Dna Report : Neural Tissue Lab Report

2. Novocain blocks action potential production at the site of injection. How do you think Novocain works on the axon membrane, and how does it block the sensation of pain?

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

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).

As well as these there are also the axon of the cell which is covered in myelin sheaths which carried information away from the cell body and hands the action potentials, these are small short bursts of change in the electrical charge of the axon membrane through openings of ion channels, off to the following neurons dendrites through terminal buttons at the end of the axons. Whenever an action potential is passed through these terminal buttons it releases a chemicals that pass on the action potential on to the next neuron through the terminal button and dendrite connection. The chemicals that are

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.

3. A nerve is a bundle of axons, and some nerves are less sensitive to lidocaine. If a nerve, rather than an axon, had been used in the lidocaine experiment, the responses recorded at R1 and R2 would be the sum of all the action potentials (called a compound action potential). Would the response at R2 after lidocaine application necessarily be zero? Why or why not?

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

2. Explain why the resting membrane potential had the same value in the cell body and in the axon.

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

Neurons communicate with each other through an electrochemical process in three steps (Stufflebeam, 2008). An electrical impulse will travel down the axon to axon terminals. This causes the vesicles to open and neurotransmitter molecules are released into the synaptic gap. Neurotransmitter molecules then cross the synaptic gap and enters the receptor sites located on the dendrites of the receiving neuron. The information is carried along axons and dendrites because of changes in electrical properties which we call action potential. An action potential is initiated when a messenger attaches itself to a receptor. This occurrence causes an electrical signal to be triggered and is generated through the neuron. Once the signal reaches the end of an axon, which is at the end of a neuron, a neurotransmitter molecule will return to the synaptic gap where they are received by the sending neuron and the process is repeated or are destroyed by enzymes (Griggs, 2014, p. 41-45).

An action potential is a short electrical impulse generated at the axon hillock which travels the length of an axon. Its generation happens in three distinct stages, depolarisation, repolarisation and hyperpolarisation. When the threshold of excitation is reached, depolarisation starts, the threshold is between -55mV and -65mV in most neurons. When the neuron is stimulated voltage-activated Sodium (Na+) channels open, allowing Na+ ions to rush into the neuron. This reverses the polarity in the neuron towards its peak of +40mV. At this peak Na+ channels

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.

When the cell reaches the resting potential, then the cell can undergo depolarization. During the process, the charge within the cell goes from negative to positive. For this to happen, many events occur along the plasma membrane. The sodium potassium pump continues to work but the voltage gated ion channels that were closed during resting potential become open due to an electrical stimulus. Sodium enters into the cell again and positive sodium ions change the charge inside the cell from negative to positive. When the inside of the cell is positively charged, depolarization is

The extracellular Na+ did not alter the membrane potential in the resting neuron because the Na+ channels were mostly closed.

As soon as the electrical signal reaches the end of the axon, mechanism of chemical alteration initiates. First, calcium ion spurt into the axon terminal, leading to the release of neurotransmitters “molecules released neurons which carries information to the adjacent cell”. Next, inside the axon terminal, neurotransmitter molecules are stored inside a membrane sac called vesicle. Finally, the neurotransmitter molecule is then discharged in synapse space to be delivered to post synaptic neuron.