CV Physiology: Reentry
The relationship between refractory period and conduction time of the AV node The significance of wavelength and excitable gap in reentrant tachycardia. which is expressed as the product of refractory period and conduction velocity. To measure the threshold, conduction velocity, and refractory period of A change in potential difference between the electrodes is recorded. Key words: Conduction velocity, sensory - Refractory period - Tissue tem- perature and . There is a positiv linear correlation between temperature and conduc-.
To speed up the warming up of the worm it will be very cold due to the iceyou can give a "worm hug" by placing your fingers alongside the worm. Take another conduction velocity reading at room temperature. Using a thermometer, you can heat up some water and test this by filling an empty worm tray with the heated solution. We leave it to you to do this experiment. The worm may start moving at the end of the experiment, causing EMG's electromyograms, or muscle electrical activity to swamp out the small neural action potentials.
Troubleshooting Our initial experiments using ice water did not slow down the conduction velocity enough for us to detect. Thus, it's important the worm lay directly on the ice to sufficiently cool it down. The effects of changing temperature on threshold electrotonus were modest Fig. These effects are all understandable in terms of the acceleration of the gating of slow potassium channels see Discussion.
Although there appears in Fig. However, by making repeated recordings of threshold electrotonus on the same nerve while temperature was altered over a wider range, we found that temperature does have consistent, but complex, effects on hyperpolarizing threshold electrotonus. In separate studies on two subjects using a cooling—warming cycle, we found that the effects of temperature on the depolarizing responses could be almost entirely separated from the effects on the hyperpolarizing responses.
The depolarizing responses were closely related to temperature itself, while the hyperpolarizing responses were much more sensitive to the direction of temperature change. Figure 3A i compares threshold electrotonus in one subject at The hyperpolarizing response curves superimpose, but accommodation to depolarizing currents occurred appreciably faster at the higher temperature.
A similar difference was found for the second subject in Fig. In this experiment, thresholds were tracked for a further 50 ms after the ends of the polarizing currents to show that recovery was also appreciably delayed at the lower temperature, presumably because this also depended on temperature-dependent channel gating. Panels A ii and B ii in Fig. For each subject, the depolarizing responses were similar, but the increase in threshold on hyperpolarization was greater when the temperature was increasing than when it was decreasing.
Figure 4A shows the plots of the time courses of the changes in temperature, CMAP latency and threshold electrotonus for the experiment shown in Fig. There is a good correspondence between the time course of skin temperature and both latency to the peak of the CMAP and depolarizing electrotonus response 40—60 ms after the start of the polarizing current. In contrast, the hyperpolarizing response, measured at 90— ms, changes most at the time the direction of temperature change is reversed.
The hyperpolarizing response was more nearly proportional to the rate of change of temperature than to temperature itself.
A similar relationship between the time courses of changes in temperature and threshold electrotonus was found for the second subject Fig. Change in the recovery cycle due to temperature The effects of temperature on the recovery cycle were more conspicuous than on any of the other excitability measures Fig. The relative refractory period, i. This is understandable, because refractoriness is due primarily to sodium channel inactivation, and recovery from inactivation, like other channel gating functions, is strongly temperature-dependent, with a Q10 close to 3.
The relative refractory period and the measure of latency were the two most temperature-sensitive parameters when compared with the intersubject variability Table 1D. The equivalent temperature deviation of 2. After the refractory period, axons enter a superexcitable phase produced by the depolarizing afterpotential Bergmans, ; Barrett and Barrett,followed by a late subexcitable period due to activation of nodal voltage-dependent slow potassium channels Baker et al.
The times to peak superexcitability and subexcitability were also clearly delayed by cooling, but these delays were not measured. The small increases in amplitude of superexcitability and subexcitability with temperature were not statistically significant Table 1. Change in latency and amplitude due to temperature Unlike the various measures of axonal excitability mentioned to date—measures that reflect the excitability of the nerve at the point of stimulation—both the latency and the amplitude of the CMAP reflect the changing temperature of the nerve throughout its course from the point of stimulation to the recording site.
By implication, measures of these parameters include contributions from temperature effects on both the neuromuscular junction and the muscle fibres that contribute to the generation of the target CMAP.
Consequently, while the present study can provide qualitative information about latency and amplitude, it is not possible to determine quantitative information about the contribution of individual components.
As temperature decreases, sodium channel gating is slowed, leading to slowing of the inward sodium current responsible for depolarization of the axonal membrane Schwarz and Eikhof, In routine nerve conduction studies, this is manifested by prolongation in latency of the compound potential and this will occur at each node of Ranvier along the nerve segment measured Burke et al.
In the present study, latency increased by 2. The amplitude of the compound potential is also inversely related to temperature Ludin and Beyeler, ; Bolton et al. As temperature decreases, inactivation of sodium channels slows and repolarization becomes delayed. There is therefore an increase in both the amplitude and the duration of the individual action potentials that contribute to the compound potential, in both the nerve segment and the contributing muscle fibres.
As the duration of the individual potentials increases, the effects of temporal dispersion are reduced, with less phase cancellation, resulting in larger compound potentials Table 1 Kiernan et al.
However, temporal dispersion is much less important for CMAPs than for sensory nerve action potentials. Discussion The present study compares the effects of temperature on different excitability properties of human motor axons.
Conduction velocity and refractory period of single motor nerve fibres in antecedent poliomyelitis.
The results are important for the interpretation of excitability measurements from patients with peripheral nerve disorders and for deciding the best strategy to adopt when testing patients with different limb temperatures.
The principle finding is that most excitability parameters are not very sensitive to temperature over the range encountered clinically, the conspicuous exception being the relative refractory period. This result is in agreement with a study of the effects of temperature on the excitability properties of cutaneous afferents Burke et al. The high sensitivity of refractoriness to temperature means that, to obtain meaningful comparisons of refractoriness between a single patient or a group of patients and controls, it is necessary either that all measurements be made at the same temperature or that temperature differences be taken into account.
The former option is often regarded as preferable in principle, even though a specified temperature can only ever be approximated and the extra time required to stabilize temperature at a new level adds to the expense and inconvenience of the test.
However, this study has shown that changing the temperature of a nerve to a standard temperature can introduce previously unexpected errors. If the sensitivity of hyperpolarizing electrotonus [TEh 90— ms ] to temperature changes reflects transient changes in membrane potential, then other potential-sensitive excitability parameters may also be sensitive to temperature changes, though this remains to be confirmed. We suggest, therefore, that for clinical studies of nerve excitability patients should be kept in a constant-temperature environment before testing and that skin temperature should be measured close to the site of stimulation during the test, but not altered if it is abnormal.
Experiment: Effect of Temperature on Nerve Conduction Velocity
Temperature corrections are best applied if temperature was stable at the time of the recordings. The primary effects of temperature on nerve function occur by altering the kinetics of channel gating. The PowerLab set up is slightly different for the Earthworm giant axon recording, but the theory is similar.
The conduction velocity of the action potential is determined by measuring the distance traveled length of the nerve in m and dividing by the time sec taken to complete the reflex arc, also called the latency.
Measurement of distance is relatively straightforward. It can be done using a ruler or a tape measure. The measurement of time is more complicated. Action potentials travel very quickly; therefore, the times to be measured are very small and require more sophisticated instrumentation. The computer with PowerLab, like the oscilloscope, is ideally suited to measure events that happen in a very short amount of time.
The conduction velocity of a particular neuron is correlated with nerve diameter and myelination. Myelin, a lipid-rich substance, acts like insulation to increase the conduction velocity of vertebrate neurons.
Invertebrates lack myelinated neurons, and conduction velocity of their action potentials increases primarily as the result of increased axon diameter. Many invertebrates have specialized "giant" axons, like the earthworm, that conduct action potentials very rapidly. Draft data tables in your lab notebook to record the Threshold voltage needed to elicit an action potential in the frog and earthworm both medial and lateral Giant Axon.
From the three timed trials record the time between stimulus artifact and action potential latency in ms and measure the distance as described in the manual. Calculate the Average conduction velocity for each using the class data. Conduction Velocity in a Human Reflex Arc When the Achilles tendon is stretched after being tapped with a reflex hammer, the induced action potential is conducted up the leg to the spinal cord and back down where it causes the gastrocnemius calf muscle to contract.
To determine the speed of conduction, the distance that the action potential travels is measured and the time between the tapping of the tendon and the contraction of the muscle is measured using PowerLab and ADinstruments software. A reflex arc is initiated by stretching a tendon, an action that stimulates stretch receptors in the muscle. Those stretch receptors respond by initiating an action potential in sensory neurons.
The action potential travels through those sensory neurons to the spinal cord where they synapse directly with motor neurons. The excitation travels back to the gastrocnemius muscle where it causes contraction of the muscle.
Thus the tendon that was initially stretched is returned to its original length through contraction, completing the reflex arc. The function of this type of reflex arc is to maintain posture. Muscles are continually stretching and returning to their original length without the intervention of the brain. Note that this response is monosynaptic.
The sensory neuron synapses directly with the motor neuron in the spinal cord; there is no interneuron involved. In the muscle the action potential spreads throughout the muscle causing contraction of the muscle fibers. The passage of the action potentials can be sensed by electrodes placed on the skin above the muscle, which when amplified as in the ECG can be displayed on a computer screen. The hammer that you will use has been modified so that when it hits the tendon, the hammer closes a circuit and generates a small signal.
This signal is used to trigger a sweep by the computer. Experimental Procedure Seat the subject on the edge of the lab bench so that her legs are hanging freely. Attach two pre-jelled electrodes to the body of the calf gastrocnemius muscle, a bit to the left or right of the midline. The two electrodes should be placed so their outer edges touch in a vertical line on the muscle See figure below.
A third ground electrode should be placed on the ankle bone. Attach the cables to the correct electrodes: A, Diagram of a reflex arc in a human. When the stretch receptor is stimulated by the hammer, the action potential travels up the sensory fibers to the spinal cord and synapses on the motor fibers The action potential then travels back down the nerve to cause the muscle contraction we observe as a reflex. B, Two electrodes are placed on the calf, close to each other as shown.
The third electrode should be placed on a bony surface, such as the knee cap or ankle. C, LabChart 8 Setup files. If you cannot find this file on the desktop, ask your instructor. To collect an EMG: The test subject should be seated and her legs and feet relaxed. Gently lift the subject's toes to stretch the Achilles tendon on the back of her leg, and firmly rap the Achilles tendon of the subject with the black rubber part of the hammer.
Repeat until you have 3 representative EMGs. When you have a good set of 3 EMGs see Fig. Repeat on different recordings and average three. Record data in your lab manual and on the spreadsheet provided by your instructor.
Refer to PowerPoint slide provided by your instructor for a diagram of how to take this measurement.
Effective refractory period
Record length and then calculate and record the conduction velocity. Place the marker "M" at the top of the first peak of the EMG. The time displayed indicates the time elapsed between the trigger signal and the gastrocnemius response, i. Conduction Velocity in a Frog Sciatic Nerve An action potential is initiated in the dissected sciatic nerve of a frog Rana pipiens or Xenopus laevis by a stimulator a device for delivering precise electrical stimuli.
The action potential travels along the nerve and is detected as it passes two external electrodes according to method 2 described in the introduction and the detected response is amplified and displayed on the computer screen.
The trace on the computer of stimulus and response is triggered by the stimulus; time and distance are measured and the speed can then be calculated. A nerve is a collection of the axons of many neurons. The axons may have different thicknesses and hence their action potentials will have different sizes and speeds.
The action potentials, recorded from the outside of the nerve extracellularly is known as a compound action potential, and represents the sum of the action potentials fired by individual neurons. A, Diagram of a biphasic action potential as an extracellular recording of a nerve.ACTION POTENTIALS IN NEUROPHYSIOLOGY by Professor Fink
The stimulus is applied to the left end of the nerve. B, Dorsal view of exposed frog left hind limb and spinal column.
Lab 9: Conduction Velocity of Nerves - OpenWetWare
The Sciatic Nerve is the large nerve running from the spinal cord to the gastrocnemius muscle. It contains both sensory and motor neurons it is the nerve that is stimulated when you stretch the Human Achilles tendon. In this lab, the frog will have been anesthetized, sacrificed, and double pithed both its brain and spinal cord will have been destroyed.
You may need to remove the skin. To Dissect the Sciatic Nerve Gently separate the dorsal thigh muscles with your fingers and use a blunt glass probe to reveal the white sciatic nerve and accompanying blood vessels see Fig. Free the nerve from the surrounding tissue in the thigh using a blunt glass hook. Cut away muscle and connective tissue around the nerve as you hold the nerve out of the way. Try not to stretch the nerve and avoid touching the nerve with anything metal to avoid damaging the nerve.