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The findings of the first experiment clearly support this theory. The peak of the compound action potential rose as the amplitude of the stimuli increased. To put it another way, the graph's form corresponded to the hypothesized trend line. Nonetheless, the compound action potential fell, specifically at 3mV. Such a decline in the compound action potential might have been caused by over exertion of the nerve (Del Bigio and Enno 2008). At this point, the nerve could not withstand the presence of the high voltage. In each of the trials, there was a slight variation of the replicates.
Some of the possible sources of errors include the slowly dying of the nerves at the time of data taking. Additionally, the fibers of the nerve might have been damaged. According to Fields (2008), other possible sources of discrepancies in the results include the having direct contact with the nerve on the stimulating electrodes and the errors in the program. In summary, the primary sources of errors involved in the experimental analysis include random and systematic errors. Fields (2008) notes that such errors must be minimized to realize more accurate lab results.
An increase in stimuli produces an increase in response amplitude. The kind of process results from the differences in both threshold and sizes of the fibres of the nerve within the frog nerve. Compared to the smaller ones, the bigger nerve fibers have lower threshold stimuli. In fact, the larger nerve fibres began firing as the strength of the stimulus started to increase. In effect, the smaller nerves start to activates in the process (Raymond 2008).
In general, there is a relationship of the peak to the individual potential action's number that passes under the first electrode of recording. In their article, Del Bigio and Enno (2008), notes that the higher peak produces, the more electrode potentials. The process of running the strength of stimuli through the load nerve make the individual action potential to become negative as they pass under the first electrode.
Notably, the increase in stimuli causes the peak to get higher due to the presence of the more individual action potentials that passes under the first electrode. As a result, the single nerves reach the action potential threshold after peaking. In turn, the amount of compound action potential is increased (Del Bigio and Enno 2008).
Naturally, there is an association of the latency to the fastest individual action potential and the application time of the stimulus (Forestier 2003). In this case, the whole process simply helps in illustrating how fast the nerve can respond. Noticeably, the peak act as the indicial action potentials number that consistently passes under the electrodes in the first experiment (Fields 2008). For this reason, any increase in the peak results in the corresponding rise in the latency.
Just like the first experiment, the second experiment's results also confirm the hypothesis. The preliminary figures reveal that the increase in temperature in the ringer solution of the Frog results in the decrease in the CAP's duration. However, such a scenario only occurs when the stimuli electrode passes through the system. Conversely, this experiment rejects the hypothesis for the control.
Even though the actual duration of the compound action potential was 0.7, it was hypothesized to be 0.5. Such discrepancies in the values of the compound action potentials might have resulted from the failure to measure the frog Ringer's solution at the time of pouring it onto the sciatic nerve. In other words, however, there was no consistency in the quantity of the Frog ringer's solution throughout the experiment. Moreover, the rapid temperature changes might have also resulted in nerve damage, hence another probable source of error in the experiment.
As already indicated, minimizing such errors is the only way to realize more accurate answers. One must always be careful during the practical sessions. All the equipment/apparatuses must also be ensured to properly work before they are used in this kind of lab (Raymond 2008).
According to the experiment, the use of electric volts to stimulate the neurons results in the production of action potentials. In this lab, an extracellular response was simulated. In effect, the resultant values were a clear depiction of the individual axons' total activity, as well as their ability to move. In this case, all the action potential that was fired from the nerve system reached the threshold.
Again, the rise in temperature caused the channels of the voltage-gated ion to close and open quicker than in the previous experiment. For this reason, both the potassium and sodium could be noticed to rush both out and in of the cell much quicker. In effect, the compound action potential was decreased in the process of the movement of potassium and sodium.
According to Fearon and Gautier (2007), multiple sclerosis refers to the nervous system's disease. Certainly, this kind of illness can cause some disruptions in the functions of the neuron. In this experiment, however, the compound action potentials duration was observed to slow down as the temperature of the extracellular fluid was decreasing. When this kind of scenario is related to a patient with damaged myelin/axons or MS, a nervous system is reported not to react quickly (Raymond 2008).
However, an increase in temperature makes the nervous system react faster. As a result, the brain fails to use the nervous system in sending the right signals to the body. On the other hand, when the body temperature of these patients is decreased, the nervous system may be able to continue transmitting more signals to the body. As a consequence, some of the health-related symptoms are greatly minimized.
First, having multiple sclerosis is the result of the nervous system's disease. In other words, both the nerve fibers, as well as the central nervous system, are damaged by such multiple sclerosis. In effect, a problem is created because there is already damage to the protective sheath in the nervous system. Any disruption to the nervous system makes the brain not function properly (Fearon and Gautier 2007). Consequently, the nerve fails to send signals to other parts of the body, including the brain. In this case, the patient suffers various symptoms.
Some of these symptoms include difficulty in controlling motor function, balance, as well as coordination (Kellie 1999). Other symptoms involve the loss of memory and visual disturbances. Practically, the areas that get affected are linked to the spinal cord and the nerves in the brain (Krogh 2009).
List any references you have used in your answers, in the panel below.
Del Bigio, M. and Enno, T. (2008). Effect of hydrocephalus on rat brain extracellular compartment. Cerebrospinal Fluid Research, 5(1), p.12.
Fearon, I. and Gautier, M. (2007). Prolonged action potentials in cardiac Purkinje cells: a distinct phenotype arising from a distinct sodium channel. Experimental Physiology, 92(1), pp.1-2.
Fields, R. (2008). Oligodendrocytes Changing the Rules: Action Potentials in Glia and Oligodendrocytes Controlling Action Potentials. The Neuroscientist, 14(6), pp.540-543.
Forestier, F. (2003). Molecular genetics of central nervous system malformations. Child's Nervous System, 19(7-8), pp.440-443.
Kellie, S. (1999). Chemotherapy of central nervous system tumors in infants. Child's Nervous System, 15(10), pp.592-612.
Krogh, A. (2009). Extracellular and intracellular fluid. Acta Medica Scandinavica, 95(S90), pp.9-18.
Raymond, C. (2008). Different requirements for action potentials in the induction of the various forms of long-term potentiation. The Journal of Physiology, 586(7), pp.1859-1865.
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