96 research outputs found
Synaptic plasticity in medial vestibular nucleus neurons: comparison with computational requirements of VOR adaptation
Background: Vestibulo-ocular reflex (VOR) gain adaptation, a longstanding experimental model of cerebellar learning, utilizes sites of plasticity in both cerebellar cortex and brainstem. However, the mechanisms by which the activity of cortical Purkinje cells may guide synaptic plasticity in brainstem vestibular neurons are unclear. Theoretical analyses indicate that vestibular plasticity should depend upon the correlation between Purkinje cell and vestibular afferent inputs, so that, in gain-down learning for example, increased cortical activity should induce long-term depression (LTD) at vestibular synapses.
Methodology/Principal Findings: Here we expressed this correlational learning rule in its simplest form, as an anti-Hebbian, heterosynaptic spike-timing dependent plasticity interaction between excitatory (vestibular) and inhibitory (floccular) inputs converging on medial vestibular nucleus (MVN) neurons (input-spike-timing dependent plasticity, iSTDP). To test this rule, we stimulated vestibular afferents to evoke EPSCs in rat MVN neurons in vitro. Control EPSC recordings were followed by an induction protocol where membrane hyperpolarizing pulses, mimicking IPSPs evoked by flocculus inputs, were paired with single vestibular nerve stimuli. A robust LTD developed at vestibular synapses when the afferent EPSPs coincided with membrane hyperpolarisation, while EPSPs occurring before or after the simulated IPSPs induced no lasting change. Furthermore, the iSTDP rule also successfully predicted the effects of a complex protocol using EPSP trains designed to mimic classical conditioning.
Conclusions: These results, in strong support of theoretical predictions, suggest that the cerebellum alters the strength of vestibular synapses on MVN neurons through hetero-synaptic, anti-Hebbian iSTDP. Since the iSTDP rule does not depend on post-synaptic firing, it suggests a possible mechanism for VOR adaptation without compromising gaze-holding and VOR performance in vivo
Cerebellar Motor Learning: When Is Cortical Plasticity Not Enough?
Classical Marr-Albus theories of cerebellar learning employ only cortical sites of plasticity. However, tests of these theories using adaptive calibration of the vestibuloβocular reflex (VOR) have indicated plasticity in both cerebellar cortex and the brainstem. To resolve this long-standing conflict, we attempted to identify the computational role of the brainstem site, by using an adaptive filter version of the cerebellar microcircuit to model VOR calibration for changes in the oculomotor plant. With only cortical plasticity, introducing a realistic delay in the retinal-slip error signal of 100 ms prevented learning at frequencies higher than 2.5 Hz, although the VOR itself is accurate up to at least 25 Hz. However, the introduction of an additional brainstem site of plasticity, driven by the correlation between cerebellar and vestibular inputs, overcame the 2.5 Hz limitation and allowed learning of accurate high-frequency gains. This βcortex-firstβ learning mechanism is consistent with a wide variety of evidence concerning the role of the flocculus in VOR calibration, and complements rather than replaces the previously proposed βbrainstem-firstβ mechanism that operates when ocular tracking mechanisms are effective. These results (i) describe a process whereby information originally learnt in one area of the brain (cerebellar cortex) can be transferred and expressed in another (brainstem), and (ii) indicate for the first time why a brainstem site of plasticity is actually required by Marr-Albus type models when high-frequency gains must be learned in the presence of error delay
Fine-Tuning and the Stability of Recurrent Neural Networks
A central criticism of standard theoretical approaches to constructing stable, recurrent model networks is that the synaptic connection weights need to be finely-tuned. This criticism is severe because proposed rules for learning these weights have been shown to have various limitations to their biological plausibility. Hence it is unlikely that such rules are used to continuously fine-tune the network in vivo. We describe a learning rule that is able to tune synaptic weights in a biologically plausible manner. We demonstrate and test this rule in the context of the oculomotor integrator, showing that only known neural signals are needed to tune the weights. We demonstrate that the rule appropriately accounts for a wide variety of experimental results, and is robust under several kinds of perturbation. Furthermore, we show that the rule is able to achieve stability as good as or better than that provided by the linearly optimal weights often used in recurrent models of the integrator. Finally, we discuss how this rule can be generalized to tune a wide variety of recurrent attractor networks, such as those found in head direction and path integration systems, suggesting that it may be used to tune a wide variety of stable neural systems
Learning the Optimal Control of Coordinated Eye and Head Movements
Various optimality principles have been proposed to explain the characteristics of coordinated eye and head movements during visual orienting behavior. At the same time, researchers have suggested several neural models to underly the generation of saccades, but these do not include online learning as a mechanism of optimization. Here, we suggest an open-loop neural controller with a local adaptation mechanism that minimizes a proposed cost function. Simulations show that the characteristics of coordinated eye and head movements generated by this model match the experimental data in many aspects, including the relationship between amplitude, duration and peak velocity in head-restrained and the relative contribution of eye and head to the total gaze shift in head-free conditions. Our model is a first step towards bringing together an optimality principle and an incremental local learning mechanism into a unified control scheme for coordinated eye and head movements
'VOR' - an interactive iPad model of the combined angular and linear vestibulo-ocular reflex
The mammalian vestibular system consists of a series of sensory organs located in the labyrinths of the inner ear that are sensitive to angular and linear movements of the head. Afferent inputs from the vestibular end organs contribute to balance, proprioception and vision. The vestibulo-ocular reflex (VOR) driven by these sensory inputs produces oculomotor responses in a direction opposite to head movement which tend to stabilise visual images on the retina. We present a model, in the form of a software application called VOR, which represents a simplified view of this complex system. The basis for our model is the hypothesis that afferent vestibular signals are integrated to maintain a notional internal representation of the head position (RHP). The vestibulo-ocular reflex maintains gaze towards a world-fixed point relative to the RHP, regardless of the actual head position. The RHP will imperfectly match the real head position when end organ input imperfectly reports head movements, such as can occur in cases of organ dysfunction and even in healthy subjects due to adaptation to motion stimuli. We do not claim that any specific observable part of the real vestibulo-ocular system corresponds to the RHP, but it seems reasonable to suggest that it might exist as a literal "neural network", trained through evolution and experience to maintain gaze during head movement. We hypothesise that the real VOR is supported by this internal representation, continually updated by afferent signals from the vestibular end organs, and that VOR eye responses tend to direct the eyes towards a fixed point in the world. Human vestibulo-ocular research typically employs equipment to which a subject is securely attached and allows rotation around, and sometimes linear movement along, one or more axes ("rotating chair") while attempting to maintain gaze on a fixation point, fixed relative to the head or world. A series of consecutive movements are referred to as a "motion profile". Meanwhile eye movements are recorded, using scleral search coils (or, more recently, video cameras and image-processing software) which can detect the horizontal, vertical and torsional components of the direction of each eye. VOR allows the user to define motion profiles and predicts the eye movements that a researcher or clinician might expect to observe in a real subject during such motion profiles. For example, the "on-centre rotation" motion profile specifies that the subject's head is positioned upright and centred around the vertical axis of the rotating chair, with a chair-fixed fixation point 1m in front of the subject. The chair accelerates angularly to 200Β°/sec over 20 seconds, rotates at a constant 200Β°/sec for 60 seconds, then decelerates to stationary over 20 seconds. The model accurately predicts the transient nystagmus that would be expected: its direction, duration, phase velocity and even the brief secondary nystagmus which is characteristic of adaptation to constant velocity rotation. VOR also allows the user to define end organ condition configurations, e.g. "normal", "bilateral vestibular loss", "unilateral superior neuritis", which are represented as a series of response gains attached to the sensory inputs from each end organ, relative to a nominal perfect gain of 1, and various other parameters which are derived from the human vestibular system, including the rate of drift of gaze to fixation point in light and dark, the rate at which the end organs adapt to constant stimuli, and quick-phase trigger dependencies. The VOR is not the only source of eye movement while attempting to maintain gaze on a fixation point. In our model, eye position drifts towards the fixation point at a nominal fixed rate. If this slow drift is insufficient to maintain gaze on the fixation point, a saccade or quick phase is triggered. Hence the transduction of mechanical forces at the labyrinths into sensory signals, subject to end organ conditions and adaptation that reduce the strength of the neuronal signals, maintain the RHP. Eye movement is then determined entirely by (a) the direction from RHP to the (world-referenced) fixation point, and (b) the disparity between eye direction and actual fixation point (which may be head-referenced). To validate the model, we prepared 24 motion profile/end organ condition combinations, compared the outputs from our model with real world observations, and found the results to be similar. Similarities include a simple first approximation of the linear and angular VOR; nystagmus caused by a subject's attempts to maintain fixation on a head-referenced target during head movement; decay of nystagmus through adaptation to stimulus, including secondary nystagmus; indefinitely prolonged nystagmus during off-vertical axis rotation (OVAR); rapid decay of nystagmus during the "tilt dump" motion profile, and dynamic cyclovergence during vertical linear acceleration. VOR is programmed in Objective-C using Xcode and runs on the Apple iPad. Its screen displays a 3d graphical representation of the virtual subject's head and eyes, including imaginary lines of sight to clarify eye movements. The user may program an effectively unlimited series of linear and angular motions of the rotating chair, and of the virtual subject's head relative to the chair. They may also program the gain (roughly, the sensitivity) associated with each end organ and other variables relating to the subject. They may select a series of internal variables to chart during the motion profile such as head velocity, eye direction, neuron firing rates, etc., while simultaneously displaying the head and eyes. VOR can record a video screen capture of the virtual head, eyes and lines of sight during the execution of a motion profile, a CSV file containing the internal variables at each time interval, a PNG image of the labelled chart, PDF descriptions of the motion profile and end organ condition configurations, and data files defining the motion profiles and end organ conditions which can then be exchanged between researchers/clinicians. Predefined motion profiles include: lateral, LARP and RALP head impulses; lateral head impulse with close fixation point; sinusoidal yaw, on-centre rotation, linear heave along Y axis, linear oscillation along X, Y and Z axes; linear sled along Y axis; forward- and backward-facing centrifugation; off-vertical axis rotation; tilt dump; and head tilt. Predefined conditions include: normal; left unilateral vestibular loss; bilateral vestibular loss; left superior neuritis; and "perfect" (unrealistic gain of 1 in otoliths, producing perfect linear VOR). All of these motion profiles and conditions may easily be modified, created and shared
'VOR' - an interactive iPad model of the combined angular and linear vestibulo-ocular reflex
The mammalian vestibular system consists of a series of sensory organs located in the labyrinths of the inner ear that are sensitive to angular and linear movements of the head. Afferent inputs from the vestibular end organs contribute to balance, proprioception and vision. The vestibulo-ocular reflex (VOR) driven by these sensory inputs produces oculomotor responses in a direction opposite to head movement which tend to stabilise visual images on the retina. We present a model, in the form of a software application called VOR, which represents a simplified view of this complex system. The basis for our model is the hypothesis that afferent vestibular signals are integrated to maintain a notional internal representation of the head position (RHP). The vestibulo-ocular reflex maintains gaze towards a world-fixed point relative to the RHP, regardless of the actual head position. The RHP will imperfectly match the real head position when end organ input imperfectly reports head movements, such as can occur in cases of organ dysfunction and even in healthy subjects due to adaptation to motion stimuli. We do not claim that any specific observable part of the real vestibulo-ocular system corresponds to the RHP, but it seems reasonable to suggest that it might exist as a literal "neural network", trained through evolution and experience to maintain gaze during head movement. We hypothesise that the real VOR is supported by this internal representation, continually updated by afferent signals from the vestibular end organs, and that VOR eye responses tend to direct the eyes towards a fixed point in the world. Human vestibulo-ocular research typically employs equipment to which a subject is securely attached and allows rotation around, and sometimes linear movement along, one or more axes ("rotating chair") while attempting to maintain gaze on a fixation point, fixed relative to the head or world. A series of consecutive movements are referred to as a "motion profile". Meanwhile eye movements are recorded, using scleral search coils (or, more recently, video cameras and image-processing software) which can detect the horizontal, vertical and torsional components of the direction of each eye. VOR allows the user to define motion profiles and predicts the eye movements that a researcher or clinician might expect to observe in a real subject during such motion profiles. For example, the "on-centre rotation" motion profile specifies that the subject's head is positioned upright and centred around the vertical axis of the rotating chair, with a chair-fixed fixation point 1m in front of the subject. The chair accelerates angularly to 200Β°/sec over 20 seconds, rotates at a constant 200Β°/sec for 60 seconds, then decelerates to stationary over 20 seconds. The model accurately predicts the transient nystagmus that would be expected: its direction, duration, phase velocity and even the brief secondary nystagmus which is characteristic of adaptation to constant velocity rotation. VOR also allows the user to define end organ condition configurations, e.g. "normal", "bilateral vestibular loss", "unilateral superior neuritis", which are represented as a series of response gains attached to the sensory inputs from each end organ, relative to a nominal perfect gain of 1, and various other parameters which are derived from the human vestibular system, including the rate of drift of gaze to fixation point in light and dark, the rate at which the end organs adapt to constant stimuli, and quick-phase trigger dependencies. The VOR is not the only source of eye movement while attempting to maintain gaze on a fixation point. In our model, eye position drifts towards the fixation point at a nominal fixed rate. If this slow drift is insufficient to maintain gaze on the fixation point, a saccade or quick phase is triggered. Hence the transduction of mechanical forces at the labyrinths into sensory signals, subject to end organ conditions and adaptation that reduce the strength of the neuronal signals, maintain the RHP. Eye movement is then determined entirely by (a) the direction from RHP to the (world-referenced) fixation point, and (b) the disparity between eye direction and actual fixation point (which may be head-referenced). To validate the model, we prepared 24 motion profile/end organ condition combinations, compared the outputs from our model with real world observations, and found the results to be similar. Similarities include a simple first approximation of the linear and angular VOR; nystagmus caused by a subject's attempts to maintain fixation on a head-referenced target during head movement; decay of nystagmus through adaptation to stimulus, including secondary nystagmus; indefinitely prolonged nystagmus during off-vertical axis rotation (OVAR); rapid decay of nystagmus during the "tilt dump" motion profile, and dynamic cyclovergence during vertical linear acceleration. VOR is programmed in Objective-C using Xcode and runs on the Apple iPad. Its screen displays a 3d graphical representation of the virtual subject's head and eyes, including imaginary lines of sight to clarify eye movements. The user may program an effectively unlimited series of linear and angular motions of the rotating chair, and of the virtual subject's head relative to the chair. They may also program the gain (roughly, the sensitivity) associated with each end organ and other variables relating to the subject. They may select a series of internal variables to chart during the motion profile such as head velocity, eye direction, neuron firing rates, etc., while simultaneously displaying the head and eyes. VOR can record a video screen capture of the virtual head, eyes and lines of sight during the execution of a motion profile, a CSV file containing the internal variables at each time interval, a PNG image of the labelled chart, PDF descriptions of the motion profile and end organ condition configurations, and data files defining the motion profiles and end organ conditions which can then be exchanged between researchers/clinicians. Predefined motion profiles include: lateral, LARP and RALP head impulses; lateral head impulse with close fixation point; sinusoidal yaw, on-centre rotation, linear heave along Y axis, linear oscillation along X, Y and Z axes; linear sled along Y axis; forward- and backward-facing centrifugation; off-vertical axis rotation; tilt dump; and head tilt. Predefined conditions include: normal; left unilateral vestibular loss; bilateral vestibular loss; left superior neuritis; and "perfect" (unrealistic gain of 1 in otoliths, producing perfect linear VOR). All of these motion profiles and conditions may easily be modified, created and shared
Active Vision for Scene Understanding
Visual perception is one of the most important sources of information for both humans and robots. A particular challenge is the acquisition and interpretation of complex unstructured scenes. This work contributes to active vision for humanoid robots. A semantic model of the scene is created, which is extended by successively changing the robot\u27s view in order to explore interaction possibilities of the scene
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Όλ¬Έ (λ°μ¬)-- μμΈλνκ΅ λνμ : μκ³Όλν μκ³Όνκ³Ό, 2019. 2. κΉμμ .Learning rule has been thought to be implemented by activity-dependent modifications of synaptic function and neuronal excitability which contributing to maximization the information flow in the neural network. Since the sensory information is conveyed by forms of action potential (AP) firing, the plasticity of the intrinsic excitability (intrinsic plasticity) has been highlighted the computational feature of the brain. Given the cerebellar Purkinje cells (PCs) is the sole output neurons in the cerebellar cortex, coordination of the synaptic plasticity at the parallel fiber (PF) to PC synapses including long-term depression (LTD) and long-term potentiation (LTP) but also the intrinsic plasticity may play a essential role in information processing in the cerebellum. In this Dissertation, I have investigated several features of intrinsic plasticity in the cerebellar PCs in an activity-dependent manner and their cellular mechanism. Furthermore, the functional implications of the intrinsic plasticity in the cerebellum-dependent behavioral output are discussed. Firstly, I first cover the ion channels regulating the spiking activity of the cerebellar PCs and the cellular mechanisms of the plastic changes in excitability. Various ion channels indeed harmonize the cellular activity and shaping the optimal ranges of the neuronal excitability. Among the ion channels expressed in the cerebellar PCs, hyperpolarization-activated cyclic nucleotide-gated (HCN) channels contribute to the non-Hebbian homeostatic intrinsic plasticity in the cerebellar PCs. Chronic activity-deprivation of PC activity caused the upregulation of agonist-independent activity of type 1 metabotropic glutamate receptor (mGluR1). The increased mGluR1 activity consequently enhanced the HCN channel current density through protein kinase A (PKA) pathway thereby downregulation of intrinsic excitability in PCs. In addition, the intrinsic excitability of PCs is found to be modulated by synaptic activity. Of interest, I investigated that the PF-PC LTD is accompanied by LTD of intrinsic excitability (LTD-IE). The LTD-IE indeed shared intracellular signal cascade for governing the synaptic LTD such as large amount of Ca2+ influx, mGluR1, protein kinase C (PKC) and Ca2+-calmodulin-dependent protein kinase II (CaMKII) activation. Interestingly, the LTD-IE reduced PC spike output without changes in patterns of synaptic integration and spike generation, suggesting that the intrinsic plasticity alters the quantity of information rather than the quality of information processing. In consistent, the LTD-IE was shown in the floccular PCs when the PF-PC LTD occurs. Notably, not only the synaptic LTD but also LTD-IE was found to be formed at the conditioned dendritic branch. Thus, synaptic plasticity could significantly affect to the neuronal net output through the synergistic coordination of synaptic and intrinsic plasticity in the dendrosomatic axis of the cerebellar PCs. In conclusion, the activity-dependent modulation of intrinsic excitability may contribute to dynamic tuning of the cerebellar PC output for appropriate signal transduction into the downstream neurons of the cerebellar PCs.μλͺ
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Abstract
General introduction
Chapter 1. Summary of the previous literatures and further implication for physiological significance of the intrinsic plasticity in the cerebellar Purkinje cells
Summary.
1.1 Ion channels and spiking activity of the cerebellar Purkinje cells
1.1.1 Voltage-gated Na+ channels
1.1.2 Voltage-gated K+ channels and Ca2+-activated K+ channels
1.2 Activity-dependent plasticity of intrinsic excitability through ion channel modulation
1.2.1 Activity-dependent plasticity of intrinsic. excitability through ion channel
1.2.2 Possible mechanisms for LTD-IE.
1.2.3 Upside down: to what extent does bidirectional intrinsic plasticity in. the cerebellar dependent-motor learning do?
1.3 The further implication of intrinsic plasticity in the memory circuits.
Chapter 2. Type 1 metabotropic glutamate receptor mediates homeostatic control of intrinsic excitability through hyperpolarization-activated current in cerebellar Purkinje cells
Introduction
Material and Method
Results
2.1 Chronic activity-deprivation reduces intrinsic excitability of the
cerebellar. Purkinje cells 35
2.2 Homeostatic intrinsic plasticity of the cerebellar Purkinje cells is mediated activity-dependent modulation of Ih
2.3 Homeostatic intrinsic plasticity of the cerebellar Purkinje cells requires agonist-independent action of mGluR1
2.4 Homeostatic intrinsic plasticity of the cerebellar Purkinje cells is mediated. PKA activity
Discussion
Chapter 3. Long-Term Depression of Intrinsic Excitability Accompanied by Synaptic Depression in Cerebellar Purkinje Cells
Introduction
Material and Method
Results
3.1 LTD of intrinsic excitability of PC accompanied by PF-PC LTD
3.2 LTD-IE has different developing kinetics from synaptic LTD
3.3 LTD-IE was not reversed by subsequent LTP-IE induction
3.4 The number of recruited synapses were not correlated to the magnitude of the neuronal
3.5 Information processing after LTD induction LTD-IE was not. reversed by subsequent LTP-IE induction
3.6 LTD-IE required the Ca2+-signal but not depended on the Ca2+-activated K+ channels
Discussion
Chapter 4. Synergies between synaptic depression and intrinsic plasticity of the cerebellar Purkinje cells determining the Purkinje cell output
Introduction
Material and Method
Restuls
4.1 Timing rules of intrinsic plasticity of floccular PCs 87
4.2 Intrinsic plasticity shares intracellular signaling for PF-PC LTD
4.3 Conditioned PF branches contributing to robust reduction of spike output of the PCs
4.4 Sufficient changes in spiking output require both of plasticity, synaptic and. intrinsic plasticity
4.5 Supralinearity of spiking output coordination after induction of PC plasticity
Discussion
Bibliography
Abstract in Korean
AcknowledgementDocto
Implementation of a line attractor-based model of the gaze holding integrator using nonlinear spiking neuron models
Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 1996.Includes bibliographical references (leaves 30-31).by Ben Y. Reis.M.Eng
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