Differentiated short latency response increases after conditioning in inferior colliculus neurons of alert rat

1977 ◽  
Vol 130 (2) ◽  
pp. 315-333 ◽  
Author(s):  
John F. Disterhoft ◽  
Duncan K. Stuart
Keyword(s):  
Inferior Colliculus ◽  
Short Latency ◽  
Alert Rat ◽  
Short Latency Response ◽  
Latency Response

scholarly journals Temporal Evolution of “Automatic Gain-Scaling”

2009 ◽  
Vol 102 (2) ◽  
pp. 992-1003 ◽  
Author(s):  
J. Andrew Pruszynski ◽  
Isaac Kurtzer ◽  
Timothy P. Lillicrap ◽  
Stephen H. Scott
Keyword(s):  
Steady State ◽  
Muscle Activity ◽  
Temporal Evolution ◽  
Rapid Decrease ◽  
Short Latency ◽  
State Activity ◽  
Long Latency ◽  
Short Latency Response ◽  
Latency Response ◽  
Steady State Activity

The earliest neural response to a mechanical perturbation, the short-latency stretch response (R1: 20–45 ms), is known to exhibit “automatic gain-scaling” whereby its magnitude is proportional to preperturbation muscle activity. Because gain-scaling likely reflects an intrinsic property of the motoneuron pool (via the size-recruitment principle), counteracting this property poses a fundamental challenge for the nervous system, which must ultimately counter the absolute change in load regardless of the initial muscle activity (i.e., show no gain-scaling). Here we explore the temporal evolution of gain-scaling in a simple behavioral task where subjects stabilize their arm against different background loads and randomly occurring torque perturbations. We quantified gain-scaling in four elbow muscles (brachioradialis, biceps long, triceps lateral, triceps long) over the entire sequence of muscle activity following perturbation onset—the short-latency response, long-latency response (R2: 50–75 ms; R3: 75–105 ms), early voluntary corrections (120–180 ms), and steady-state activity (750–1250 ms). In agreement with previous observations, we found that the short-latency response demonstrated substantial gain-scaling with a threefold increase in background load resulting in an approximately twofold increase in muscle activity for the same perturbation. Following the short-latency response, we found a rapid decrease in gain-scaling starting in the long-latency epoch (∼75-ms postperturbation) such that no significant gain-scaling was observed for the early voluntary corrections or steady-state activity. The rapid decrease in gain-scaling supports our recent suggestion that long-latency responses and voluntary control are inherently linked as part of an evolving sensorimotor control process through similar neural circuitry.

Neuronal Responses in Vestibular Nuclei to Dorsal Raphe Electrical Activation

1995 ◽  
Vol 5 (2) ◽  
pp. 137-145
Author(s):  
Flora Licata ◽  
Guido Li Volsi ◽  
Giuseppe Maugeri ◽  
Francesca Santangelo
Keyword(s):  
Vestibular Nuclei ◽  
Dorsal Raphe ◽  
Short Latency ◽  
Response Patterns ◽  
Neuronal Responses ◽  
Short Latency Response ◽  
Anaesthetized Rats ◽  
Latency Response ◽  
The Mean ◽  
Dorsal Raphé

The effects of dorsal raphe (DR) electrical stimulation on the neuronal activity of vestibular nuclei were studied in anaesthetized rats. The aim was to establish whether the central systems classically involved in nociceptive functions are able to influence vestibular secondary neurons. DR activation induced modifications of the firing in 70% of the tested neurons, the percentage being similar in the lateral (LVN), superior (SVN), and spinal (SpVN) vestibular nuclei. Three different types of responses were recorded: long-lasting modifications (generally enhancements) of the mean firing rate (43%), short-latency response patterns (14%), both (43%). Short-latency response patterns were more numerous in LVN than in SVN. Iontophoretic applications of 5-HT antagonists Methysergide and Ketanserin blocked long-lasting effects but were scarcely effective on the short-latency response patterns evoked by DR stimulation. It is concluded that DR exerts a double control on secondary vestibular neurons: a generalised excitatory influence by serotoninergic fibers and a specific action mostly targeted on LVN, by nonserotoninergic pathways.

Contrasting neuronal activity in supplementary and precentral motor cortex of monkeys. II. Responses to movement triggering vs. nontriggering sensory signals

1985 ◽  
Vol 53 (1) ◽  
pp. 142-152 ◽  
Author(s):  
K. Kurata ◽  
J. Tanji
Keyword(s):  
Motor Cortex ◽  
Neuronal Activity ◽  
Anterior Part ◽  
Short Latency ◽  
Vibrotactile Stimulus ◽  
Auditory Signal ◽  
Activity Increase ◽  
Key Press ◽  
Short Latency Response ◽  
Latency Response

This report compares neuronal activity in the supplementary motor area (SMA) and the precentral motor cortex (PCM) in response to auditory and vibrotactile signals that required a monkey either to start a key-press movement or to refrain from initiating such a movement. Confirming previous reports (3, 9), a vibrotactile stimulus that triggered movement gave rise to two phases of neuronal activity in PCM neurons: a short-latency response time-locked to the occurrence of the vibrotactile stimulus, and a response related to the time of onset of the movement. When the animal was required to refrain from moving in response to the vibrotactile signal, the short-latency response was often attenuated and there was rarely any later activity. There was no attenuation of the short-latency response to the nontriggering vibrotactile stimulus in the anterior part of the postcentral somatosensory cortex. As reported previously (23), short-latency stimulus-locked responses of SMA neurons to a vibrotactile signals were less frequent and the magnitude of the responses was smaller than in the PCM. However, the properties of the later-occurring responses of SMA neurons were often different from those of PCM neurons. Many SMA neurons responded to both the triggering and nontriggering vibrotactile signals. Twenty-nine SMA neurons responded to the nontriggering signal only and not to the movement-triggering signal. Most of the PCM neurons were active after the auditory signal only when the signal was a trigger to start the key-press movement; three neurons exhibited a slight activity increase after the nontriggering auditory signal. In contrast, a number of SMA neurons responded to the nontriggering auditory signal as well as the movement-triggering auditory signal. Twenty-three neurons responded exclusively to the nontriggering auditory signal. These results indicate the extent to which SMA neuronal activity, in contrast to that of the PCM, is related to factors other than the execution of movement.

Ready Signal and Definition of a CR in Classical Eyelid Conditioning

1968 ◽  
Vol 23 (3) ◽  
pp. 995-1001
Author(s):  
Milton D. Suboski ◽  
Robert T. Greenner
Keyword(s):  
Eyelid Conditioning ◽  
Short Latency ◽  
Ready Signal ◽  
Short Latency Response ◽  
Latency Response ◽  
Definition Of ◽  
Classical Eyelid Conditioning

In both within- and between- Ss designs, the ready signal was shown to increase the frequency of short-latency eyelid responses, most of which are below the latency usually regarded as defining a CR. Since the occurrence of a short latency response sharply reduces the probability of a longer latency response, fewer responses are scored as CRs when a ready signal is used. These factors appear to explain the decrement obtained with a ready signal in eyelid conditioning.

scholarly journals Short-term pressure induced suppression of the short-latency response: a new methodology for investigating stretch reflexes

2009 ◽  
Vol 107 (4) ◽  
pp. 1051-1058 ◽  
Author(s):  
Christian Leukel ◽  
Jesper Lundbye-Jensen ◽  
Markus Gruber ◽  
Abraham T. Zuur ◽  
Albert Gollhofer ◽  
...  
Keyword(s):  
Sensory Nerve ◽  
Muscle Spindles ◽  
Length Change ◽  
Short Latency ◽  
Afferent Feedback ◽  
Short Term ◽  
Short Latency Response ◽  
Inflated Cuff ◽  
Reflex Arc ◽  
Latency Response

During experiments involving ischemic nerve block, we noticed that the short-latency response (SLR) of evoked stretches in m. soleus decreased immediately following inflation of a pneumatic cuff surrounding the lower leg. The present study aimed to investigate this short-term effect of pressure application in more detail. Fifty-eight healthy subjects were divided into seven protocols. Unilateral stretches were applied to the calf muscles to elicit a SLR, and bilateral stretches to evoke a subsequent medium-latency response (MLR). Furthermore, H-reflexes and sensory nerve action potentials (SNAPs) were recorded. Additionally, stretches were applied with different velocities and amplitudes. Finally, the SLR was investigated during hopping and in two protocols that modified the ability of the muscle-tendon complex distal to the cuff to stretch. All measurements were performed with deflated and inflated cuff. Results of the protocols were as follows: 1) inflation of the cuff reduced the SLR but not the MLR; 2) the H-reflex, the M-wave, and, 3) SNAPs of n. tibialis remained unchanged with deflated and inflated cuff; 4) the SLR was dependent on the stretch velocity with deflated and also inflated cuff; 5 and 6) the reduction of the SLR by the cuff was dependent on the elastic properties of the muscle-tendon complex distal to the cuff; and 7) the cuff reduced the SLR during hopping. The present results suggest that the cuff did not affect the reflex arc per se. It is proposed that inflation restricted stretch of the muscles underlying the cuff so that most of the length change occurred in the muscle-tendon complex distal to the cuff. As a consequence, the muscle spindles lying within the muscle may be less excited, resulting in a reduced SLR. Due to its applicability in functional tasks, the introduced method can be a useful tool to study afferent feedback in motor control.

scholarly journals Impact of Experimental Tonic Pain on Corrective Motor Responses to Mechanical Perturbations

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Elodie Traverse ◽  
Clémentine Brun ◽  
Émilie Harnois ◽  
Catherine Mercier
Keyword(s):  
Sensory Feedback ◽  
Pain Model ◽  
Voluntary Response ◽  
Long Latency ◽  
Short Latency Response ◽  
Latency Response ◽  
Tonic Pain ◽  
Underlying Mechanisms ◽  
The Impact ◽  
Muscle Responses

Movement is altered by pain, but the underlying mechanisms remain unclear. Assessing corrective muscle responses following mechanical perturbations can help clarify these underlying mechanisms, as these responses involve spinal (short-latency response, 20-50 ms), transcortical (long-latency response, 50-100 ms), and cortical (early voluntary response, 100-150 ms) mechanisms. Pairing mechanical (proprioceptive) perturbations with different conditions of visual feedback can also offer insight into how pain impacts on sensorimotor integration. The general aim of this study was to examine the impact of experimental tonic pain on corrective muscle responses evoked by mechanical and/or visual perturbations in healthy adults. Two sessions (Pain (induced with capsaicin) and No pain) were performed using a robotic exoskeleton combined with a 2D virtual environment. Participants were instructed to maintain their index in a target despite the application of perturbations under four conditions of sensory feedback: (1) proprioceptive only, (2) visuoproprioceptive congruent, (3) visuoproprioceptive incongruent, and (4) visual only. Perturbations were induced in either flexion or extension, with an amplitude of 2 or 3 Nm. Surface electromyography was recorded from Biceps and Triceps muscles. Results demonstrated no significant effect of the type of sensory feedback on corrective muscle responses, no matter whether pain was present or not. When looking at the effect of pain on corrective responses across muscles, a significant interaction was found, but for the early voluntary responses only. These results suggest that the effect of cutaneous tonic pain on motor control arises mainly at the cortical (rather than spinal) level and that proprioception dominates vision for responses to perturbations, even in the presence of pain. The observation of a muscle-specific modulation using a cutaneous pain model highlights the fact that the impacts of pain on the motor system are not only driven by the need to unload structures from which the nociceptive signal is arising.

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