A Respiratory Reflex as Affected by an Anticholinesterase

1956 ◽  
Vol 185 (1) ◽  
pp. 142-144 ◽  
Author(s):  
Bernard Metz
Keyword(s):  
Electrical Stimulation ◽  
Respiratory Failure ◽  
Respiratory Control ◽  
Reflex Response ◽  
Suggestive Evidence ◽  
Small Doses ◽  
Respiratory Reflex ◽  
Stimulation Of

Small doses of the potent anticholinesterase, TEPP, introduced via a cisternal puncture produce a marked potentiation of the respiratory reflex response induced by electrical stimulation of Hering's nerve in the dog. Larger doses of TEPP cause an inhibition of this reflex followed by respiratory failure. These experiments lend suggestive evidence that a neurohumoral mediator (e.g. acetylcholine) may be a component of respiratory control.

Correlation between respiratory reflex and acetylcholine content of pons and medulla

1962 ◽  
Vol 202 (1) ◽  
pp. 80-82 ◽  
Author(s):  
Bernard Metz
Keyword(s):  
Electrical Stimulation ◽  
Intravenous Administration ◽  
Respiratory Function ◽  
Cholinergic System ◽  
Respiratory Control ◽  
Gradual Decrease ◽  
Reflex Response ◽  
Additional Support ◽  
Respiratory Reflex ◽  
Stimulation Of

Experiments indicate that there is a significant correlation between respiratory function (as measured by the reflex response to electrical stimulation of Hering's nerve) and the total acetylcholine (ACh) concentrations in the pons and medulla, after intravenous administration of the hemicholinium, HC-3 (α,α', dimethylethanolamino 4,4' biacetophenone), a drug which inhibits the synthesis of ACh. With a decreasing respiratory reflex response there is a corresponding progressive and gradual decrease in the total ACh content in the pons and medulla. These experiments lend additional support to the hypothesis of the participation of a cholinergic factor in central respiratory control, particularly in view of the fact that these investigations are in harmony with earlier studies in which other biochemical rearrangements were induced within the cholinergic system.

Brain Acetylcholinesterase and a Respiratory Reflex

1957 ◽  
Vol 192 (1) ◽  
pp. 101-105 ◽  
Author(s):  
Bernard Metz
Keyword(s):  
Ache Activity ◽  
Respiratory Control ◽  
Reflex Response ◽  
Brain Areas ◽  
Progressive Decline ◽  
Anesthetized Dogs ◽  
The Brain ◽  
Brain Acetylcholinesterase ◽  
Respiratory Reflex ◽  
Stimulation Of

Experiments were carried out to determine the correlation, if any, between the level of acetylcholinesterase (AChE) activity in the brain and the degree of respiratory reflex potentiation and inhibition which occurs after the administration of varied doses of an anticholinesterase, tetraethyl pyrophosphate (TEPP). After a steady state of reflex response was reached (elicited by electrical stimulation of Hering's Nerve), TEPP was injected in varying doses via a cisternal puncture, and the anesthetized dogs were killed at various stages of reflex potentiation and inhibition. Analyses of the AChE activity of representative brain areas indicated that following an initial marked potentiation, maximal at AChE values approximately 84–88% of the controls, there is a gradual but progressive decline in the potentiated respiratory reflex which parallels the fall in the AChE activities of the brain areas vitally concerned with respiration, until respiratory failure was evident when the enzyme activity was 8–11% of the control values. These experiments lend suggestive evidence that a neurohumoral component (e.g. acetylcholine) may be factor in respiratory control.

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.

Increased H-Reflex Response Induced by Intramuscular Electrical Stimulation of Latent Myofascial Trigger Points

2009 ◽  
Vol 27 (4) ◽  
pp. 150-154 ◽  
Author(s):  
Hong-You Ge ◽  
Mariano Serrao ◽  
Ole K Andersen ◽  
Thomas Graven-Nielsen ◽  
Lars Arendt-Nielsen
Keyword(s):  
Electrical Stimulation ◽  
Conduction Velocity ◽  
Tibial Nerve ◽  
Trigger Points ◽  
H Reflex ◽  
Reflex Response ◽  
Muscle Spindle Afferents ◽  
Myofascial Trigger Points ◽  
Reflex Threshold ◽  
Stimulation Of

Background Myofascial trigger points (MTrPs) present with mechanical hyperalgesia and allodynia. No electrophysiological evidence exists as to the excitability of muscle spindle afferents at myofascial trigger points MTrPs. The purpose of this current study was to explore whether an H-reflex response could be elicited from intramuscular electrical stimulation. If so, to assess the possibility of increased reflex response at MTrPs. Methods The H-reflex latency and the conduction velocity were first determined from electrical stimulation of the tibial nerve in 13 healthy subjects. Then an intramuscular monopolar needle electrode was inserted randomly into a latent MTrP or a non-MTrP in the gastrocnemius muscle. Electrical stimuli at different intensities were delivered via the intramuscular recording electrode to the MTrP or non-MTrP. Results The average conduction velocity (44.3 ± 1.5 m/s) of the electrical stimulation of tibial nerve was similar (p>0.05) with the conduction velocity (43.9 ± 1.4 m/s) of intramuscular electrical stimulation. The intramuscular H-reflex at MTrPs was higher in amplitude than non-MTrPs (p<0.001). The reflex threshold was lower for MTrPs than non-MTrPs (p<0.001). Conclusion The current study provides first electrophysiological evidence that intramuscular electrical stimulation can evoke H-reflex, and that higher H-reflex amplitude and lower H-reflex threshold exist at MTrPs than non-MTrPs respectively, suggesting that muscle spindle afferents may be involved in the pathophysiology of MTrPs.

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.

Phase-linked variations in the amplitude of the digastric nerve jaw-opening reflex response during fictive mastication in the rabbit

1983 ◽  
Vol 61 (10) ◽  
pp. 1122-1128 ◽  
Author(s):  
J. P. Lund ◽  
S. Enomoto ◽  
H. Hayashi ◽  
K. Hiraba ◽  
M. Katoh ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Sensory Feedback ◽  
Motor Program ◽  
Reflex Response ◽  
Upper Lip ◽  
Reflex Amplitude ◽  
Jaw Opening ◽  
Jaw Opening Reflex ◽  
Repetitive Electrical Stimulation ◽  
Stimulation Of

The digastric nerve reflex response to stimulation of the upper lip was studied in urethan-anesthetized rabbits paralysed with pancuronium bromide. Rhythmic bursts of masticatory activity were evoked in the nerve by repetitive electrical stimulation of the motor cortex. The amplitude and latency of the reflex responses during fictive mastication were compared with preceding control values. When stimuli close to threshold were given, the largest and earliest responses occurred during the digastric burst. When intense stimuli were employed, the largest responses were out of phase with the burst, although the latency was still shortest when the motoneurons were rhythmically active. Since the pattern is essentially the same as that seen during normal mastication, we conclude that the cyclical modulation of reflex amplitude and latency is not the result of sensory feedback generated by the movements themselves but is instead governed by the central motor program.

Comparison of the inhibitory response to tendon and cutaneous afferent stimulation in the human lower limb

2012 ◽  
Vol 107 (2) ◽  
pp. 564-572 ◽  
Author(s):  
Nigel C. Rogasch ◽  
John A. Burne ◽  
Kemal S. Türker
Keyword(s):  
Electrical Stimulation ◽  
Achilles Tendon ◽  
Nerve Stimulation ◽  
Sural Nerve ◽  
Time Course ◽  
Triceps Surae ◽  
Reflex Response ◽  
Cutaneous Afferents ◽  
Similar Data ◽  
Stimulation Of

A powerful early inhibition is seen in triceps surae after transcutaneous electrical stimulation of the Achilles tendon [tendon electrical stimulation (TES)]. The aim of the present study was to confirm results from surface electromyogram (SEMG) recordings that the inhibition is not wholly or partly due to stimulation of cutaneous afferents that may lie within range of the tendon electrodes. Because of methodological limitations, SEMG does not reliably identify the time course of inhibitory and excitatory reflex components. This issue was revisited here with an analysis of changes in single motor unit (SMU) firing rate [peristimulus frequencygram (PSF)] and probability [peristimulus time histogram (PSTH)] to reexamine the time course of inhibitory SMU events that follow purely cutaneous (superficial sural) nerve stimulation. Results were then compared with similar data from TES. When compared with the reflex response to TES, sural nerve stimulation resulted in a longer onset latency of the primary inhibition and a weaker effect on SMU firing probability and rate. PSF also revealed that decreased SMU firing rates persisted during the excitation phase in SEMG, suggesting that the initial inhibition was more prolonged than previously reported. In a further study, the transcutaneous SEMG Achilles tendon response was compared with that from direct intratendon stimulation with insulated needle electrodes. This method should attenuate the SEMG response if it is wholly or partly dependent on cutaneous afferents. However, subcutaneous stimulation of the tendon produced similar components in the SEMG, confirming that cutaneous afferents made little or no contribution to the initial inhibition following TES.

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