ADAPTIVE CEREBELLAR SPIKING MODEL EMBEDDED IN THE CONTROL LOOP: CONTEXT SWITCHING AND ROBUSTNESS AGAINST NOISE

2011 ◽  
Vol 21 (05) ◽  
pp. 385-401 ◽  
Author(s):  
N. R. LUQUE ◽  
J. A. GARRIDO ◽  
R. R. CARRILLO ◽  
S. TOLU ◽  
E. ROS
Keyword(s):  
Degrees Of Freedom ◽  
Mossy Fibers ◽  
Long Term Potentiation ◽  
Biologically Inspired ◽  
Context Switching ◽  
Term Potentiation ◽  
Spiking Network ◽  
Three Degrees Of Freedom ◽  
Spiking Model

This work evaluates the capability of a spiking cerebellar model embedded in different loop architectures (recurrent, forward, and forward&recurrent) to control a robotic arm (three degrees of freedom) using a biologically-inspired approach. The implemented spiking network relies on synaptic plasticity (long-term potentiation and long-term depression) to adapt and cope with perturbations in the manipulation scenario: changes in dynamics and kinematics of the simulated robot. Furthermore, the effect of several degrees of noise in the cerebellar input pathway (mossy fibers) was assessed depending on the employed control architecture. The implemented cerebellar model managed to adapt in the three control architectures to different dynamics and kinematics providing corrective actions for more accurate movements. According to the obtained results, coupling both control architectures (forward&recurrent) provides benefits of the two of them and leads to a higher robustness against noise.

Effect of tolbutamide on tetraethylammonium-induced postsynaptic zinc signals at hippocampal mossy fiber-CA3 synapses

2017 ◽  
Vol 95 (9) ◽  
pp. 1058-1063 ◽  
Author(s):  
Fatima C. Bastos ◽  
Vanessa N. Corceiro ◽  
Sandra A. Lopes ◽  
José G. de Almeida ◽  
Carlos M. Matias ◽  
...  
Keyword(s):  
Mossy Fiber ◽  
Mossy Fibers ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Chemical Stimulation ◽  
Term Potentiation ◽  
Voltage Dependent ◽  
Zinc Release ◽  
Ca3 Pyramidal Cells

The application of tetraethylammonium (TEA), a blocker of voltage-dependent potassium channels, can induce long-term potentiation (LTP) in the synaptic systems CA3–CA1 and mossy fiber-CA3 pyramidal cells of the hippocampus. In the mossy fibers, the depolarization evoked by extracellular TEA induces a large amount of glutamate and also of zinc release. It is considered that zinc has a neuromodulatory role at the mossy fiber synapses, which can, at least in part, be due to the activation of presynaptic ATP-dependent potassium (KATP) channels. The aim of this work was to study properties of TEA-induced zinc signals, detected at the mossy fiber region, using the permeant form of the zinc indicator Newport Green. The application of TEA caused a depression of those signals that was partially blocked by the KATP channel inhibitor tolbutamide. After the removal of TEA, the signals usually increased to a level above baseline. These results are in agreement with the idea that intense zinc release during strong synaptic events triggers a negative feedback action. The zinc depression, caused by the LTP-evoking chemical stimulation, turns into potentiation after TEA washout, suggesting the existence of a correspondence between the observed zinc potentiation and TEA-evoked mossy fiber LTP.

Rapid Translocation of Zn2+ From Presynaptic Terminals Into Postsynaptic Hippocampal Neurons After Physiological Stimulation

2001 ◽  
Vol 86 (5) ◽  
pp. 2597-2604 ◽  
Author(s):  
Yang Li ◽  
Christopher J. Hough ◽  
Sang Won Suh ◽  
John M. Sarvey ◽  
Christopher J. Frederickson
Keyword(s):  
Hippocampal Neurons ◽  
Hippocampal Slices ◽  
Mossy Fibers ◽  
Synaptic Cleft ◽  
Immediate Release ◽  
Long Term Potentiation ◽  
Anatomical Location ◽  
Term Potentiation ◽  
Presynaptic Boutons

Zn2+ is found in glutamatergic nerve terminals throughout the mammalian forebrain and has diverse extracellular and intracellular actions. The anatomical location and possible synaptic signaling role for this cation have led to the hypothesis that Zn2+ is released from presynaptic boutons, traverses the synaptic cleft, and enters postsynaptic neurons. However, these events have not been directly observed or characterized. Here we show, using microfluorescence imaging in rat hippocampal slices, that brief trains of electrical stimulation of mossy fibers caused immediate release of Zn2+ from synaptic terminals into the extracellular microenvironment. Release was induced across a broad range of stimulus intensities and frequencies, including those likely to induce long-term potentiation. The amount of Zn2+ release was dependent on stimulation frequency (1–200 Hz) and intensity. Release of Zn2+ required sodium-dependent action potentials and was dependent on extracellular Ca2+. Once released, Zn2+ crosses the synaptic cleft and enters postsynaptic neurons, producing increases in intracellular Zn2+ concentration. These results indicate that, like a neurotransmitter, Zn2+ is stored in synaptic vesicles and is released into the synaptic cleft. However, unlike conventional transmitters, it also enters postsynaptic neurons, where it may have manifold physiological functions as an intracellular second messenger.

scholarly journals Fast and flexible sequence induction in spiking neural networks via rapid excitability changes

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Rich Pang ◽  
Adrienne L Fairhall
Keyword(s):  
Neural Networks ◽  
Cognitive Flexibility ◽  
Long Term Potentiation ◽  
Spiking Neural Networks ◽  
Intrinsic Excitability ◽  
Stimulus Response ◽  
Term Potentiation ◽  
Spiking Network ◽  
Sequence Induction

Cognitive flexibility likely depends on modulation of the dynamics underlying how biological neural networks process information. While dynamics can be reshaped by gradually modifying connectivity, less is known about mechanisms operating on faster timescales. A compelling entrypoint to this problem is the observation that exploratory behaviors can rapidly cause selective hippocampal sequences to ‘replay’ during rest. Using a spiking network model, we asked whether simplified replay could arise from three biological components: fixed recurrent connectivity; stochastic ‘gating’ inputs; and rapid gating input scaling via long-term potentiation of intrinsic excitability (LTP-IE). Indeed, these enabled both forward and reverse replay of recent sensorimotor-evoked sequences, despite unchanged recurrent weights. LTP-IE ‘tags’ specific neurons with increased spiking probability under gating input, and ordering is reconstructed from recurrent connectivity. We further show how LTP-IE can implement temporary stimulus-response mappings. This elucidates a novel combination of mechanisms that might play a role in rapid cognitive flexibility.

scholarly journals Enhancements in mossy fibers long‐term potentiation (LTP) are neurotrophin‐specific.

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Esther Angelica Jimenez‐Nunez ◽  
Kenira Thompson ◽  
James Porter
Keyword(s):  
Mossy Fibers ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Pathophysiology of Cerebellar Tremor: The Forward Model-Related Tremor and the Inferior Olive Oscillation-Related Tremor

2021 ◽  
Vol 12 ◽  
Author(s):  
Shinji Kakei ◽  
Mario Manto ◽  
Hirokazu Tanaka ◽  
Hiroshi Mitoma
Keyword(s):  
Degrees Of Freedom ◽  
Inferior Olive ◽  
Red Nucleus ◽  
Distinct Type ◽  
Long Term Potentiation ◽  
Cerebellar Nuclei ◽  
Forward Model ◽  
Term Potentiation ◽  
Generation Mechanisms

Lesions in the Guillain–Mollaret (G–M) triangle frequently cause various types of tremors or tremor-like movements. Nevertheless, we know relatively little about their generation mechanisms. The deep cerebellar nuclei (DCN), which is a primary node of the triangle, has two main output paths: the primary excitatory path to the thalamus, the red nucleus (RN), and other brain stem nuclei, and the secondary inhibitory path to the inferior olive (IO). The inhibitory path contributes to the dentato-olivo-cerebellar loop (the short loop), while the excitatory path contributes to the cerebrocerebellar loop (the long loop). We propose a novel hypothesis: each loop contributes to physiologically distinct type of tremors or tremor-like movements. One type of irregular tremor-like movement is caused by a lesion in the cerebrocerebellar loop, which includes the primary path. A lesion in this loop affects the cerebellar forward model and deteriorates its accuracy of prediction and compensation of the feedback delay, resulting in irregular instability of voluntary motor control, i.e., cerebellar ataxia (CA). Therefore, this type of tremor, such as kinetic tremor, is usually associated with other symptoms of CA such as dysmetria. We call this type of tremor forward model-related tremor. The second type of regular tremor appears to be correlated with synchronized oscillation of IO neurons due, at least in animal models, to reduced degrees of freedom in IO activities. The regular burst activity of IO neurons is precisely transmitted along the cerebellocerebral path to the motor cortex before inducing rhythmical reciprocal activities of agonists and antagonists, i.e., tremor. We call this type of tremor IO-oscillation-related tremor. Although this type of regular tremor does not necessarily accompany ataxia, the aberrant IO activities (i.e., aberrant CS activities) may induce secondary maladaptation of cerebellar forward models through aberrant patterns of long-term depression (LTD) and/or long-term potentiation (LTP) of the cerebellar circuitry. Although our hypothesis does not cover all tremors or tremor-like movement disorders, our approach integrates the latest theories of cerebellar physiology and provides explanations how various lesions in or around the G–M triangle results in tremors or tremor-like movements. We propose that tremor results from errors in predictions carried out by the cerebellar circuitry.

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