PhysioEx3NeurophysioogyHWKQUestions Wolf

Explain why a change in extracellular Na+ did not alter the membrane potential in the resting neuron. ___

The nervous system is responsible for registering extrinsic and intrinsic factors and communicating them with the entirety of the body. Dendrites acquire these signals from other neurons and then the signal is transmitted through the cell body and down the axon. Graded potentials create an electrical charge that eventually leads to threshold being met and action potentials being generated. These action potentials send the signals down the axon. Signals will sometimes struggle to hike up stream due to threshold recently being met. This absolute refractory state inhibits signals from traveling up the axon unless myelin is present to increase signaling. It takes longer to conduct a signal down an un-myelinated axon because voltage-gated ion channels

These layers are made of myelin, produced by Schwann cells that are assigned early in the organism’s development. As these layers develop they become tightly packed around the axons, and the main benefit of this coating is that it prevents the exiting and entering of ions for a distance along the axons. This protection allows the ions to travel further and cause action potentials at a faster rate (Norton and Cammer, 1984). Action potentials are caused by the influx of sodium ions followed by the slow efflux of potassium ions. The process of rapid action potentials jumping from one node to the next is called salutatory conductance (Black et al., 1991).

Two laws govern the generation and propagation of an action potential, the All-or-None Law and the Rate Law. The All-or-None Law states that if an action potential occurs it will continue to the terminal buttons without interruption. The Rate Law, however, describes how the different rates of an action potential represent different stimulus

You are working with a squid giant axon with a resting potential of -70mV. What would the voltage change look like if (a) the axon is bathed in tetrodotoxin, and (b) the axon is bathed in TEA? In both cases, supra-threshold current is applied to the axon, enough to cause an action potential in a seawater only

Finally, please manipulate the various options available in this simulation to improve your understanding of the mechanism responsible for action potentials.

A. Depolarization; excitatory postsynaptic potential. Sodium would depolarize the membrane and increase the likelihood that the post synaptic neuron would fire an action potential.

The action potential occurs in the space between the myelinated sections of the axon. The diffusion and electrostatic pressure pushes sodium ion Na+ into the cell despite the lack of permeability of the membrane. The cell uses sodium-potassium transporters to pump out three Na+ and pump in two potassium ions K+ resulting in a low intracellular levels of Na+. this creates a voltage difference of -70mv which is the neurons resting potential. When the neuron is stimulated by a presynaptic neuron the sodium channels open, letting in positive sodium ions in. this changes the electrical environment inside the cell more positive than the outside. This process is called depolarization, and it causes a chain reaction with the rest of the

[3]. Boundless: Stages of the Action Potential [Internet]. Boundless Open Textbook: September 20, 2016. Available from:

When the channels open (in response to depolarization in transmembrane voltage[b]), they allow an inward flow of sodium ions, which changes the electrochemical gradient, which in turn produces a further rise in the membrane potential. This then causes more channels to open, producing a greater electric current across the cell membrane, and so on. The process proceeds explosively until all of the available ion channels are open, resulting in a large upswing in the membrane potential. The rapid influx of sodium ions causes the polarity of the plasma membrane to reverse, and the ion channels then rapidly inactivate. As the sodium channels close, sodium ions can no longer enter the neuron, and then they are actively transported back out of the plasma membrane. Potassium channels are then activated, and there is an outward current of potassium ions, returning the electrochemical gradient to the resting state. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization or refractory period, due to additional potassium currents. This mechanism prevents an action potential from traveling back the way it just

A compound action potential is the sum of electrical activity produced by all the individual neurons in a nerve that are brought to a critical membrane potential by a local stimulus. This critical membrane potential, referred to as threshold potential, is needed to be reached during depolarization to elicit an action potential. Two sub-threshold potentials occurring in quick succession can summate and cause an action potential to occur even though each individual potential would not trigger an action potential. This is referred to as temporal summation. After the depolarization phase of the membrane, the membrane becomes completely unresponsive to stimulation, known as an absolute refractory period. The speed at which an action potentials are

The electrical begins as neurotransmitters stimulate a cascade of reaction that lead to the depolarization and repolarization of the axon. The neuron is not processing a signal, it is in a state known as resting potential; the resting potential is a net charge of the cell based on the ion gradient established in the intracellular and extracellular matrix (~70 mV). The interior of the cell is negatively charged at rest, while the exterior of the cell is positively charged. When a neuron receives a signal from another neuron, it begins its action potential, causing a depolarization of the cell. This process is said to be “all or none” because once the cell reaches are certain level of depolarization, the action potential is inevitable. So, as a neuron receives a signal and reaches it threshold of depolarization (~65 mV), sodium begins to enter the cell through sodium channels, causing the cell to quickly depolarize until it reaches a maximum (~40 mV). Once the cell reaches the maximum depolarization, potassium begins to leave the cell, causing the neuron to repolarize. A refractory period occurs after this repolarization in which the cell becomes less than 70 mV in charge and is unable to transmit another action potential. This entire process occurs in less than 2 milliseconds. Several action potentials occur down the length of the axon until the chemical signaling is activated. Myelin, a type of axon insulator, is able to transmit action potential over a longer length of the axon, making this process occur more quickly; the spaces between myelinated cells where the action potential occurs are called nodes of Ranvier. Once the action potential reaches the axon

A compound action potential (CAP) is a recording demonstrating the sum of multiple action potential simultaneously occurring in the various axons in a nerve. A CAP relates to the nerve’s excitability, how quickly it generates an action potential, which is associated to its firing threshold. This experiment demonstrates the interconnected effects of stimulus intensity and duration on CAP amplitude. Using extracellular recording, the lowest stimulus intensity was measured for which a CAP was present. This was repeated at various increments of stimulus duration. An inverse relationship between stimulus intensity and duration was observed; when stimulus duration

In Activity 1 we set our hypothesis to find out the potential voltage difference across a cell that’s at rest. We used a computer to simulate explaining how the membrane is permeable more to potassium than sodium due to potassium has more leak channels than sodium does. The cell maintains a stable resting membrane thus the membrane is polarized. In Activity 2, our hypothesis is to find out how stimulus modalities induce amplitude receptor potential. We used three sensory neurons. Pacinian corpuscle had a resting potential of -70mv except a receptor potential of the biggest amplitude to pressure. Olfactory receptor had an increase with chemical modality only. Heat, light and pressure this receptor stayed in the resting membrane potential. The free nerve ending stayed in the resting membrane potential except to heat. In Activity 3 our hypothesis was to find out how much stimulus voltage would it take to cause an action potential? With our computer simulation, we started at 10 mv with no action potential results. We increased to 20 mv and we had an action potential. Action potentials are all or none. You could keep increasing voltage from this point on and continue to achieve action potentials. In Activity 7 we are using a computer simulation. We have three fibers, all with different myelination and

In early 1950, Hodgkin and Huxley carried out an elegant series of electrophysiological experiments on a segment of squid axon. On the basis of these experiments, they have given a quantitative description of membrane current and its application to conduction and excitation in nerve [1]-[2]. From these experimental results, they have proposed an equivalent circuit to account for the resistive and capacitive properties of a patch of membrane [3].