The Experts below are selected from a list of 32199 Experts worldwide ranked by ideXlab platform
David M. Halliday - One of the best experts on this subject based on the ideXlab platform.
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Axial current reversal promotes synchronous correlation between dendritic membrane potentials during large-scale Synaptic Input
Neurocomputing, 2004Co-Authors: M. Griffin, David M. HallidayAbstract:Abstract We report two results from a simulation study of spatial temporal interactions in a dendritic tree during large-scale Synaptic Input. The first is a feedback mechanism following individual Synaptic Inputs, which results in a reversal of the axial current 1– 2 ms after activation of an Input. The second is a time domain transfer function analysis between the membrane potential fluctuations at different sites. During large-scale Synaptic Input, this has a symmetrical structure, indicative of a two-way flow of axial current in the dendritic tree. We interpret this as an indication of a synchronous correlation structure between membrane potential fluctuations during large-scale Synaptic Input, which may have implications for our understanding of Synaptic integration.
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Weak, Stochastic Temporal Correlation of Large-Scale Synaptic Input Is a Major Determinant of Neuronal Bandwidth
Neural computation, 2000Co-Authors: David M. HallidayAbstract:We determine the bandwidth of a model neurone to large-scale Synaptic Input by assessing the frequency response between the outputs of a two-cell simulation that share a percentage of the total Synaptic Input. For temporally uncorrelated Inputs, a large percentage of common Inputs are required before the output discharges of the two cells exhibit significant correlation. In contrast, a small percentage (5%) of the total Synaptic Input that involves stochastic spike trains that are weakly correlated over a broad range of frequencies exert a clear influence on the output discharge of both cells over this range of frequencies. Inputs that are weakly correlated at a single frequency induce correlation between the output discharges only at the frequency of correlation. The strength of temporal correlation required is sufficiently weak that analysis of a sample pair of Input spike trains could fail to reveal the presence of correlated Input. Weak temporal correlation between Inputs is therefore a major determinant of the transmission to the output discharge of frequencies present in the spike discharges of preSynaptic Inputs, and therefore of neural bandwidth.
Eunjoon Kim - One of the best experts on this subject based on the ideXlab platform.
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Data_Sheet_2_GABA Neuronal Deletion of Shank3 Exons 14–16 in Mice Suppresses Striatal Excitatory Synaptic Input and Induces Social and Locomotor Abnormalities.PDF
2018Co-Authors: Taesun Yoo, Heejin Cho, Jiseok Lee, Haram Park, Ye-eun Yoo, Esther Yang, Jin Yong Kim, Hyun Kim, Eunjoon KimAbstract:Shank3 is an excitatory postSynaptic scaffolding protein implicated in multiple brain disorders, including autism spectrum disorders (ASD) and Phelan-McDermid syndrome (PMS). Although previous neurobiological studies on Shank3 and Shank3-mutant mice have revealed diverse roles of Shank3 in the regulation of Synaptic, neuronal and brain functions, whether Shank3 expression in specific cell types distinctly contributes to mouse phenotypes remains largely unclear. In the present study, we generated two Shank3-mutant mouse lines (exons 14–16) carrying global and GABA neuron-specific deletions and characterized their electrophysiological and behavioral phenotypes. These mouse lines show similar decreases in excitatory Synaptic Input onto dorsolateral striatal neurons. In addition, the abnormal social and locomotor behaviors observed in global Shank3-mutant mice are strongly mimicked by GABA neuron-specific Shank3-mutant mice, whereas the repetitive and anxiety-like behaviors are only partially mimicked. These results suggest that GABAergic Shank3 (exons 14–16) deletion has strong influences on striatal excitatory Synaptic transmission and social and locomotor behaviors in mice.
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GABA Neuronal Deletion of Shank3 Exons 14–16 in Mice Suppresses Striatal Excitatory Synaptic Input and Induces Social and Locomotor Abnormalities
Frontiers Media S.A., 2018Co-Authors: Taesun Yoo, Heejin Cho, Jiseok Lee, Haram Park, Ye-eun Yoo, Esther Yang, Jin Yong Kim, Hyun Kim, Eunjoon KimAbstract:Shank3 is an excitatory postSynaptic scaffolding protein implicated in multiple brain disorders, including autism spectrum disorders (ASD) and Phelan-McDermid syndrome (PMS). Although previous neurobiological studies on Shank3 and Shank3-mutant mice have revealed diverse roles of Shank3 in the regulation of Synaptic, neuronal and brain functions, whether Shank3 expression in specific cell types distinctly contributes to mouse phenotypes remains largely unclear. In the present study, we generated two Shank3-mutant mouse lines (exons 14–16) carrying global and GABA neuron-specific deletions and characterized their electrophysiological and behavioral phenotypes. These mouse lines show similar decreases in excitatory Synaptic Input onto dorsolateral striatal neurons. In addition, the abnormal social and locomotor behaviors observed in global Shank3-mutant mice are strongly mimicked by GABA neuron-specific Shank3-mutant mice, whereas the repetitive and anxiety-like behaviors are only partially mimicked. These results suggest that GABAergic Shank3 (exons 14–16) deletion has strong influences on striatal excitatory Synaptic transmission and social and locomotor behaviors in mice
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GABA neuronal deletion of Shank3 exons 14-16 in mice suppresses striatal excitatory Synaptic Input and induces social and locomotor abnormalities
'Frontiers Media SA', 2018Co-Authors: Taesun Yoo, Heejin Cho, Jiseok Lee, Haram Park, Ye-eun Yoo, Esther Yang, Jin Yong Kim, Hyun Kim, Eunjoon KimAbstract:Shank3 is an excitatory postSynaptic scaffolding protein implicated in multiple brain disorders, including autism spectrum disorders (ASD) and Phelan-McDermid syndrome (PMS). Although previous neurobiological studies on Shank3 and Shank3-mutant mice have revealed diverse roles of Shank3 in the regulation of Synaptic, neuronal and brain functions, whether Shank3 expression in specific cell types distinctly contributes to mouse phenotypes remains largely unclear. In the present study, we generated two Shank3-mutant mouse lines (exons 14?16) carrying global and GABA neuron-specific deletions and characterized their electrophysiological and behavioral phenotypes. These mouse lines show similar decreases in excitatory Synaptic Input onto dorsolateral striatal neurons. In addition, the abnormal social and locomotor behaviors observed in global Shank3-mutant mice are strongly mimicked by GABA neuron-specific Shank3-mutant mice, whereas the repetitive and anxiety-like behaviors are only partially mimicked. These results suggest that GABAergic Shank3 (exons 14?16) deletion has strong influences on striatal excitatory Synaptic transmission and social and locomotor behaviors in mice. (c) 2018 Yoo, Cho, Lee, Park, Yoo, Yang, Kim, Kim and Ki
Upinder S Bhalla - One of the best experts on this subject based on the ideXlab platform.
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Synaptic Input sequence discrimination on behavioral timescales mediated by reaction diffusion chemistry in dendrites
eLife, 2017Co-Authors: Upinder S BhallaAbstract:Sequences of events are ubiquitous in sensory, motor, and cognitive function. Key computational operations, including pattern recognition, event prediction, and plasticity, involve neural discrimination of spatio-temporal sequences. Here, we show that Synaptically-driven reaction-diffusion pathways on dendrites can perform sequence discrimination on behaviorally relevant time-scales. We used abstract signaling models to show that selectivity arises when Inputs at successive locations are aligned with, and amplified by, propagating chemical waves triggered by previous Inputs. We incorporated biological detail using sequential Synaptic Input onto spines in morphologically, electrically, and chemically detailed pyramidal neuronal models based on rat data. Again, sequences were recognized, and local channel modulation downstream of putative sequence-triggered signaling could elicit changes in neuronal firing. We predict that dendritic sequence-recognition zones occupy 5 to 30 microns and recognize time-intervals of 0.2 to 5 s. We suggest that this mechanism provides highly parallel and selective neural computation in a functionally important time range.
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Synaptic Input sequence discrimination on behavioral time scales mediated by reaction diffusion chemistry in dendrites
bioRxiv, 2017Co-Authors: Upinder S BhallaAbstract:Sequences of events are ubiquitous in sensory, motor, and cognitive function. Key computational operations, including pattern recognition, event prediction, and plasticity, involve neural discrimination of spatio-temporal sequences. Here we show that Synaptically-driven reaction-diffusion pathways on dendrites can perform sequence discrimination on behaviorally relevant time-scales. We used abstract signaling models to show that this selectivity arises when Inputs at successive locations are aligned with, and amplified by, propagating chemical waves triggered by previous Inputs. We incorporated biological detail using sequential Synaptic Input onto spines in morphologically, electrically, and chemically detailed pyramidal neuronal models. Again, sequences were recognized, and local channel modulation on the length-scale of sequence Input could elicit changes in neuronal firing. We predict that dendritic sequence-recognition zones occupy 5 to 20 microns and recognize time-intervals of 0.2 to 5s. We suggest that this mechanism provides highly parallel and selective neural computation in a functionally important time range.
J H Szurszewski - One of the best experts on this subject based on the ideXlab platform.
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Circumferential, not longitudinal, colonic stretch increases Synaptic Input to mouse prevertebral ganglion neurons
American journal of physiology. Gastrointestinal and liver physiology, 2003Co-Authors: Steven M. Miller, J H SzurszewskiAbstract:The relationship between longitudinal and circular muscle tension in the mouse colon and mechanosensory excitatory Synaptic Input to neurons in the superior mesenteric ganglion (SMG) was investigat...
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Relationship between colonic motility and cholinergic mechanosensory afferent Synaptic Input to mouse superior mesenteric ganglion.
Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 2002Co-Authors: Steven M. Miller, J H SzurszewskiAbstract:Abstract Abdominal prevertebral ganglion neurones receive excitatory Synaptic Input from intestinofugal neurones. To better understand the physiological significance of this Input, we examined the relationship between Synaptic Input to mouse superior mesenteric ganglion (SMG) neurones and intracolonic pressure and volume changes that accompany spontaneous colonic contractions in vitro. Electrical activity was recorded intracellularly from SMG neurones in ganglia attached to a segment of distal colon. The majority of neurones examined received ongoing fast excitatory potentials (F-EPSPs). F-EPSP frequency increased when the colon was distended with fluid and during spontaneous increases in colonic volume that accompanied colonic relaxation. In contrast, F-EPSP frequency in SMG neurones decreased when the colon emptied, and remained at a reduced frequency until the colon refilled and volume increased. Nicotinic blockade of the colon abolished spontaneous colonic contractions and reduced or abolished Synaptic Input to SMG neurones, suggesting that most of the Synaptic Input arose from second or higher order neurones. Retrograde labelling identified cell bodies of intestinofugal neurones in myenteric ganglia. Most had short, club-like dendritic processes and appeared uni-axonal. These results show that mechanosensory intestinofugal afferent nerves monitor intracolonic volume changes.
Charles J. Heckman - One of the best experts on this subject based on the ideXlab platform.
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Alterations in Synaptic Input to motoneurons during partial spinal cord injury
Medicine and science in sports and exercise, 1994Co-Authors: Charles J. HeckmanAbstract:An acute animal model (dorsal hemisection of the spinal cord in the decerebrate cat preparation) has been developed that closely mimics the spasticity in humans that occurs subsequent to partial spinal cord injury and hemiparetic stroke. In this animal model, there are severe disruptions in the pattern of recruitment and rate modulation of motoneurons. The cellular mechanisms of these deficits are being studied with a combined experimental/computer simulation approach. The initial studies indicate that changes in the intrinsic properties of motoneurons are not important, which means the mechanism for changes in recruitment and rate patterns must reside in an alteration in the organization of the Synaptic Input to motoneurons. Computer simulation studies of the effects of different Synaptic Inputs on motoneuron outputs show that inhibitory Inputs can, under certain conditions, generate substantial disruptions in recruitment and rate modulation. Recent data indicate that the monoamines noradrenalin and serotonin, which are released by fiber tracts originating in the brainstem, may play an important role in maintaining normal levels of inhibition in spinal circuits. Pharmacological interventions based on the monoamines may provide effective means of reducing the deficits in recruitment and rate modulation.
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Computer simulations of the effects of different Synaptic Input systems on motor unit recruitment
Journal of neurophysiology, 1993Co-Authors: Charles J. Heckman, Marc D. BinderAbstract:1. The effects of four different Synaptic Input systems on the recruitment order within a mammalian motoneuron pool were investigated using computer simulations. The Synaptic Inputs and motor unit ...
