|Biology 450 - Animal Physiology Lab||Fall 2004|
My goal in providing this sample is to give you an idea of what I am expecting from you in your lab reports. However, I want to avoid having you slavishly follow every aspect of a model that I provide. I'm therefore poviding just the first part of a lab report - in other words, the introduction. Be sure to see Writing a Physiology Lab Report for hints on the remaining sections. If you are unsure about your approach, feel free to bring a draft by my office, or email me one, and I will take a brief look to make sure you are on the right track
The introduction below is for the lab exercise we did examining action potentials in the giant axons of earthworms. Here are a few important points about the general format:
One of the pathways used in animals to communicate information from one area of the body to another involves the cells of the nervous system. Signals are carried along neurons in the form of action potentials (AP's), in which there is a rapid change in a neuron's membrane potential, from negative to positive and back again (Germann and Stanfield 2004, pp. 226-234). This pattern of quick depolarization and repolarization occurs because an initial membrane depolarization of sufficient strength triggers voltage-gated sodium channels, which open to allow an influx of positive sodium ions before closing again. Depolarization also triggers voltage-gated potassium channels, which open more slowly, allowing a delayed efflux of potassium ions that help to repolarize the membrane. Because depolarization and repolarization involve the activity of these voltage-gated ion channels, the action potential shows a consistent pattern once the membrane is initially depolarized enough to trigger the start of the AP. Thus action potentials are often described as showing an "all-or-none" response.
Once initiated, action potentials are propagated along the axon without a loss of amplitude (Germann and Stanfield 2004, pp. 234-236). This occurs because the strong depolarization associated with the AP depolarizes adjacent regions enough to trigger the voltage-gated sodium channels in those regions, thus triggering a new AP a short distance from the original one. As this process continues, the AP effectively travels along the axon as a wave of depolarization and repolarization. The AP can only travel in one direction because recently depolarized regions of the membrane are in the refractory period, during which voltage-gated ion channels will not yet reopen. The speed of AP propagation is limited primarily by the cable properties of the axon, which determine how far the voltage change associated with a depolarization travels along the axon. In vertebrates, a myelin covering on the axons improves their cable properties and results in a rapid type of AP propagation called saltatory conduction. Invertebrates, on the other hand, lack any additional insulation on their axons, and conduction speed is relatively slow because changes in membrane potential degrade more quickly with distance. One adaptation that invertebrates have shown to help increase conduction speed is an increase in the diameter of axons, which results in improved cable properties. Behaviors in which reaction speed is critical, such as escape responses, often involve these giant axons.
In the study reported here, we examined the generation and propagation of action potentials in giant axons of the earthworm Lumbricus terrestris. The ventral nerve cord of this animal has one medial and two lateral giant axons. In our experiments, we placed stimulating electrodes around the nerve cord near the head of the animal and recording electrodes near the nerve cord along the length of the animal's body. We could then apply a voltage to depolarize neurons and look for resulting action potentials traveling along the axons. Our goals were to verify that action potentials show an "all-or-none" response, to measure the approximate duration of an AP, and to determine the speed of propagation along the giant axons of this animal. We also attempted to verify that activity of the giant axons was associated with stimuli that would be expected to elicit escape responses.