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David McNeely HPHY322 Lab T 1400 Week 2 Lab: Nerve Conduction Velocity Introduction: Action potentials (APs) are the basal method of function of all neurons; they allow information to be interpreted, converted, and passed along to subsequent neurons or to a destination structure (e.g.: a muscle or gland). Muscles, for example, involve a rather complex series of steps that ultimately result in muscle contraction or relaxation. Electromyography (EMG) is used to measure the “sum of the action potential’s electrical activity within the muscle” (Matern 2019) and produces an “M-wave” curve on its output graph that can be used to calculate the conduction velocity of the neurons in the tissue through which the data was obtained. Knowing this information, this experiment was conducted in order to determine how the nerve conduction velocity (NCV) of the median nerve changed in response to changes in temperature. It was hypothesized that an increased nerve temperature (IT) would result in an increased NCV, and a decreased nerve temperature (DT) would result in a decreased NCV. Methods: A bar electrode was placed over the subject’s left median nerve at wrist level, the negative electrode was placed over the left abductor pollicis brevis muscle in line with the metacarpophalangeal joint, the positive electrode was placed about 2 cm distally along the left thumb, and the ground electrode was arbitrarily placed on the ventral surface of the right wrist. All stimuli were transmitted, and all data collected via a PowerLab data acquisition console. For the control condition, three trials were conducted with the stimulus intensity set to 20mA, and the data were automatically graphed by the PowerLab software. The latency periods of each trial were measured and recorded by measuring the time between the stimulus onset and peak of the M-wave. NCV was then calculated by dividing the distance between the stimulatory section of the bar electrode and the negative electrode by the average, previously obtained latency period. Two more sets of 3 trials were conducted following the same procedure listed above; however, one set of trials (IT condition) was anteceded by the application of a HotHands® hand warmer across the section of the subject’s wrist between the bar electrode and negative electrode for 5 mins, and the other set of trials (DT condition) was anteceded by the application of an ice pack across the subject’s wrist for 8 mins. Latency periods and NCV were then calculated and recorded for each subsequent condition. Results: Nerve Conduction Velocity (cm/s)

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Experimental Condition

Figure 1. Changes in NCV with temperature

David McNeely HPHY322 Lab T 1400 Discussion: This experiment was conducted in order to determine the effect of temperature on NCV. It was determined that NCV decreased with the IT (hot) condition and did not change with the DT (cold) condition. Upon post-experiment collaboration with other laboratory groups, it was determined that this conclusion is not correct, in fact. If accurate data were to have been measured, the conclusion should have been that NCV increased with the IT (hot) condition and decreased with the DT (cold) condition. Potential explanations for this inaccurate data will be discussed later. The anatomical path of an AP officially begins at the axon hillock (in between the cell body and axon of the neuron), but certain events must occur before the AP can be propagated and further transmitted down the axon. Before a neuronal AP fires, smaller graded potentials must be propagated on the dendrosomatic aspect of the neuron, sending ion-electric changes in charge across the neuron’s plasma membrane until it reaches the axon hillock region. Here, the density of electro-gated sodium and potassium pumps increases dramatically, thereby allowing a full-on AP to propagate. The AP then continues propagating down the neuronal axon before reaching the axon terminal and signaling vesicles of neurotransmitters to exocytose across the synaptic cleft (among other things) where they will be recognized and responded to by the postsynaptic neuron. Most often, this response involves membrane depolarization, which then performs the same actions just described to propagate an AP down its own axon and into the subsequent neuron. In order for an AP to be propagated, an initiation depolarization event must depolarize the membrane potential above a certain limit (i.e.: the threshold potential) before sodium ions begin flooding into the cell. At the same time that sodium ions begin rushing in, potassium ions begin to slowly leave the cell through their own ion channel membranes. After a certain amount of time, sodium ion influx eventually slows down and potassium efflux begins to speed up. Once enough of this ion exchange has occurred, the membrane potential begins to repolarize once again; sodium ions are no longer entering the cell to any significant degree, but potassium ions are flooding outward. The gates on the potassium channels close slightly slower than one might think, so the membrane potential actually hyperpolarizes (going even lower than its resting potential) before the gates close and potassium efflux stops. At this point, the sodium-potassium pump does its job to concentrate sodium ions outside of the cell and potassium ions inside the cell. As previously discussed, the conclusion from the data obtained from this experimental procedure was not accurate. There exist a number of reasons why these data could be inaccurate; for example, anatomical/physiological abnormalities of the experimental subject, incorrect apparatus setup/manipulation, or faulty equipment could have all contributed to improper data acquisition. As Li, Baizhan, et al. (2018) determined, as nerve temperature increased, NCV should have increased due to increased kinetic energy (i.e.: faster ion movement and channel protein opening/closing), and as nerve temperature decreased, NCV should have decreased due to decreased kinetic energy (. Directly affected by channel protein movement speed and ion kinetic energy, AP propagation speed (i.e.: NCV) is positively correlated with changes in temperature. An absolute refractory period is a certain amount of time during the propagation of an AP in which it is impossible for another AP to fire; the local membrane potential of the cell must be at or below the threshold potential for another AP to be propagated. If, however, an initiation stimulus is strong enough to depolarize the membrane potential above threshold potential before

David McNeely HPHY322 Lab T 1400 it has resettled to resting potential, it is possible to propagate another AP during this period known as the relative refractory period. These refractory periods are mostly responsible for the unidirectional movement of APs down neuronal axons, ensuring APs are unable to travel both up and downstream from the site of AP propagation. References: 1. Li, Baizhan, et al. “Regulation of Sensory Nerve Conduction Velocity of Human Bodies Responding to Annual Temperature Variations in Natural Environments.” Indoor Air, vol. 29, no. 2, 2018, pp. 308–319., doi:10.1111/ina.12525. Web of Science (times cited): 0 2. Matern, Philip. “Lab 2 Nerve Conduction Velocity.” University of Oregon, 2019....