THE CAUSE OF REFLEX AFTERDISCHARGE IN THE FROG'S SPINAL CORD

1956 ◽  
Vol 34 (3) ◽  
pp. 456-465 ◽  
Author(s):  
B. Delisle Burns
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Biceps Femoris ◽  
Single Stimulus ◽  
Spinal Reflex ◽  
Reflex Response ◽  
Strong Stimulus ◽  
Spinal Animal ◽  
Reflex Stimulation ◽  
Stimulation Of

It is usually assumed that spinal reflex afterdischarge in the decerebrate or spinal animal is due to functional circuits of interneurons around which excitation can "chase its own tail" until fatigue brings the process to an end. This hypothesis has been tested in the frog. Reflex afterdischarge of motoneurons innervating the biceps femoris was produced by electrical stimulation of the ipsilateral foot. After the end of reflex stimulation, but during the afterdischarge, a direct single stimulus was applied to the animal's spinal cord. A strength of stimulus (of duration greater than five milliseconds) could always be found which would terminate the afterdischarge abruptly. This strong stimulus did not halt the afterdischarge by producing transient damage to the neurons of the cord, for when the stimulus was given during stimulation of the foot, there was no interruption of either reflex response or afterdischarge. Such experimental results are consistent with Forbes' hypothesis of reverberatory circuits.

THE CAUSE OF REFLEX AFTERDISCHARGE IN THE FROG'S SPINAL CORD

1956 ◽  
Vol 34 (1) ◽  
pp. 456-465
Author(s):  
B. Delisle Burns
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Biceps Femoris ◽  
Single Stimulus ◽  
Spinal Reflex ◽  
Reflex Response ◽  
Strong Stimulus ◽  
Spinal Animal ◽  
Reflex Stimulation ◽  
Stimulation Of

It is usually assumed that spinal reflex afterdischarge in the decerebrate or spinal animal is due to functional circuits of interneurons around which excitation can "chase its own tail" until fatigue brings the process to an end. This hypothesis has been tested in the frog. Reflex afterdischarge of motoneurons innervating the biceps femoris was produced by electrical stimulation of the ipsilateral foot. After the end of reflex stimulation, but during the afterdischarge, a direct single stimulus was applied to the animal's spinal cord. A strength of stimulus (of duration greater than five milliseconds) could always be found which would terminate the afterdischarge abruptly. This strong stimulus did not halt the afterdischarge by producing transient damage to the neurons of the cord, for when the stimulus was given during stimulation of the foot, there was no interruption of either reflex response or afterdischarge. Such experimental results are consistent with Forbes' hypothesis of reverberatory circuits.

Micturition reflexes in the in vitro neonatal rat brain stem-spinal cord-bladder preparation

1994 ◽  
Vol 266 (3) ◽  
pp. R658-R667 ◽  
Author(s):  
K. Sugaya ◽  
W. C. De Groat
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Brain Stem ◽  
Rat Brain ◽  
Bladder Wall ◽  
Spinal Reflex ◽  
Neonatal Rat ◽  
Evoked Contractions ◽  
Stimulation Of

An in vitro neonatal (1-7 day) rat brain stem-spinal cord-bladder (BSB) preparation was used to examine the central control of micturition. Isovolumetric bladder contractions occurred spontaneously or were induced by electrical stimulation of the ventrolateral brain stem, spinal cord, bladder wall (ES-BW), or by perineal tactile stimulation (PS). Transection of the spinal cord at the L1 segment increased the amplitude of ES-BW- and PS-evoked contractions, and subsequent removal of the spinal cord further increased spontaneous and ES-BW-evoked contractions but abolished PS-evoked contractions. Hexamethonium (1 mM), a ganglionic blocking agent, mimicked the effect of cord extirpation. Tetrodotoxin (1 microM) blocked ES-BW- and PS-evoked contractions but enhanced spontaneous contractions. Bicuculline methiodide (10-50 microM), a gamma-aminobutyric acid A receptor antagonist, increased the amplitude of spontaneous, ES-BW- and PS-evoked contractions. These results indicate that PS-evoked contractions are mediated by spinal reflex pathways, whereas spontaneous and ES-BW-evoked contractions that are elicited by peripheral mechanisms are subject to a tonic inhibition dependent on an efferent outflow from the spinal cord. PS-evoked micturition is also subject to inhibitory modulation arising from sites rostral to the lumbosacral spinal cord. Although electrical stimulation of bulbospinal excitatory pathways can initiate bladder contractions in the neonatal rat, these pathways do not appear to have an important role in controlling micturition during the first postnatal week.

Electrical Stimulation of the Spinal Cord and Peripheral Nerves for Pain Control

1981 ◽  
Vol 44 (4) ◽  
pp. 207-217 ◽  
Author(s):  
Don M. Long ◽  
Donald Erickson ◽  
James Campbell ◽  
Richard North
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Peripheral Nerves ◽  
Pain Control ◽  
Stimulation Of

The effect of transcranial magnetic stimulation on the excitability of the motor neuron pools of the muscles of the lower extremities

2021 ◽  
Author(s):  
S.S. Ananiev ◽  
D.A. Pavlov ◽  
R.N. Yakupov ◽  
V.A. Golodnova ◽  
M.V. Balykin
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Transcranial Magnetic Stimulation ◽  
Motor Cortex ◽  
Magnetic Stimulation ◽  
Primary Motor Cortex ◽  
Lower Extremities ◽  
Transcutaneous Electrical Stimulation ◽  
Stimulation Of

The study was conducted on 22 healthy men aged 18-23 years. The primary motor cortex innervating the lower limb was stimulated with transcranial magnetic stimulation. Using transcutaneous electrical stimulation of the spinal cord, evoked motor responses of the muscles of the lower extremities were initiated when electrodes were applied cutaneous between the spinous processes in the Th11-Th12 projection. Research protocol: Determination of the thresholds of BMO of the muscles of the lower extremities during TESCS; determination of the BMO threshold of the TA muscle in TMS; determination of the thresholds of the BMO of the muscles of the lower extremities during TESCS against the background of 80% and 90% TMS. It was found that magnetic stimulation of the motor cortex of the brain leads to an increase in the excitability of the neural structures of the lumbar thickening of the spinal cord and an improvement in neuromuscular interactions. Key words: transcranial magnetic stimulation, transcutaneous electrical stimulation of the spinal cord, neural networks, excitability, neuromuscular interactions.

Epidural electrical stimulation to facilitate locomotor recovery after spinal cord injury

2021 ◽  
Author(s):  
Johannie Audet ◽  
Charly G. Lecomte
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Electrical Stimulation ◽  
Clinical Implementation ◽  
Preclinical Models ◽  
Lumbosacral Region ◽  
Locomotor Recovery ◽  
Promising Therapeutic Approach ◽  
Cord Injury ◽  
Stimulation Of

Tonic or phasic electrical epidural stimulation of the lumbosacral region of the spinal cord facilitates locomotion and standing in a variety of preclinical models with severe spinal cord injury. However, the mechanisms of epidural electrical stimulation that facilitate sensorimotor functions remain largely unknown. This review aims to address how epidural electrical stimulation interacts with spinal sensorimotor circuits and discusses the limitations that currently restrict the clinical implementation of this promising therapeutic approach.

scholarly journals A Fully Implantable Miniaturized Liquid Crystal Polymer (LCP)-Based Spinal Cord Stimulator for Pain Control

Sensors ◽  
2022 ◽  
Vol 22 (2) ◽  
pp. 501
Author(s):  
Seunghyeon Yun ◽  
Chin Su Koh ◽  
Jungmin Seo ◽  
Shinyong Shim ◽  
Minkyung Park ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Liquid Crystal ◽  
Mechanical Stimulation ◽  
Spinal Cord Stimulation ◽  
Pulse Generator ◽  
Spinal Cord Stimulator ◽  
Stimulation Threshold ◽  
Crystal Polymer ◽  
Stimulation Of

Spinal cord stimulation is a therapy to treat the severe neuropathic pain by suppressing the pain signal via electrical stimulation of the spinal cord. The conventional metal packaged and battery-operated implantable pulse generator (IPG) produces electrical pulses to stimulate the spinal cord. Despite its stable operation after implantation, the implantation site is limited due to its bulky size and heavy weight. Wireless communications including wireless power charging is also restricted, which is mainly attributed to the electromagnetic shielding of the metal package. To overcome these limitations, here, we developed a fully implantable miniaturized spinal cord stimulator based on a biocompatible liquid crystal polymer (LCP). The fabrication of electrode arrays in the LCP substrate and monolithically encapsulating the circuitries using LCP packaging reduces the weight (0.4 g) and the size (the width, length, and thickness are 25.3, 9.3, and 1.9 mm, respectively). An inductive link was utilized to wirelessly transfer the power and the data to implanted circuitries to generate the stimulus pulse. Prior to implantation of the device, operation of the pulse generator was evaluated, and characteristics of stimulation electrode such as an electrochemical impedance spectroscopy (EIS) were measured. The LCP-based spinal cord stimulator was implanted into the spared nerve injury rat model. The degree of pain suppression upon spinal cord stimulation was assessed via the Von Frey test where the mechanical stimulation threshold was evaluated by monitoring the paw withdrawal responses. With no spinal cord stimulation, the mechanical stimulation threshold was observed as 1.47 ± 0.623 g, whereas the stimulation threshold was increased to 12.7 ± 4.00 g after spinal cord stimulation, confirming the efficacy of pain suppression via electrical stimulation of the spinal cord. This LCP-based spinal cord stimulator opens new avenues for the development of a miniaturized but still effective spinal cord stimulator.

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