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Dominique Debanne - One of the best experts on this subject based on the ideXlab platform.
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plasticity of intrinsic Neuronal Excitability
Current Opinion in Neurobiology, 2019Co-Authors: Dominique Debanne, Yanis Inglebert, Michael RussierAbstract:Long-term synaptic modification is not the exclusive mode of memory storage, and persistent regulation of voltage-gated ion channels also participates in memory formation. Intrinsic plasticity is expressed in virtually all Neuronal types including principal cells and interneurons. Activation of synaptic glutamate receptors initiates long-lasting changes in Neuronal Excitability at presynaptic and postsynaptic side. As synaptic plasticity, intrinsic plasticity is bi-directional and expresses a certain level of input-specificity or cell-specificity. We discuss here the nature of the learning rules shared by intrinsic and synaptic plasticity and the impact of intrinsic plasticity on temporal processing.
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Spike-timing dependent plasticity beyond synapse - pre- and post-synaptic plasticity of intrinsic Neuronal Excitability.
Frontiers in Synaptic Neuroscience, 2010Co-Authors: Dominique DebanneAbstract:Long-lasting plasticity of synaptic transmission is classically thought to be the cellular substrate for information storage in the brain. Recent data indicate however that it is not the whole story. Persistent changes in the intrinsic Neuronal Excitability have been shown to occur in parallel to the induction of long-term synaptic modifications. This form of plasticity depends on the regulation of voltage-gated ion channels. Here we review the experimental evidence for plasticity of Neuronal Excitability induced at pre- or post-synaptic sites when long-term plasticity of synaptic transmission is induced with Spike-Timing-Dependent Plasticity (STDP) protocols. We describe the induction and expression mechanisms of the induced changes in Excitability. Finally, the functional synergy between synaptic and non-synaptic plasticity and their spatial extent are discussed.
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Plasticity of Neuronal Excitability in vivo.
The Journal of Physiology, 2009Co-Authors: Dominique DebanneAbstract:For years, long-lasting plasticity of synaptic transmission was the favourite mechanism to account for information storage in the brain. While bidirectional long-term synaptic plasticity is computationally appealing (in part because of synapse-specific changes among a large array of inputs), it is not the whole story. Recent evidence indicates that the Neuronal message is also persistently filtered through regulation of voltage-gated ion channels. Excitatory postsynaptic potentials (EPSPs) measured at the axon hillock result from a tight interplay between synaptic and intrinsic voltage-gated conductances that either amplify or attenuate the synaptic potentials (review in Spruston, 2008). Any modifications in this fragile equilibrium may in turn facilitate or diminish the probability that a given synaptic input triggers an action potential. For instance, induction of long-term synaptic potentiation (LTP) in CA1 hippocampal neurons down-regulates A-type K+ (Frick et al. 2004) and hyperpolarization-activated cationic (H) currents (Campanac et al. 2008) in the dendrites, and in turn facilitates the generation of an action potential by the EPSP. In paired recordings of connected neurons, LTP is associated with an increase in Excitability of the presynaptic neuron that results from a facilitation of the transient sodium current (Ganguly et al. 2000). Independently of synaptic activation, rapid elevation in Neuronal Excitability may also be induced by directly conditioning the neuron with repeated action potential bursting of the recorded neuron (Cudmore & Turrigiano, 2004). Here, the global increase in Excitability is accompanied by modifications in the threshold for action potential generation. Plasticity of Neuronal Excitability may therefore be defined as the persistent modification of intrinsic electrical properties of a neuron induced by Neuronal (action potential firing) or synaptic activity. It is mediated by changes in the expression level or biophysical properties of ion channels and may thus alter a large range of functional processes such as dendritic integration, spike generation, signal propagation in the dendrite and the axon, and regulation of plasticity thresholds. Most of the recent advances in understanding induction and expression mechanisms of intrinsic plasticity come from in vitro studies on brain slices or cultures of dissociated neurons. Less attention has been devoted to the search for cellular Excitability correlates of learning and memory in the mammalian brain. Eye-blink conditioning in the cat or the rabbit provides, however, representative examples of learning-driven changes in Neuronal Excitability in hippocampal, cerebellar and cortical neurons. In conditioned animals, neurons that are active during conditioning display in vitro Excitability that is significantly higher than that of neurons recorded from naive or pseudo-conditioned animals (Disterhoft et al. 1986). Changes in Excitability of physiologically characterized neurons in vivo remain, however, uncertain because Excitability changes were generally measured in separate populations of neurons before and after conditioning (Aou et al. 1992). In this issue of The Journal of Physiology, Paz and co-workers filled the gap by providing direct evidence that rat motor cortex neurons recorded intracellularly in vivo express a long-lasting increase in Excitability following cellular conditioning (Paz et al. 2009). The authors accomplished here a technical tour-de-force by obtaining stable intracellular recordings from identified L5 neurons in anaesthetized rats. Excitability changes were quantified by current–firing curves established before and after conditioning which consisted of repeated postsynaptic bursting at 30 Hz. Two main parameters are classically measured in input–output curves: the firing threshold and the gain (Carvalho & Buonomano, 2009). Changes in firing threshold signify modification in Excitability drive (e.g. sodium current) whereas modifications in the gain usually indicate regulation of the Excitability brake (e.g. after-hyperpolarizing potential). Consistent with previous in vitro findings (Cudmore & Turrigiano, 2004), repeated postsynaptic bursting induced by direct injection of depolarizing current in the neuron produced a long-lasting (> 30 min) increase in Excitability in the great majority of changes (Paz et al. 2009; Fig. 1). The induction mechanisms have not been characterized here because of the complexity of the experiment, but one may suppose that action potential bursting triggers postsynaptic calcium influx that will activate an enzymatic cascade controlling the activity of one (or several) ion channel(s). In fact, the Excitability changes displayed heterogeneous behaviour. In one-third of cases, an increase in Excitability was associated with a reduction in the firing threshold. In the second third, the gain of the input–output curve was altered and in the remaining third, both changes were observed, suggesting multiple expression mechanisms. Figure 1 Repeated bursting of layer 5 pyramidal neuron induces long-term potentiation of intrinsic Excitability in rat cortical motor neurons in vivo. The report by Paz and colleagues extends our knowledge of the potential of functional plasticity observed in the whole brain in vivo. Furthermore, this study will certainly motivate many other investigations in the future because several major questions are pending. Here, intrinsic plasticity was induced by postsynaptic bursting in the recorded neuron but the effects of physiologically relevant synaptic stimulation remain unknown. In addition, the precise conditions allowing induction of a persistent decrease in Excitability will require clarification. Finally, the potential of intrinsic plasticity in other Neuronal types including pyramidal and non-pyramidal cells must be defined.
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Plasticity of Neuronal Excitability: Hebbian rules beyond the synapse.
Archives Italiennes De Biologie, 2007Co-Authors: Emilie Campanac, Dominique DebanneAbstract:Activity-dependent synaptic plasticity is classically though to be the cellular substrate for learning and memory. Recent data show that activation of glutamate receptors initiates a long-term modification in pre- or post-synaptic Neuronal Excitability. Similarly to synaptic plasticity, intrinsic plasticity is bidirectional and input- or cell-specific. In addition to an increase in the reliability of the input-output function, temporal precision of the Neuronal discharge is improved. These forms of plasticity not only share common learning rules and induction pathways with the better known synaptic plasticity but may also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram.
Chong Ding - One of the best experts on this subject based on the ideXlab platform.
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Repetitive transcranial magnetic stimulation significantly improves cognitive impairment and Neuronal Excitability during aging in mice
Journal of Biomedical Engineering, 2020Co-Authors: Chong Ding, Yang Li, Guizhi XuAbstract:Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive brain stimulation technique that has been paid attention to with increasing interests as a therapeutic neural rehabilitative tool. Studies confirmed that high-frequency rTMS could improve the cognitive performance in behavioral test as well as the Excitability of the neuron in animals. This study aimes to investigate the effects of rTMS on the cognition and Neuronal Excitability of Kunming mice during the natural aging. Twelve young mice, 12 adult mice, and 12 aged mice were used, and each age group were randomly divided into rTMS group and control group. rTMS-treated groups were subjected to high-frequency rTMS treatment for 15 days, and control groups were treated with sham stimulation for 15 days. Then, novel object recognition and step-down tests were performed to examine cognition of learning and memory. Whole-cell patch clamp technique was used to record and analyze resting membrane potential, action potential (AP), and related electrical properties of AP of hippocampal dentate gyrus (DG) granule neurons. Data analysis showed that cognition of mice and Neuronal Excitability of DG granule neurons were degenerated significantly as the age increased. Cognitive damage and degeneration of some electrical properties were alleviated under the condition of high-frequency rTMS. It may be one of the mechanisms of rTMS to alleviate cognitive damage and improve cognitive ability by changing the electrophysiological properties of DG granule neurons and increasing Neuronal Excitability.
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The effects of repetitive transcranial magnetic stimulation on the cognition and Neuronal Excitability of mice.
Electromagnetic Biology and Medicine, 2019Co-Authors: Guizhi Xu, Lingdi Fu, Yang Li, Rui Fu, Dongshuai Zhao, Chong DingAbstract:This study aimed to investigate the effects of repetitive transcranial magnetic stimulation (rTMS) on the cognition and Neuronal Excitability of Kunming mice during the natural aging of the brain. ...
James E Porter - One of the best experts on this subject based on the ideXlab platform.
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GABAB Receptor Activation Inhibits Neuronal Excitability and Spatial Learning in the Entorhinal Cortex by Activating TREK-2 K+ Channels
Neuron, 2009Co-Authors: Panyue Deng, Zhaoyang Xiao, Lalida Rojanathammanee, Chuanxiu Yang, Laurel A Grisanti, John A. Watt, Jonathan D. Geiger, James E PorterAbstract:Summary The entorhinal cortex (EC) is regarded as the gateway to the hippocampus and thus is essential for learning and memory. Whereas the EC expresses a high density of GABA B receptors, the functions of these receptors in this region remain unexplored. Here, we examined the effects of GABA B receptor activation on Neuronal Excitability in the EC and spatial learning. Application of baclofen, a specific GABA B receptor agonist, inhibited significantly Neuronal Excitability in the EC. GABA B receptor-mediated inhibition in the EC was mediated via activating TREK-2, a type of two-pore domain K + channels, and required the functions of inhibitory G proteins and protein kinase A pathway. Depression of Neuronal Excitability in the EC underlies GABA B receptor-mediated inhibition of spatial learning as assessed by Morris water maze. Our study indicates that GABA B receptors exert a tight control over spatial learning by modulating Neuronal Excitability in the EC.
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noradrenergic depression of Neuronal Excitability in the entorhinal cortex via activation of trek 2 k channels
Journal of Biological Chemistry, 2009Co-Authors: Zhaoyang Xiao, Panyue Deng, Lalida Rojanathammanee, Chuanxiu Yang, Laurel A Grisanti, Kannika Permpoonputtana, David Weinshenker, Van A Doze, James E PorterAbstract:The entorhinal cortex is closely associated with the consolidation and recall of memories, Alzheimer disease, schizophrenia, and temporal lobe epilepsy. Norepinephrine is a neurotransmitter that plays a significant role in these physiological functions and neurological diseases. Whereas the entorhinal cortex receives profuse noradrenergic innervations from the locus coeruleus of the pons and expresses high densities of adrenergic receptors, the function of norepinephrine in the entorhinal cortex is still elusive. Accordingly, we examined the effects of norepinephrine on Neuronal Excitability in the entorhinal cortex and explored the underlying cellular and molecular mechanisms. Application of norepinephrine-generated hyperpolarization and decreased the Excitability of the neurons in the superficial layers with no effects on Neuronal Excitability in the deep layers of the entorhinal cortex. Norepinephrine-induced hyperpolarization was mediated by α2A adrenergic receptors and required the functions of Gαi proteins, adenylyl cyclase, and protein kinase A. Norepinephrine-mediated depression on Neuronal Excitability was mediated by activation of TREK-2, a type of two-pore domain K+ channel, and mutation of the protein kinase A phosphorylation site on TREK-2 channels annulled the effects of norepinephrine. Our results indicate a novel action mode in which norepinephrine depresses Neuronal Excitability in the entorhinal cortex by disinhibiting protein kinase A-mediated tonic inhibition of TREK-2 channels.
Guizhi Xu - One of the best experts on this subject based on the ideXlab platform.
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Repetitive transcranial magnetic stimulation significantly improves cognitive impairment and Neuronal Excitability during aging in mice
Journal of Biomedical Engineering, 2020Co-Authors: Chong Ding, Yang Li, Guizhi XuAbstract:Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive brain stimulation technique that has been paid attention to with increasing interests as a therapeutic neural rehabilitative tool. Studies confirmed that high-frequency rTMS could improve the cognitive performance in behavioral test as well as the Excitability of the neuron in animals. This study aimes to investigate the effects of rTMS on the cognition and Neuronal Excitability of Kunming mice during the natural aging. Twelve young mice, 12 adult mice, and 12 aged mice were used, and each age group were randomly divided into rTMS group and control group. rTMS-treated groups were subjected to high-frequency rTMS treatment for 15 days, and control groups were treated with sham stimulation for 15 days. Then, novel object recognition and step-down tests were performed to examine cognition of learning and memory. Whole-cell patch clamp technique was used to record and analyze resting membrane potential, action potential (AP), and related electrical properties of AP of hippocampal dentate gyrus (DG) granule neurons. Data analysis showed that cognition of mice and Neuronal Excitability of DG granule neurons were degenerated significantly as the age increased. Cognitive damage and degeneration of some electrical properties were alleviated under the condition of high-frequency rTMS. It may be one of the mechanisms of rTMS to alleviate cognitive damage and improve cognitive ability by changing the electrophysiological properties of DG granule neurons and increasing Neuronal Excitability.
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The effects of repetitive transcranial magnetic stimulation on the cognition and Neuronal Excitability of mice.
Electromagnetic Biology and Medicine, 2019Co-Authors: Guizhi Xu, Lingdi Fu, Yang Li, Rui Fu, Dongshuai Zhao, Chong DingAbstract:This study aimed to investigate the effects of repetitive transcranial magnetic stimulation (rTMS) on the cognition and Neuronal Excitability of Kunming mice during the natural aging of the brain. ...
Robert H Lipsky - One of the best experts on this subject based on the ideXlab platform.
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mice lacking the transcriptional regulator bhlhe40 have enhanced Neuronal Excitability and impaired synaptic plasticity in the hippocampus
PLOS ONE, 2018Co-Authors: Kelly A Hamilton, Yue Wang, Sophia M Raefsky, Sean T Berkowitz, Ryan D Spangler, Caitlin N Suire, Simonetta Camandola, Robert H LipskyAbstract:Bhlhe40 is a transcription factor that is highly expressed in the hippocampus; however, its role in Neuronal function is not well understood. Here, we used Bhlhe40 null mice on a congenic C57Bl6/J background (Bhlhe40 KO) to investigate the impact of Bhlhe40 on Neuronal Excitability and synaptic plasticity in the hippocampus. Bhlhe40 KO CA1 neurons had increased miniature excitatory post-synaptic current amplitude and decreased inhibitory post-synaptic current amplitude, indicating CA1 Neuronal hyperExcitability. Increased CA1 Neuronal Excitability was not associated with increased seizure severity as Bhlhe40 KO relative to +/+ (WT) control mice injected with the convulsant kainic acid. However, significant reductions in long term potentiation and long term depression at CA1 synapses were observed in Bhlhe40 KO mice, indicating impaired hippocampal synaptic plasticity. Behavioral testing for spatial learning and memory on the Morris Water Maze (MWM) revealed that while Bhlhe40 KO mice performed similarly to WT controls initially, when the hidden platform was moved to the opposite quadrant Bhlhe40 KO mice showed impairments in relearning, consistent with decreased hippocampal synaptic plasticity. To investigate possible mechanisms for increased Neuronal Excitability and decreased synaptic plasticity, a whole genome mRNA expression profile of Bhlhe40 KO hippocampus was performed followed by a chromatin immunoprecipitation sequencing (ChIP-Seq) screen of the validated candidate genes for Bhlhe40 protein-DNA interactions consistent with transcriptional regulation. Of the validated genes identified from mRNA expression analysis, insulin degrading enzyme (Ide) had the most significantly altered expression in hippocampus and was significantly downregulated on the RNA and protein levels; although Bhlhe40 did not occupy the Ide gene by ChIP-Seq. Together, these findings support a role for Bhlhe40 in regulating Neuronal Excitability and synaptic plasticity in the hippocampus and that indirect regulation of Ide transcription may be involved in these phenotypes.