1. Explain what happened to the CAP amplitude as voltage applied to the neuron was changed. Be specific with your results and explain why the amplitude was smaller with some voltages and larger with other voltages. Increasing the shock voltage recruits more axons into the response until all of the axons in the sciatic nerve are above threshold, and an action potential is produced. Thus, the compound action potential would increase as the shocks of voltage increased. The amplitude was smaller with some voltages, because a mild shock only brought a few axons to threshold, which elicits a small compound action potential. A few of the voltages produced no response, because the shock did not produce any action potentials. This can be seen on the …show more content…
Discuss what happend to the second CAP as the interval was changed between the shocks. Explain why these results were seen in relationship to absolute and relative refractory periods.
As the time interval was changed between the shocks, the amplitude of the second CAP began to increase. This was seen when the time interval increased from 1.0 to 1.5. The compound action potential went from 0 to 0.1. The height (or maximum threshold) of the amplitude was seen at about 2.6. Once the time interval was increased past that point the compound action potential fell back down to zero. This was seen in the intervals of 8.0 to 9.0, where the amplitude is 0. To understand why these results were seen in relation to absolute, and relative refractory periods one should understand there definitions. The absolute refractory period, “is a time during which another stimulus given to the neuron (no matter how strong) will not lead to a second action potential” (PhysiologyWeb,2012). This period takes about 1 to 2 milliseconds, and it is a time when the sodium ion channels are inactive. The relative refractory period, “is a period during which a stronger than normal stimulus is needed in order to elicit an action potential”
In the beginning phases of muscle contraction, a “cocked” motor neuron in the spinal cord is activated to form a neuromuscular junction with each muscle fiber when it begins branching out to each cell. An action potential is passed down the nerve, releasing calcium, which simultaneously stimulates the release of acetylcholine onto the sarcolemma. As long as calcium and ATP are present, the contraction will continue. Acetylcholine then initiates the resting potential’s change under the motor end plate, stimulates the action potential, and passes along both directions on the surface of the muscle fiber. Sodium ions rush into the cell through the open channels to depolarize the sarcolemma. The depolarization spreads. The potassium channels open while the sodium channels close off, which repolarizes the entire cell. The action potential is dispersed throughout the cell through the transverse tubule, causing the sarcoplasmic reticulum to release
In conclusion, regardless of Macropoland’s current economic condition, it is fair to say that it is all part of the business cycle. The business cycle has three parts: peak, trough, and peak. The peak is the date that the recession starts. In Macropoland’s case, the peak would be at the beginning of 1973, its trough somewhere between 1973 and 1974, and then its peak again at 1974. In the second scenario, Macropoland is either at its trough, where it is about to head up again because of its low inflation rate, or it is at its expansion, on its way to heading to its next peak.
The amount of time taken in seconds for her pulse rate to return to normal is the recovery time. The number of steps taken in a minute remained constant for both
Each sensation has its own neuronal receptor, such as: “mechanosensation, thermosensation, vibration, joint position, chemosensation, and electrosensation.” Oaklander then discusses “nocifensive sensations,” or senses that defend us from danger, such as pain and itch. These sensations trigger reflexes and strong movements. However, something that is often left undetected is chronic neuropathic pain, which can cause nerve damage. Shingles is a result of chronic neuropathic pain.
...ending on the size and tolerances of the patients, the voltages could have ranged anywhere form 70 to 130 volts. As a direct effect from the large amounts of electricity being imposed into the patient’s body they will lose consciousness almost immediately. The shocks sent them in to convulsions or seizures and therefore increased their insulin levels. After a patient regains consciousness, he or she will not remember any of the events of being shocked. (Noyes and Kolb).
Peripheral and central mechanisms involving nerve lesions and their input are substantial when perceiving phantom pain. Due to the impairment of peripheral nerves in the process of amputation, regenerative sprouting of damaged axons occurs and the activity rate of inflamed C-fibres and demyelinated A-fibres spontaneously increases (Flor, 2002). As a consequence of this nerve injury, a neuroma, which is a mass of pruned and tangled axons, may form in the residual limb producing abnormal (ectopic) activity (Katz, 1992). Flor, Nikolajsen and Jenson (2006) proposed that ectopic discharge from a neuroma in the stump illustrates abnormal afferent input to the spinal cord, which is a possible mechanism for unpro...
How many ancestors does a node at level n in a binary tree have? Provide justification.
Less inhibition should result in positive rates of change. Given the instruction is to make circles smaller, the authors asked them to inhibit more, is that correct? If you have more intracortical inhibition, why are RTs faster? For example, anodal tDCS shortens RT (Hummel et al. 2006, BMC Neuroscience) and decreases SICI (inducing larger MEP ratios, Kidgell et al. 2013, Neural Plasticity). Assuming participants can change intracortical excitability at will and this method is perhaps equivalent to using non-invasive stimulation (anodal tDCS), it would be expected that RT would become larger.
This reduces the amount of current that would otherwise leak out of the axon and increases the distance that the current can flow passively. Myelination, aka axon insulation, increases action potential conduction up to 150m/s compared to 0.5-10m/s conduction velocities of unmyelinated axons! Speedy delivery of current information along axons is also due to the nodes of Ranvier. Nodes of Ranvier are gaps between insulated portions of the axon. The gaps create a place where the current can flow out of the axon so an action potential can be generated.
The occurrence of action potential is a very short process. When action potential occurs in the neuron the sodium channels open along the axon and sodium comes in. Because the sodium is positive it make the inside of the axon positive. When both the inside and outside are comparative in charge the sodium storms rushing in and starts the depolarization of the action potential. After this happens the sodium channels begin to close and the potassium channels begin to ...
Johnson, J. S., & Newport, E. L. (1991). Critical period effects on universal properties of
...ical impulse, repeating the mechanism described above. The neurons received signal, they crumble up the information passed it down until they get to the last one.
More specifically, the ability to shift input-output functions could show an intrinsic property of the spiral ganglion neurons that allows them to respond to varying inputs, in this case, frequencies. However, over time, input-output functions tend to shift on their own with repeated stimulation. Determining the cause of this shift will allow for a more accurate representation of the neurons true electrophysiological properties. In order to test for these results, patch-clamping technology will be utilized, in order to inject current directly into spiral ganglion neurons. By creating successive input-output functions over time, with varying internal solutions, potential trends can be defined, and from that, a potential mechanism can be established that could be responsible for any changes that are noticed. An ATP-regenerative internal solution will help in the stability of the neuron and aid in determining the true nature of the input-output function shift. Data pertaining to both voltage and current-dependent properties of the spiral ganglion neurons will also be analyzed. The properties of channels that are activated by both hyperpolarization and depolarization will be analyzed to identify a mechanism for the differing properties of the lower and upper half of an input-output function as well as its double Boltzmann character. Comparing any potential changes in both of these properties could help to discover an underlying mechanism that contributes to the changes that are seen in the input-output functions. Over time, it is expected that the input-output functions of spiral ganglion neurons will shift in varying way depending on the internal solution in
The Transient Analysis Tool has 2 fundamental components. (1) Preparation of raw data, and (2) transient analysis of the prepared data. With regard to the first component, there are four subcomponents. (i) Import data (ii) Cell separation (iii) Information marks (cell deletion and -background) and (iv) Transient separation. The second more substantive component can be subdivided into polynomial fitting of the baseline phase, deflection phase, peak phase and reflection phase and exponential fitting of the return phase. According parameters reflecting the kinetics of intracellular calcium concentrations and contractility are extracted from the fit results.