This article is investing the effects of speed of the action potential across many neurons through investigating two diseases and performing related lab simulations. Multiple sclerosis and epilepsy are the two disease which are investigated and through the use of Neurons in Action lab simulations, we saw the effects that demyelination and channelopathy can have. As my hypothesis guessed, demyelination is the main cause of multiple sclerosis and channelopathy is the main cause of epilepsy. Introduction
The nervous system is susceptible to many disease and disorders. Nervous system degenerative diseases are those where neurons, parts of neurons, or any part of the nervous system become damaged and die. The purpose of this study is to understand the mechanisms of epilepsy and multiple sclerosis. “The term “channelopathy” was coined by Louis Ptácěk to describe dysfunction of a Na+ channel underlying inherited hyperkalemic periodic paralysis. Since then, the concept of channelopathy has been expanded to cover a number of syndromes with dysfunction of ion channels at their foundation, including myopathy, pain, cardiac arrhythmia, and epilepsy.” (Poolos and Johnston, 2012) My hypothesis was that demyelination is the underlying cause of multiple sclerosis, and channelopathy is the underlying cause of epilepsy. Myelin is made of lipids, proteins, and protective layers of nerve fiber. Myelin functions to insulate nerve fibers and thus speed up action potentials between neurons. Demyelination is degeneration of the myelin. (Canbay, 2010). I performed simulations with a group, and we manipulated factors in the axon to see the effect upon the action potential, if propagated at all. Materials and Methods
Over a series of three labs, my group performed several Neurons in Action Lab Simulations in the following order (with no changes to the original instructions): The Membrane Tutorial (Resting Membrane Potential) (Manipulates which ion channels are present as leak channels), Equilibrium Potentials (Eion) (Manipulates the ion’s resting potential with only one type of ion present, sodium or potassium), The Na+ Action Potential (manipulates action potential by using sodium), Refractory Period (manipulated factors affecting the refractory period), Threshold, Voltage Clamping a Patch (differs pulse length and number of pulses), The Passive Axon, The Unmyelinated Axon (manipulates speed and propagation of action potential with differing amounts of insulation), The Myelinated Axon (shows speed and propagaton of properly insulated neurons), Partial Demyelination (manipulates speed and propagation of action potential with differing amounts of insulation). Each tutorial manipulated different independent variables, as listed below. Results
The results from the simulations which my group ran are recorded below as required by the worksheets: Resting Membrane Potential
2) Mv at beginning: 0 at end: 200, after current the current pulse, mV remains constant at 200mV 3) Vm is 75 lower at all points than #2. Starts at -75mV and ends up at 125mV staying constant at 125mV. 4) It is similar I that the charge becomes more positive before reaching a maximum. However, the changes are much less pronounced, and, with the addition of leak channels, the membrane can repolarize after the stimulus current has ended. The graph shows the Mv going from -70 to -7 to -50 (and still decreasing). 5) This graph has three spikes (the second being slightly less drastic, and the third being very slight). One from -65mV to 50mV to -73mV followed by the other from -65mV to 30mV to -73mV. The third spike looks similar to the graph in #4. The voltage-gated channels have an inactivation gate for sodium which closes at specified mV and the membrane repolarizes before initiating another action potential. Equilibrium Potential
1) Because there are no sodium channels.
2) EK became more positive. The value of EK is not equal to the membrane potential.It changed in the...
References: Bitsch, A.. "Acute axonal injury in multiple sclerosis: Correlation with demyelination and inflammation." Brain 123.6 (2000): 1174-1183. Print.
Canbay, Cahit. "The Essential Environmental Cause Of Multiple Sclerosis Disease." Progress In Electromagnetics Research 101 (2010): 375-391. Print.
Minagar, A.. "A Channelopathy Contributes to Cerebellar Dysfunction in a Model of Multiple Sclerosis." Yearbook of Neurology and Neurosurgery 2012 (2012): 69-70. Print.
Poolos, Nicholas P.. "HCN channelopathy in epilepsy." Epilepsia 51 (2010): 12-12. Print.
Poolos, Nicholas P., and Daniel Johnston. "Dendritic ion channelopathy in acquired epilepsy." Epilepsia 53 (2012): 32-40. Print.
Please join StudyMode to read the full document