plasticity over age remains poorly understood. In visual cortex, the robust plasticity induced in juvenile mice by brief monocular deprivation during the critical period is abrogated by genetic deletion of Arc, an activity-dependent regulator of excitatory synaptic modification. Here, we report that augmenting Arc expression in adult mice prolongs juvenile-like plasticity in visual cortex, as assessed by recordings of ocular dominance (OD) plasticity in vivo. A distinguishing characteristic of juvenile OD plasticity is the weakening of deprived-eye responses, believed to be accounted for by the mechanisms of homosynaptic long-term depression (LTD). Accordingly, we also found increased LTD in visual cortex of adult mice with augmented Arc expression and impaired LTD in visual cortex of juvenile mice that lack Arc or have been treated in vivo with a protein synthesis inhibitor. Further, we found that although activity-dependent ...
This new research might unite neurobiologists studying circadian rhythms with those studying developmental brain plasticity, Kobayashi notes. It could open inquiries into the role of circadian rhythm genes beyond the visual system, including brain regions that control cognition and social behaviors.. Specifically, the findings may have implications for disorders such as autism and schizophrenia. A number of genes associated with mental illness were expressed differently in the PV-cells of Clock-deficient versus control mice. The Hensch group and others have long proposed a link between neurodevelopmental disorders and timing defects in critical periods of brain plasticity. And finally, factors that influence circadian rhythms-sleep deprivation, seasonal changes limiting sunlight exposure, night shift work, etc.-have been linked to mood disorders.. By implicating circadian rhythm genes in the control of developmental brain plasticity, the new study may help bridge these ideas and suggests that ...
We used the rat visual cortex as a model system to examine the changes in protein synthesis during experience-induced synaptic plasticity. Dark-rearing rats from birth results in a relatively immature visual cortex that maintains the high de- gree of synaptic plasticity characteristic of the critical period (Kirkwood et al., 1995). Exposure of dark-reared rats to light results in a rapid, robust and coordinated burst of experience- driven synaptic plasticity that can be readily monitored at the biochemical and electrophysiological level (Quinlan et al., 1999). In previous work, we showed that visual experience evokes the polyadenylation of ␣-CaMKII mRNA in visual cortex and the elevation of ␣-CaMKII protein in synaptic fractions from this brain region. Moreover, this increase was a direct result of new synthesis because it was sensitive to the translation inhibitor cycloheximide (Wu et al., 1998). Here we show that the experience-induced increase of ␣-CaMKII pro- tein does not require new ...
The activity-regulated cytoskeletal protein Arc (also known as Arg3.1) is required for long-term memory formation and synaptic plasticity. Arc expression is robustly induced by activity, and Arc protein localizes to both active synapses and the nucleus. Whereas its synaptic function has been examined, it is not clear why or how Arc is localized to the nucleus. We found that murine Arc nuclear expression is regulated by synaptic activity in vivo and in vitro. We identified distinct regions of Arc that control its localization, including a nuclear localization signal, a nuclear retention domain and a nuclear export signal. Arc localization to the nucleus promotes an activity-induced increase in the expression of promyelocytic leukemia nuclear bodies, which decreases GluA1 (also called Gria1) transcription and synaptic strength. We further show that Arc nuclear localization regulates homeostatic plasticity. Thus, Arc mediates the homeostatic response to increased activity by translocating to the ...
While stroke-related deaths have decreased in recent years, stroke is still the leading cause of long-term disability in the United States. Adequate rehabilitation is dependant upon plasticity, a multidimensional and adaptive process underlying recovery of function in both the human and rodent brain. The complexity of processes underlying plasticity in the central nervous system is still largely unknown, but manipulating this spontaneous state of the healing brain is of the utmost importance as it will allow maximum therapeutic effect. Characterization of lesion-induced local and remote rewiring, initial behavioral deficit and their long-term relationships to behavioral outcome are required to fill some of the gaps in our understanding of brain repair mechanisms after stroke. The experiments outlined in this dissertation take advantage of hypothesized neuroplasticity foundations of learning and memory, as well as an established model of forelimb motor cortex injury in rats in order to examine ...
TY - JOUR. T1 - Adult cortical plasticity depends on an early postnatal critical period. AU - Greenhill, Stuart D.. AU - Juczewski, Konrad. AU - de Haan, Annelies M.. AU - Seaton, Gillian. AU - Fox, Kevin. AU - Hardingham, Neil R.. N1 - This is the authors version of the work. It is posted here by permission of the AAAS for personal use, not for redistribution. The definitive version was published in Science on Volume 349 Issue 6246 24 July 2015], DOI: 10.1126/science.aaa8481. PY - 2015/7/24. Y1 - 2015/7/24. N2 - Development of the cerebral cortex is influenced by sensory experience during distinct phases of postnatal development known as critical periods. Disruption of experience during a critical period produces neurons that lack specificity for particular stimulus features, such as location in the somatosensory system. Synaptic plasticity is the agent by which sensory experience affects cortical development. Here, we describe, in mice, a developmental critical period that affects plasticity ...
Postnatal sensory experience plays a significant role in the maturation and synaptic stabilization of sensory cortices, such as the primary auditory cortex (A1). Here, we examined the effects of patterned sound deprivation (by rearing in continuous white noise, WN) during early postnatal life on short- and long-term plasticity of adult male rats using an|i| in vivo|/i| preparation (urethane anesthesia). Relative to age-matched control animals reared under unaltered sound conditions, rats raised in WN (from postnatal day 5 to 50–60) showed greater levels of long-term potentiation (LTP) of field potentials in A1 induced by theta-burst stimulation (TBS) of the medial geniculate nucleus (MGN). In contrast, analyses of short-term plasticity using paired-pulse stimulation (interstimulus intervals of 25–1000 ms) did not reveal any significant effects of WN rearing. However, LTP induction resulted in a significant enhancement of paired-pulse depression (PPD) for both rearing conditions|i|.
article{ef532af8-d218-4166-9ec2-b39930c591ef, abstract = {,p,Following stroke, complete cellular death in the ischemic brain area may ensue, with remaining brain areas undergoing tissue remodelling to various degrees. Experience-dependent brain plasticity exerted through an enriched environment (EE) promotes remodelling after central nervous system injury, such as stroke. Post-stroke tissue reorganization is modulated by growth inhibitory molecules differentially expressed within the ischemic hemisphere, like chondroitin sulfate proteoglycans found in perineuronal nets (PNNs). PNNs in the neocortex predominantly enwrap parvalbumin-containing GABAergic (PV/GABA) neurons, important in sensori-information processing. Here, we investigate how extracellular matrix (ECM) proteases and their inhibitors may participate in the regulation of PNN integrity during stroke recovery. Rats were subjected to photothrombotic stroke in the motor cortex, and functional deficits were assessed at 7 days of recovery. ...
Resum: Although there is a decline in brain plasticity across lifespan, neurons in certain areas of the adult brain retain the ability to undergo synaptic, dendritic and spine remodeling in response to different stimuli. This neuronal structural plasticity seems to be the basis for many cognitive processes and it is crucial for adaptive responses to aversive experiences and recovery from brain damage and disease. Among the numerous candidate molecules that have been identified for mediating this neuronal remodeling, cell adhesion molecules and, specially, the neural cell adhesion molecule (NCAM), are of particular interest. The addition of polysialic acid (PSA) to the NCAM is critical for the structural changes that underlie plasticity; not only because it prevents both homotypic and heterotypic NCAM bindings (anti-adhesive properties) but also because it interacts with a large number of molecules and signaling pathways that regulate synaptic strength. In consonance with this fact, PSA-NCAM ...
TY - JOUR. T1 - Neuronal networks and synaptic plasticity in Parkinsons disease. T2 - beyond motor deficits. AU - Calabresi, Paolo. AU - Galletti, Francesca. AU - Saggese, Emanuele. AU - Ghiglieri, Veronica. AU - Picconi, Barbara. PY - 2007. Y1 - 2007. N2 - The excitatory corticostriatal pathway, which plays a critical role in the building up and storage of adaptive motor behaviours, can undergo long-lasting, activity-dependent changes in the efficacy of synaptic transmission, named long-term potentiation (LTP) and long- term depression (LTD). Both forms of plasticity are thought to underlie motor learning and depend upon the concomitant activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways. Accordingly, corticostriatal LTP and LTD are altered in Parkinsons Disease (PD) models. The dopamine (DA)/acetylcholine(Ach) synaptic unbalance could be responsible of some of the cognitive deficits described in PD patients. The impairment of DA/ACh-dependent cellular learning ...
Abstract. It is now accepted that immune molecules are not only present within the brain during pathology but they exert physiological functions in the healthy brain as well. Increasing evidence points to a neuro-modulatory role of cytokines and chemokines (CHEMOtactic cytoKINES) in basal transmission and plasticity processes where signaling between peri-synaptic astrocytes, microglia and neurons plays an important role. Nevertheless, the exact mechanisms as to how cytokines, and in particular chemokines, participate in the molecular and cellular processes thought to subserve memory formation, plasticity processes and responsiveness to environmental stimuli remain to be clarified. Interestingly, in in vitro preparations, molecules like TNF-a, interleukin (IL)-1ß, IL-6, CX3CL1, CXCL12, CCL2 and CCL3 are implicated in synaptic formation and scaling, in modulation of glutamatergic transmission, in plasticity and neurogenesis, in particular in the hippocampus. The hippocampus is an extremely ...
The two fundamental forms of short-term plasticity, short-term depression and facilitation, coexist at most synapses, but little is known about their interaction. Here, we studied the interplay between short-term depression and facilitation at calyx of Held synapses. Stimulation at a low frequency of 10 or 20 Hz, which is in the range of the spontaneous activity of these auditory neurons in vivo, induced synaptic depression. Surprisingly, an instantaneous increase of the stimulation frequency to 100 or 200 Hz following the low-frequency train uncovered a robust facilitation of EPSCs relative to the predepressed amplitude level. This facilitation decayed rapidly (similar to 30 ms) and depended on presynaptic residual Ca2+, but it was not caused by Ca2+ current facilitation. To probe the release probability of the remaining readily releasable vesicles following the low-frequency train we made presynaptic Ca2+ uncaging experiments in the predepressed state of the synapse. We found that low-frequency
Author Summary Recent brain imaging and neurophysiological studies suggest that the striatum, the start of the basal ganglia circuit, plays a major role in value-based decision making and behavioral disorders such as drug addiction. The plasticity of synaptic input from the cerebral cortex to output neurons of the striatum, which are medium spiny neurons, depends on interactions between glutamate input from the cortex and dopaminergic input from the midbrain. It also links sensory and cognitive states in the cortex with reward-oriented action outputs. The mechanisms involved in molecular cascades that transmit glutamate and dopamine inputs to changes in postsynaptic glutamate receptors are very complex and it is difficult to intuitively understand the mechanism. Therefore, a biochemical network model was constructed, and computer simulations were performed. The model reproduced dopamine-dependent and calcium-dependent forms of long-term depression (LTD) and potentiation (LTP) of corticostriatal synapses
Does severe acute pain provoke lasting changes in attentional and emotional mechanisms of pain-related processing? A longitudinal ...
Tinnitus is a phantom auditory sensation that reduces quality of life for millions of people worldwide, and for which there is no medical cure. Most cases of tinnitus are associated with hearing loss caused by ageing or noise exposure. Exposure to loud recreational sound is common among the young, and this group are at increasing risk of developing tinnitus.
The world was originally introduced to the concept of synaptic plasticity over 60 years ago, when Dr. Donald Hebb first clearly defined a physiological mechanism for learning and memory in his seminal work The Organization of Behavior. It took another 20 years for Bliss and Lomo to scientifically validate Hebbs postulate, and show that neurons could alter their ability to communicate with one another in a persistent manner. Together, these works started off what has grown to become the field of synaptic plasticity. The years following the initial discovery were exciting times for learning and memory young researchers like myself, and each discovery over the next 20 years seemed to push us closer to elucidating the biological mechanisms responsible for memory formation. This seemed particularly true in the mid-1980s when the NMDA receptor was being heralded as the key to learning and memory processes. However, more recently it has become obvious that the activation of membrane receptors is ...
TY - JOUR. T1 - Chapter 27 Neural Plasticity After Nerve Injury and Regeneration. AU - Navarro, Xavier. PY - 2009/1/1. Y1 - 2009/1/1. N2 - Injuries to the peripheral nerves result in partial or total loss of motor, sensory, and autonomic functions in the denervated segments of the body due to the interruption of axons, degeneration of distal nerve fibers, and eventual death of axotomized neurons. Functional deficits caused by nerve injuries can be compensated by reinnervation of denervated targets by regenerating injured axons or by collateral branching of undamaged axons, and remodeling of nervous system circuitry related to the lost functions. Plasticity of central connections may compensate functionally for the lack of adequate target reinnervation; however, plasticity has limited effects on disturbed sensory localization or fine motor control after injuries, and may even result in maladaptive changes, such as neuropathic pain and hyperreflexia. After axotomy, neurons shift from a transmitter ...
His recommendations for healthy life (brisk walking, entertaining sporting activities, etc.) can be found in many books. This is supposed to be a book on neuroplasticity. Unfortunately, you hardly find real recommendations on how we can handle problems by using neuroplasticity tools. Title of the book and chapters do not reflect the real subject ...
The trajectory of the somatic membrane potential of a cortical neuron exactly reflects the computations performed on its afferent inputs. However, the spikes of such a neuron are a very low-dimensional and discrete projection of this continually evolving signal. We explored the possibility that the neurons efferent synapses perform the critical computational step of estimating the membrane potential trajectory from the spikes. We found that short-term changes in synaptic efficacy can be interpreted as implementing an optimal estimator of this trajectory. Short-term depression arose when presynaptic spiking was sufficiently intense as to reduce the uncertainty associated with the estimate; short-term facilitation reflected structural features of the statistics of the presynaptic neuron such as up and down states. Our analysis provides a unifying account of a powerful, but puzzling, form of plasticity.. ...
Coupling the control of expression stochasticity (noise) to the ability of expression change (plasticity) can alter gene function and influence adaptation. A number of factors, such as transcription re-initiation, strong chromatin regulation or genome neighboring organization, underlie this coupling. However, these factors do not necessarily combine in equivalent ways and strengths in all genes. Can we identify then alternative architectures that modulate in distinct ways the linkage of noise and plasticity? Here we first show that strong chromatin regulation, commonly viewed as a source of coupling, can lead to plasticity without noise. The nature of this regulation is relevant too, with plastic but noiseless genes being subjected to general activators whereas plastic and noisy genes experience more specific repression. Contrarily, in genes exhibiting poor transcriptional control, it is translational efficiency what separates noise from plasticity, a pattern related to transcript length. This
GABAergic (GABA = gamma-aminobutyric acid) neurons from different brain regions contain high levels of parvalbumin, both in their soma and in their neurites. Parvalbumin is a slow Ca(2+) buffer that may affect the amplitude and time course of intracellular Ca(2+) transients in terminals after an action potential, and hence may regulate short-term synaptic plasticity. To test this possibility, we have applied paired-pulse stimulations (with 30- to 300-ms intervals) at GABAergic synapses between interneurons and Purkinje cells, both in wild-type (PV+/+) mice and in parvalbumin knockout (PV-/-) mice. We observed paired-pulse depression in PV+/+ mice, but paired-pulse facilitation in PV-/- mice. In paired recordings of connected interneuron-Purkinje cells, dialysis of the presynaptic interneuron with the slow Ca(2+) buffer EGTA (1 mM) rescues paired-pulse depression in PV-/- mice. These data show that parvalbumin potently modulates short-term synaptic plasticity. ...
This laboratory pilot study will explore the effects of varenicline tartrate on long-term potentiation (LTP)-like mechanisms of (1) the motor cortex and (2) the dorsolateral prefrontal cortex (DLPFC) and working memory in non-smoking patients with schizophrenia and healthy controls using a Paired Associative Stimulation (PAS) method. The present study will use this novel PAS method to evaluate the effects of five doses of varenicline (Champix) 0.5 mg BID treatment on neuroplasticity changes and working memory in 28 non-smokers with schizophrenia and 28 non-smoking controls in a placebo-controlled, double-blinded, cross-over design. The hypothesis is that varenicline will increase LTP-like facilitation of the DLPFC as compared with placebo in patients with schizophrenia, with less or a null effect in healthy controls. Likewise, it is hypothesized that varenicline will specifically improve working memory in patients with schizophrenia as compared with placebo and healthy controls. We Hypothesize ...
Valentina received her Ph.D. in Neuroscience from Tor Vergata University (Rome), where she explored the role of FMRP in the regulation of transport, translation and stability of dendritic mRNAs. Later she worked extensively on learning-dependent synaptic plasticity at the Hospital for Sick Children, Toronto.. Valentina ...
TY - CHAP. T1 - Translating memories. T2 - The role of protein biosynthesis in synpatic plasticity. AU - Westmark, Cara J.. AU - Malter, James S.. PY - 2009/1/1. Y1 - 2009/1/1. N2 - The 1990s, The Decade of the Brain, resulted in major scientific advances involving brain imaging, gene therapy, brain/robotic interfacing and the neurobiology and molecular biology of learning and memory. However, despite these critical insights, we still do not know exactly how thoughts or memories are formed or stored in the brain, which leaves much exciting research for the twenty-first and probably centuries to come. This review will elaborate on recent advances in the field of protein biosynthesis as related to synaptic plasticity. We will discuss the molecular players (RNA binding proteins and neuronal mRNAs), the signal transduction pathways that have been implicated in learning and memory and how localized translation of selected mRNAs is involved in synaptic plasticity. We will also discuss the pathology ...
Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.: Impairments of synaptic plasticity are a hallmark o
It is an open question how the multiple special and temporal scales involved in intracellular Ca2+ handling within the STDP models affect the plasticity outcomes predicted by these models. Hebbian or associative plasticity is triggered by postsynaptic Ca2+ influx which activates calmodulin and CaMKII. The influx of Ca2+ through voltage-dependent NMDA receptors and Ca2+ channels is regulated by Ca2+ -activated K+ channels (SK-channels) providing negative feedback regulation of postsynaptic [Ca2+]. Using 3-dimensional modelling of Ca2+ and calmodulin dynamics within dendritic spines we show that the non-linear relationship between Ca2+ influx and calmodulin activation endows SK-channels with the ability to gate calmodulin activation and therefore the induction of Hebbian synaptic plasticity. Since SK-channels are inhibited by several neuro-modulator receptors including acetylcholine and noradrenaline, the gating of synaptic plasticity by SK-channels could represent a common mechanism by which ...
We unravel how functional plasticity and redundancy are essential mechanisms underlying the ability to survive of metabolic networks. We perform an exhaustive computational screening of synthetic lethal reaction pairs in Escherichia coli in a minimal medium and we find that synthetic lethal pairs divide in two different groups depending on whether the synthetic lethal interaction works as a backup or as a parallel use mechanism, the first corresponding to essential plasticity and the second to essential redundancy. In E. coli, the analysis of pathways entanglement through essential redundancy supports the view that synthetic lethality affects preferentially a single function or pathway. In contrast, essential plasticity, the dominant class, tends to be inter-pathway but strongly localized and unveils Cell Envelope Biosynthesis as an essential backup for Membrane Lipid Metabolism. When comparing E. coli and Mycoplasma pneumoniae, we find that the metabolic networks of the two organisms exhibit a ...
DataMed is a prototype biomedical data search engine. Its goal is to discover data sets across data repositories or data aggregators. In the future it will allow searching outside these boundaries. DataMed supports the NIH-endorsed FAIR principles of Findability, Accessibility, Interoperability and Reusability of datasets with current functionality assisting in finding datasets and providing access information about them.
ST7103 Theory Of Elasticity And Plasticity Important Questions Bank Reg 2013. Noteskik.com Provides Important Questions Banks for all departments. We are Collected From Various Places To Provide Our Service for the Students. Questions Bank provided here are the Expected Important questions Bank for 1th Semester Department of structural Engineering for that are possible to appear in the upcoming exams & make use of the below questions and prepare for your exams.. We have provided ST7103 Theory Of Elasticity And Plasticity Important Questions Bank Reg 2013 2015-16. Here ST7103 Theory Of Elasticity And Plasticity Important Questions Bank Reg 2013 are posted and Students can download the Questions and make use of it. Anna University 1th Semester ST7103 Theory Of Elasticity And Plasticity Important Questions Bank Reg 2013 are provided Below.. ...
Maheu ME, Ressler KJ. Developmental pathway genes and neural plasticity underlying emotional learning and stress-related disorders. Learn Mem. 2017 09; 24(9):492-501 ...
If you have a question about this talk, please contact Dr Etienne Gaudrain.. Abstract not available. This talk is part of the Hearing Group Meetings series.. ...
Nitrogen (N) is central for plant growth, and metabolic plasticity can provide a strategy to respond to changing N availability. We showed that two local A. thaliana populations exhibited differential plasticity in the compounds of photorespiratory and starch degradation pathways in response to three N conditions. Association of metabolite levels with growth-related and fitness traits indicated that controlled plasticity in these pathways could contribute to local adaptation and play a role in plant evolution.
Myelin sheaths in the vertebrate nervous system enable faster impulse propagation, while myelinating glia provide vital support to axons. Once considered a static insulator, converging evidence now suggests that myelin in the central nervous system can be dynamically regulated by neuronal activity and continues to participate in nervous system plasticity beyond development. While the link between experience and myelination gains increased recognition, it is still unclear what role such adaptive myelination plays in facilitating and shaping behaviour. Additionally, fundamental mechanisms and principles underlying myelin remodelling remain poorly understood. In this review, we will discuss new insights into the link between myelin plasticity and behaviour, as well as mechanistic aspects of myelin remodelling that may help to elucidate this intriguing process.