The Experts below are selected from a list of 249 Experts worldwide ranked by ideXlab platform
Michael P Nusbaum - One of the best experts on this subject based on the ideXlab platform.
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intercircuit control of motor pattern modulation by Presynaptic Inhibition
The Journal of Neuroscience, 1997Co-Authors: Marlene Bartos, Michael P NusbaumAbstract:Rhythmically active neural networks can control the modulatory input that they receive via their synaptic effects onto modulatory neurons. This synaptic control of network modulation can occur Presynaptically, at the axon terminals of the modulatory neuron. For example, in the crab stomatogastric ganglion (STG), a gastric mill network neuron Presynaptically inhibits transmitter release from a modulatory projection neuron called modulatory commissural neuron 1. We showed previously that the gastric mill rhythm-timed Presynaptic Inhibition of the STG terminals of MCN1 is pivotal for enabling MCN1 to activate this rhythm. We also showed that MCN1 excites the pyloric rhythm within the STG. Here we show that, because MCN1 stimulation conjointly excites the gastric mill and pyloric rhythms, the gastric mill rhythm-timed Presynaptic Inhibition of MCN1 causes a rhythmic interruption in the MCN1-mediated excitation of the pyloric rhythm. Consequently, during each protraction phase of the gastric mill rhythm, Presynaptic Inhibition suppresses MCN1 excitation of the pyloric rhythm, thereby weakening the pyloric rhythm. During the retraction phase, Presynaptic Inhibition is absent and MCN1 elicits a faster, stronger, and modified pyloric rhythm. Thus, in addition to its role in enabling a neural circuit to regulate the modulatory transmission that it receives, Presynaptic Inhibition is also used effectively to rhythmically control the activity level of a distinct, but behaviorally related, neural circuit.
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a switch between two modes of synaptic transmission mediated by Presynaptic Inhibition
Nature, 1995Co-Authors: Michael P Nusbaum, Melissa J Coleman, Pierre MeyrandAbstract:Presynaptic Inhibition reduces chemical synaptic transmission in the central nervous system between pairs of neurons 1-4 , but its role(s) in shaping the multisynaptic interactions underlying neural network activity are not well studied. We therefore used the crustacean stomatogastric nervous system to study how Presynaptic Inhibition of the identified projection neuron, modulatory commissural neuron 1 (MCN1), influences the MCN1 synaptic effects on the gastric mill neural network. Tonic MCN1 discharge excites gastric mill network neurons and activates the gastric mill rhythm 5,6 . One network neuron, the lateral gastric (LG) neuron, Presynaptically inhibits MCN1 and is electrically coupled to its terminals 5,6 . We show here that this Presynaptic Inhibition selectively reduces or eliminates transmitter-mediated excitation from MCN1 without reducing its electrically mediated excitatory effects, thereby switching the network neurons excited by MCN1. By switching the type of synaptic output from MCN1 and, hence, the activated network neurons, this Presynaptic Inhibition is pivotal to motor pattern generation.
Melissa J Coleman - One of the best experts on this subject based on the ideXlab platform.
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a switch between two modes of synaptic transmission mediated by Presynaptic Inhibition
Nature, 1995Co-Authors: Michael P Nusbaum, Melissa J Coleman, Pierre MeyrandAbstract:Presynaptic Inhibition reduces chemical synaptic transmission in the central nervous system between pairs of neurons 1-4 , but its role(s) in shaping the multisynaptic interactions underlying neural network activity are not well studied. We therefore used the crustacean stomatogastric nervous system to study how Presynaptic Inhibition of the identified projection neuron, modulatory commissural neuron 1 (MCN1), influences the MCN1 synaptic effects on the gastric mill neural network. Tonic MCN1 discharge excites gastric mill network neurons and activates the gastric mill rhythm 5,6 . One network neuron, the lateral gastric (LG) neuron, Presynaptically inhibits MCN1 and is electrically coupled to its terminals 5,6 . We show here that this Presynaptic Inhibition selectively reduces or eliminates transmitter-mediated excitation from MCN1 without reducing its electrically mediated excitatory effects, thereby switching the network neurons excited by MCN1. By switching the type of synaptic output from MCN1 and, hence, the activated network neurons, this Presynaptic Inhibition is pivotal to motor pattern generation.
Jens Nielsen - One of the best experts on this subject based on the ideXlab platform.
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sensitivity of h reflexes and stretch reflexes to Presynaptic Inhibition in humans
Journal of Neurophysiology, 1998Co-Authors: Hiroshi Morita, N Petersen, L O D Christensen, Thomas Sinkjaer, Jens NielsenAbstract:Morita, H., N. Petersen, L.O.D. Christensen, T. Sinkjaer, and J. Nielsen. Sensitivity of H-reflexes and stretch reflexes to Presynaptic Inhibition in humans. J. Neurophysiol. 80: 610–620, 1998. The ...
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is Presynaptic Inhibition distributed to corticospinal fibres in man
The Journal of Physiology, 1994Co-Authors: Jens Nielsen, N PetersenAbstract:1. A tendon tap of the biceps femoris tendon was found to evoke a depression of the soleus and tibialis anterior H reflexes with a duration of 300-400 ms and with an onset at a conditioning-test interval of 20-30 ms. It is suggested that the depression is caused by Presynaptic Inhibition of the terminals of the Ia afferents mediating the reflexes. 2. This possibility was tested by a method in which the H reflex is facilitated by a monosynaptic Ia volley from the quadriceps muscle. The attenuation of this facilitation when another pathway is stimulated is probably caused by Presynaptic Inhibition of Ia afferents. It was shown that the biceps femoris tendon tap depressed the size of the femoral nerve-induced facilitation of the soleus and tibialis anterior H reflexes. This suggests that the depression of the reflexes by the tendon tap was indeed caused by Presynaptic Inhibition. 3. To investigate whether the terminals of descending fibres were similarly susceptible to Presynaptic Inhibition, the stimulation of the femoral nerve was replaced by magnetic stimulation of the contralateral motor cortex. This stimulation has been shown to evoke a facilitation of the tibialis anterior and soleus H reflexes which (within its initial 0.5-1 ms) is probably caused exclusively by direct monosynaptic projections from the cortex to the motoneurones. In contrast to the facilitation evoked by Ia afferents, the descending facilitation was not influenced by the biceps tendon tap. 4. Similarly, the monosynaptic peak in the post-stimulus time histogram (PSTH) of single voluntarily activated tibialis anterior motor units evoked by stimulation of the common peroneal nerve was depressed by the tendon tap, whereas this was not the case for the presumed monosynaptic peak evoked by brain stimulation. 5. It is suggested that the tendon tap evoked Presynaptic Inhibition of the terminals of flexor as well as extensor Ia afferents terminating on both soleus and tibialis anterior motoneurones. In contrast, the tap failed to elicit any Presynaptic Inhibition of the terminals of descending fibres on the motoneurones. We suggest that descending pathways in general are free from the Presynaptic control which attenuates peripheral input to motoneurones. Through modulation of Presynaptic Inhibition the brain may thus selectively hinder the access of peripheral feedback mechanisms to the motoneurones, while still maintaining control of the output from the spinal cord through direct and indirect projections to the motoneurones.
E Pierrot-deseilligny - One of the best experts on this subject based on the ideXlab platform.
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Cortical control of Presynaptic Inhibition of Ia afferents in humans
Experimental Brain Research, 1998Co-Authors: Stéphane Meunier, E Pierrot-deseillignyAbstract:The effect of transcranial magnetic stimulation was investigated on Presynaptic Inhibition of Ia terminals in the human upper and lower limb. Presynaptic Inhibition of Ia afferents was assessed by three different and independent methods: (1) heteronymous Ia facilitation of the H-reflex (assessing ongoing Presynaptic Inhibition of Ia afferents in the conditioning volley); (2) long-lasting Inhibition of the H-reflex by a group I volley (D1 Inhibition, assessing Presynaptic Inhibition on Ia afferents in the test volley); (3) measurement of the monosynaptic Ia peak evoked in single motor units by a homonymous or heteronymous volley (post stimulus time histogram method). The first two methods were used on the lower limb; the last two on the upper limb. Provided that the corticospinal volley and the explored Ia volley were directed to the same target motoneurones, cortical stimulation evoked significant and congruent changes: (1) In the lower limb, transcranial stimulation provided increased heteronymous Ia facilitation and decreased D1 Inhibition, both of which suggest a decrease in Presynaptic Inhibition of Ia afferents; (2) in the upper limb, transcranial stimulation provided an increase in the radial-induced Inhibition of the wrist flexor H-reflex and a decrease in the peak of monosynaptic Ia excitation in single units, both of which suggest an increase in Presynaptic Inhibition. Selectivity of corticospinal effects was explored by testing Presynaptic Inhibition of Ia afferents to soleus motoneurones and focusing the transcranial stimulation to excite preferentially different motor nuclei (soleus, quadriceps and tibialis anterior). A cortical-induced decrease in Presynaptic Inhibition of Ia afferents was seen when, and only when, cortical and peripheral Ia volleys were directed to the same motor nucleus.
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Assessing changes in Presynaptic Inhibition of Ia afferents during movement in humans
Journal of Neuroscience Methods, 1997Co-Authors: E Pierrot-deseillignyAbstract:Different methods, based on different principles, have been proposed to estimate changes in Presynaptic Inhibition of Ia terminals (accompanied by primary afferent depolarization, (PAD)) during voluntary contraction in humans. (i) A discrepancy between the H-reflex amplitude, at an equal level of EMG activity, in two situations (e.g., walking and standing) may be taken as suggesting a different control of PAD interneurones in the two cases. (ii) A conditioning stimulation (vibration or electrical stimulation) is used to activate PAD interneurones and to evoke Presynaptic Inhibition of the afferent volley of the test reflex. The resulting long-lasting depression of the reflex depends on the excitability of PAD interneurones, but can be contaminated by long-lasting post-synaptic effects. (iii) The amount of reflex facilitation evoked by a purely monosynaptic Ia volley varies inversely with the on-going Presynaptic Inhibition of Ia afferents mediating the conditioning volley, and can he used to assess this on-going Presynaptic Inhibition. None of these methods can provide by itself unequivocal evidence for a change in Presynaptic Inhibition of Ia terminals, but reasonably reliable interpretations may be proposed when congruent results are obtained with different methods. Thus it has been shown that, during selective voluntary contraction, Presynaptic Inhibition is decreased on Ia afferents projecting on motoneurones of the contracting muscle and increased on Ia afferents projecting on motor nuclei not involved in the contraction.
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Changes in Presynaptic Inhibition of afferents to propriospinal-like neurones in man during voluntary contractions
The Journal of Physiology, 1992Co-Authors: David Burke, Sabine Meunier, J M Gracies, E Pierrot-deseillignyAbstract:1. The possibility was investigated that the facilitation of the transmission in the propriospinal-like system during voluntary contraction, documented in the companion paper (Burke, Gracies, Mazevet, Meunier & Pierrot-Deseilligny, 1992), is due to a decrease in Presynaptic Inhibition of afferents projecting to propriospinal-like neurones. 2. The radial nerve was stimulated to evoke Presynaptic Inhibition of the monosynaptic Ia projections to forearm flexor motoneurones (Berardelli, Day, Marsden & Rothwell, 1987) and, hopefully, of the afferent input to propriospinal-like neurones projecting to these motoneurones. 3. The propriospinal-like excitation of forearm motoneurones evoked from mixed afferent inputs was depressed by radial nerve stimulation, and this depression was long-lasting (200 ms). Despite the convergence of mixed nerve and cutaneous afferents onto common propriospinal-like neurones, the radial stimulation did not depress the cutaneous-induced excitation. This differential effect and the time course of the depression suggest that it results from Presynaptic Inhibition of mixed nerve afferents (presumably large muscle afferents) projecting to propriospinal-like neurones. 4. With voluntary contractions, phasic or tonic, the radial-induced depression of the propriospinal-like excitation evoked by mixed nerve afferents was much greater than at rest, but the cutaneous-evoked excitation was unchanged. Thus, with voluntary contractions, there was no evidence of decreased gating of the afferent input to propriospinal-like neurones whether the input was of muscle or cutaneous origin and it is concluded that changes in Presynaptic Inhibition cannot account for the facilitation of the transmission in the propriospinal-like system during voluntary contraction. 5. By contrast, Presynaptic Inhibition of the monosynaptic Ia projections to motoneurones was consistently reduced at the onset of contraction, and to a much lesser extent during a weak tonic contraction.
N Petersen - One of the best experts on this subject based on the ideXlab platform.
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sensitivity of h reflexes and stretch reflexes to Presynaptic Inhibition in humans
Journal of Neurophysiology, 1998Co-Authors: Hiroshi Morita, N Petersen, L O D Christensen, Thomas Sinkjaer, Jens NielsenAbstract:Morita, H., N. Petersen, L.O.D. Christensen, T. Sinkjaer, and J. Nielsen. Sensitivity of H-reflexes and stretch reflexes to Presynaptic Inhibition in humans. J. Neurophysiol. 80: 610–620, 1998. The ...
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is Presynaptic Inhibition distributed to corticospinal fibres in man
The Journal of Physiology, 1994Co-Authors: Jens Nielsen, N PetersenAbstract:1. A tendon tap of the biceps femoris tendon was found to evoke a depression of the soleus and tibialis anterior H reflexes with a duration of 300-400 ms and with an onset at a conditioning-test interval of 20-30 ms. It is suggested that the depression is caused by Presynaptic Inhibition of the terminals of the Ia afferents mediating the reflexes. 2. This possibility was tested by a method in which the H reflex is facilitated by a monosynaptic Ia volley from the quadriceps muscle. The attenuation of this facilitation when another pathway is stimulated is probably caused by Presynaptic Inhibition of Ia afferents. It was shown that the biceps femoris tendon tap depressed the size of the femoral nerve-induced facilitation of the soleus and tibialis anterior H reflexes. This suggests that the depression of the reflexes by the tendon tap was indeed caused by Presynaptic Inhibition. 3. To investigate whether the terminals of descending fibres were similarly susceptible to Presynaptic Inhibition, the stimulation of the femoral nerve was replaced by magnetic stimulation of the contralateral motor cortex. This stimulation has been shown to evoke a facilitation of the tibialis anterior and soleus H reflexes which (within its initial 0.5-1 ms) is probably caused exclusively by direct monosynaptic projections from the cortex to the motoneurones. In contrast to the facilitation evoked by Ia afferents, the descending facilitation was not influenced by the biceps tendon tap. 4. Similarly, the monosynaptic peak in the post-stimulus time histogram (PSTH) of single voluntarily activated tibialis anterior motor units evoked by stimulation of the common peroneal nerve was depressed by the tendon tap, whereas this was not the case for the presumed monosynaptic peak evoked by brain stimulation. 5. It is suggested that the tendon tap evoked Presynaptic Inhibition of the terminals of flexor as well as extensor Ia afferents terminating on both soleus and tibialis anterior motoneurones. In contrast, the tap failed to elicit any Presynaptic Inhibition of the terminals of descending fibres on the motoneurones. We suggest that descending pathways in general are free from the Presynaptic control which attenuates peripheral input to motoneurones. Through modulation of Presynaptic Inhibition the brain may thus selectively hinder the access of peripheral feedback mechanisms to the motoneurones, while still maintaining control of the output from the spinal cord through direct and indirect projections to the motoneurones.
