Action Potential Lab Report

1. Exceeding the threshold depolarization at the trigger zone DECREASES the likelihood of generation of action potential.

As result, the bonding causes the sodium and potassium gates to open. As result, end plate potential is formed and excites areas of muscle tissue. Action potential is created and the muscle moves or contracts.

A voltage-gated sodium ion channel opens when there is a change in the voltage of the membrane and allows sodium ions to flow across its electrochemical gradient. These voltage-gated channels are made up of amino acids and they aid in generating and moving an action potential down a membrane or axon (Brooker, Robert, 106).

b. What phenomena must take place for the small postsynaptic potentials to reach threshold and produce action potentials?

This stage is called repolarisation. The K+ channels then close, the sodium-potassium pump restarts, restoring the normal distribution of ions either side of the cell surface membrane and thus restoring the resting potential. In response to this the Na+ channels in that area would open up, allowing Na+ ions to flood into the cell and thus reducing the resting potential of the cells. If the resting potential of the cell drops to the threshold level, then an action potential has been generated and an impulse will be fired.

Both electrical and chemical forces combine to determine the resting membrane potential of the cell. Although the resting membrane potential of most cells is normally negative, the selective permeability of the membrane allows certain ions in and out, causing the neuronal membrane voltage to become depolarized (more positive), or hyperpolarized (more negative). Key ions involved in muscle membrane potential are sodium, potassium, and chloride, which move via passive or active diffusion through ion channels and transporter pumps (Baierlein et al. 2011). The Nernst equation predicts the membrane voltage based on the assumption that the membrane is only permeable to one type of ion. In this investigation, we are seeking to understand the basis for how different ions interact to produce the membrane potential of DEM, DEL1, and DEL2 crayfish muscle

As an action potential travels down the axon of the presynaptic neuron, the action potential reaches the axon terminal synaptic vesicles which migrate toward the synapse. They then release neurotransmitters into the synaptic cleft. The neurotransmitters travel through the synaptic cleft and bind to ligand-gated ion channels on the postsynaptic neuron membrane. The channels open and allow chemicals to enter the cell (i.e. sodium). Then positively charged sodium enters the cell and causes the cell to depolarize. The depolarization spreads down the axon and an action potential is generated. The process then starts over at the axon terminals.

When a membrane is excited depolarization begins. When the membrane depolarizes the resting membrane potential of -70 mV becomes less negative. When the membrane potential reaches 0 mV, indicating there is no charge difference across the membrane. the sodium ion channels start to close and potassium ion channels open. By the time the sodium ion channels finally close. The membrane potential has reached +35 mV. The opening of the potassium channels allows K+ to flow out of the cell down its electrochemical gradient ( ion of like charge are repelled from each other). The flow of K+ out of the cell causes the membrane potential to move in a negative direction. This is referred to as repolarization. ( Marieb & Mitchell, 2009). As the transmembrane potential comes back down towards its resting potential level and the potassium channels begins to close, the trasmembrane potential level goes just below -90mV, causing a brief period of hyperpolarization (Martini, Nath & Bartholomew, 2012). Finally, as the potassium channels close, the membrane turns back to its resting potential until it is excited or inhibited again.

Once a presynaptic neuron is passive, an electrical current is spread along the length of the axon (Schiff, 2012). This is known as action potential (Pinel, 2011). Action potential happens once an abundant amount of depolarisation reaches the limit through the entry of sodium, by means of voltage gated sodium channels

Hence, this would allow for an influx of sodium into the cell down its electrochemical gradient. It would also allow for the flow of potassium outward, as it has a 140mM concentration inside the cell and wants to shift down its concentration gradient to 5.4mM. Therefore, this great driving force for the influx of sodium and efflux of potassium helps to explain the findings at this point. As Table 1 shows, the findings within this figure are statistically supported. The fact that there is not significant difference between the findings of this experiment and the calculated Nernst at the 10, 20 and 40mM of potassium is an indicator that sodium is the largest determinant of the resting membrane potential. However, some findings defy the expectations, as the last two concentrations elicit a resting membrane potential significantly more negative than expected. This can be explained by the fact that at this point, each muscle at their respective muscle groups has been protruded many

A lesser amount of Potassium ions diffuse out across the membrane, leaving behind a less negative charge. The

Depolarization in membrane potential triggers an action potential because nearby axonal membranes will be depolarized to values near or above threshold voltage.

Whenever the balance is altered, the process of transmitting electrical signals, which is called action potential initiates by carrying information across a neuron’s axon; which is called resting membrane potential. This process occurs as uneven ions distribution flow across cell membrane, creating electrical potential. As a result, the duration of active potential can be as fast as 1 ms. Similarly, the average resting membrane is between -40 mV and -80 mV. Since the membrane from inside is more negatively charged than the outside, it reflected on the negative average voltage readings of the resting membrane.

When neurotransmitter molecules are stuck to receptors located on a neuron 's dendrites, the part of a neuron which receives signals from other neurons, ion channels are opened. At an excitatory synapse, the opening of ion channels enable positive ions to enter the neuron and results in the loss of difference in the charge between the inside and the outside of the membrane, this is called depolarization. Sodium channels open first and sodium ions rush into the neuron. When potassium channels open, potassium ions rush out of the cell and the depolarization is reversed. Sodium ion channels begin to close which results in the action potential to go past -70 mV because the

A nerve cell has a negative charge at a resting state due to negatively charged proteins within the cell.[3] Although the inside of the cell contains positively charged potassium ions as well, overall the charge is still negative. Along with potassium on the inside of the cell, positively charged sodium ions are located around the exterior of the cell.[3] When an action potential occurs, the cell becomes even more negatively charged. In turn, this causes sodium transport molecules in the membrane of the cell to open.[3] Sodium will then enter the cell during active transport. The positively charged sodium will cancel out the negatively charged active potential which will depolarize the cell. This allows neurotransmitters to transfer from cell to cell.[3] These neurotransmitters are what allows the body to feel pain. Local anesthetics work by diffusing through nerve fibers. Once they’ve reached the cells, they block the sodium transport molecules in the cell.[2] Therefore neurotransmitters cannot transfer information from cell to cell and the feeling of