scholarly journals Reversed timing-dependent associative plasticity in the human brain through interhemispheric interactions

2013 ◽  
Vol 109 (9) ◽  
pp. 2260-2271 ◽  
Author(s):  
Virginia Conde ◽  
Henning Vollmann ◽  
Marco Taubert ◽  
Bernhard Sehm ◽  
Leonardo G. Cohen ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Human Brain ◽  
Primary Motor Cortex ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
In Vivo Model ◽  
Sensorimotor Network ◽  
Median Nerve Stimulation

Spike timing-dependent plasticity (STDP) has been proposed as one of the key mechanisms underlying learning and memory. Repetitive median nerve stimulation, followed by transcranial magnetic stimulation (TMS) of the contralateral primary motor cortex (M1), defined as paired-associative stimulation (PAS), has been used as an in vivo model of STDP in humans. PAS-induced excitability changes in M1 have been repeatedly shown to be time-dependent in a STDP-like fashion, since synchronous arrival of inputs within M1 induces long-term potentiation-like effects, whereas an asynchronous arrival induces long-term depression (LTD)-like effects. Here, we show that interhemispheric inhibition of the sensorimotor network during PAS, with the peripheral stimulation over the hand ipsilateral to the motor cortex receiving TMS, results in a LTD-like effect, as opposed to the standard STDP-like effect seen for contralateral PAS. Furthermore, we could show that this reversed-associative plasticity critically depends on the timing interval between afferent and cortical stimulation. These results indicate that the outcome of associative stimulation in the human brain depends on functional network interactions (inhibition or facilitation) at a systems level and can either follow standard or reversed STDP-like mechanisms.

scholarly journals Heat-Evoked Experimental Pain Induces Long-Term Potentiation-Like Plasticity in Human Primary Motor Cortex

2012 ◽  
Vol 23 (8) ◽  
pp. 1942-1951 ◽  
Author(s):  
A. Suppa ◽  
A. Biasiotta ◽  
D. Belvisi ◽  
L. Marsili ◽  
S. La Cesa ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Experimental Pain ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Plasticity of the Cortical Motor System

2008 ◽  
Vol 20 (1) ◽  
pp. 5-22 ◽  
Author(s):  
Bogdan Sadowski
Keyword(s):  
Motor Cortex ◽  
Motor System ◽  
Primary Motor Cortex ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Skill Learning ◽  
Dynamic Features ◽  
Cortical Motor

Plasticity of the Cortical Motor SystemThe involvement of brain plastic mechanisms in the control of motor functions under normal and pathological conditions is described. These mechanisms are based on a similar principle as the neuronal models of neuronal plasticity - long-term potentiation (LTP), and long-term depression (LTD). In the motor cortex, LTP-like phenomena play a role in strengthening synaptic connections between pyramidal neurons. LTD is important for the elimination of unnecessary inputs to the cortex. The dynamic features of the primary motor cortex activity depend on particular neuronal interconnectivity within this area. The pyramidal cells send horizontal collaterals to adjacent subregions of the primary motor cortex, and so can either excite or inhibit remote pyramidal cells. These connections can expand or shrink depending on actual physiological demands, and play a role in skill learning.

Spike Timing-Dependent Plasticity: From Synapse to Perception

2006 ◽  
Vol 86 (3) ◽  
pp. 1033-1048 ◽  
Author(s):  
Yang Dan ◽  
Mu-Ming Poo
Keyword(s):  
Neuronal Excitability ◽  
Human Perception ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Functional Changes

Information in the nervous system may be carried by both the rate and timing of neuronal spikes. Recent findings of spike timing-dependent plasticity (STDP) have fueled the interest in the potential roles of spike timing in processing and storage of information in neural circuits. Induction of long-term potentiation (LTP) and long-term depression (LTD) in a variety of in vitro and in vivo systems has been shown to depend on the temporal order of pre- and postsynaptic spiking. Spike timing-dependent modification of neuronal excitability and dendritic integration was also observed. Such STDP at the synaptic and cellular level is likely to play important roles in activity-induced functional changes in neuronal receptive fields and human perception.

Inducing Homeostatic-Like Plasticity in Human Motor Cortex Through Converging Corticocortical Inputs

2009 ◽  
Vol 102 (6) ◽  
pp. 3180-3190 ◽  
Author(s):  
Monika Pötter-Nerger ◽  
Sarah Fischer ◽  
Claudia Mastroeni ◽  
Sergiu Groppa ◽  
Günther Deuschl ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Median Nerve ◽  
Primary Motor Cortex ◽  
Premotor Cortex ◽  
Long Term Potentiation ◽  
Corticospinal Excitability ◽  
Human Motor Cortex ◽  
Induced Changes ◽  
Homeostatic Response

Transcranial stimulation techniques have revealed homeostatic-like metaplasticity in the hand area of the human primary motor cortex (M1HAND) that controls stimulation-induced changes in corticospinal excitability. Here we combined two interventional protocols that induce long-term depression (LTD)–like or long-term potentiation (LTP)–like plasticity in left M1HAND through different afferents. We hypothesized that the left M1HAND would integrate LTP- and LTD-like plasticity in a homeostatic fashion. In ten healthy volunteers, low-intensity repetitive transcranial magnetic stimulation (rTMS) of the left dorsal premotor cortex (PMD) was first applied to produce an LTP-like increase (5 Hz rTMS) or LTD-like decrease (1 Hz rTMS) in corticospinal excitability in left M1HAND via premotor-to-motor inputs. Following PMD rTMS, paired-associative stimulation (PAS) was applied to the right median nerve and left M1HAND to induce spike-time–dependent plasticity in sensory-to-motor inputs to left M1HAND. We adjusted the interstimulus interval to the N20 latency of the median nerve somatosensory-evoked cortical potential to produce an LTP-like increase (PASN20+2ms) or an LTD-like decrease (PASN20−5ms) in corticospinal excitability. The amplitude of motor-evoked potentials was recorded from intrinsic hand muscles to assess stimulation-induced changes in corticospinal excitability. Premotor-to-motor preconditioning triggered a homeostatic response to subsequent sensory-to-motor PAS. After facilitatory 5 Hz rTMS, “facilitatory” PASN20+2ms suppressed corticospinal excitability. Likewise, “inhibitory” PASN20−5ms facilitated corticospinal excitability after “inhibitory” 1 Hz rTMS. There was a negative linear relationship between the excitability changes induced by PMD rTMS and those elicited by subsequent PAS. Excitability changes were not paralleled by changes in performance during a finger-tapping task. These results provide evidence for a homeostatic response pattern in the human M1HAND that integrates acute plastic changes evoked through different “input channels.”

Skilled Motor Learning Does Not Enhance Long-Term Depression in the Motor Cortex In Vivo

2005 ◽  
Vol 93 (3) ◽  
pp. 1486-1497 ◽  
Author(s):  
Jeremy D. Cohen ◽  
Manuel A. Castro-Alamancos
Keyword(s):  
Neural Networks ◽  
Motor Cortex ◽  
Motor Learning ◽  
Primary Motor Cortex ◽  
Short Term ◽  
Long Term Depression ◽  
Short Term Plasticity ◽  
Horizontal Connections

Learning of motor skills may occur as a consequence of changes in the efficacy of synaptic connections in the primary motor cortex. We investigated if learning in a reaching task affects the excitability, short-term plasticity, and long-term plasticity of horizontal connections in layers II–III of the motor cortex. Because training in this task requires animals to be food-deprived, we compared the trained animals with similarly food-deprived untrained animals and normal controls. The results show that the excitability, short-term plasticity, and long-term plasticity of the studied horizontal connections were unaffected by motor learning. However, stress-related effects produced by food deprivation and handling significantly enhanced the expression of long-term depression in these pathways. These results are compatible with the hypothesis that the acquisition of a complex motor skill produces bi-directional changes in synaptic strength that are distributed throughout the complex neural networks of motor cortex, which remains synaptically balanced during learning. The results are incompatible with the idea that learning causes large unidirectional changes in the population response of these neural networks, which may occur instead during certain behavioral states, such as stress.

scholarly journals Associative spike timing-dependent potentiation of the basal dendritic excitatory synapses in the hippocampus in vivo

2016 ◽  
Vol 115 (6) ◽  
pp. 3264-3274 ◽  
Author(s):  
Thomas K. Fung ◽  
Clayton S. Law ◽  
L. Stan Leung
Keyword(s):  
Current Source ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Stratum Radiatum ◽  
Adult Rats ◽  
Synaptic Excitation ◽  
Stratum Oriens ◽  
Term Potentiation

Spike timing-dependent plasticity in the hippocampus has rarely been studied in vivo. Using extracellular potential and current source density analysis in urethane-anesthetized adult rats, we studied synaptic plasticity at the basal dendritic excitatory synapse in CA1 after excitation-spike (ES) pairing; E was a weak basal dendritic excitation evoked by stratum oriens stimulation, and S was a population spike evoked by stratum radiatum apical dendritic excitation. We hypothesize that positive ES pairing—generating synaptic excitation before a spike—results in long-term potentiation (LTP) while negative ES pairing results in long-term depression (LTD). Pairing (50 pairs at 5 Hz) at ES intervals of −10 to 0 ms resulted in significant input-specific LTP of the basal dendritic excitatory sink, lasting 60–120 min. Pairing at +10- to +20-ms ES intervals, or unpaired 5-Hz stimulation, did not induce significant basal dendritic or apical dendritic LTP or LTD. No basal dendritic LTD was found after stimulation of stratum oriens with 200 pairs of high-intensity pulses at 25-ms interval. Pairing-induced LTP was abolished by pretreatment with an N-methyl-d-aspartate receptor antagonist, 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), which also reduced spike bursting during 5-Hz pairing. Pairing at 0.5 Hz did not induce spike bursts or basal dendritic LTP. In conclusion, ES pairing at 5 Hz resulted in input-specific basal dendritic LTP at ES intervals of −10 ms to 0 ms but no LTD at ES intervals of −20 to +20 ms. Associative LTP likely occurred because of theta-rhythmic coincidence of subthreshold excitation with a backpropagated spike burst, which are conditions that can occur naturally in the hippocampus.

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