The Effect Of Acetylcholine On The Heart Rate Of Daphnia Magna

The Effects of Temperature, Acetylcholine, and Adrenaline on the Heart Rate of Daphnia magna
Hieu Duong
6 April 2011

Introduction The heart is a muscular organ that constantly pumps blood throughout the human body. The continuous flow of blood creates a system for vital organs within the body to gain oxygen and nutrients. The timely delivery of oxygen to the body’s organs is very crucial. Brain cells, for example, will die within minutes if the flow of oxygen is obstructed. For the blood to be pumped out of the heart and into the body, contraction of the heart must take place. The rate of contraction is also referred to as the heart rate, which is usually measured in beats per minute. In this experiment, the effect
Acetylcholine is a common neurotransmitter that has an inhibitory effect on vertebrate cardiac muscle. The neurotransmitter does this by releasing neurons which activates a signal transduction pathway. As a result, the G protein in the pathway stops adenylyl cyclase and opens the muscle cell membrane’ potassium channels. These two actions result in a reduction in the cardiac muscle contraction.
Another chemical known as epinephrine has the opposite effect on cardiac muscle. In the wall of the right atrium, there is a cluster of cells called the sinoatrial node that sets the rate for which all cardiac muscle contracts. Hormones, such as epinephrine, within the body can influence the sinoatrial node and cause the heart rate to increase (Campbell and Reese, 2009).
Hypothesis
The Effect of Temperature on the Heart Rate of Daphnia magna
The alternate hypothesis is that the D. magna heart rate will increase as the temperature increases. The D. magna heart rate will decrease as the temperature decreases.
The Effect of Chemicals on the Heart Rate of Daphnia magna
The alternate hypothesis is that Acetylcholine will decrease the heart rate and Adrenaline will increase the heart rate of D. magna.
Materials and
The heart rate increased with the addition of acetylcholine whereas acetylcholine was predicted to reduce muscle cell contraction. G proteins in the signal transduction pathway of acetylcholine prevented adenylyl cyclase and the opening of potassium channels which was supposed to reduce cardiac muscle contraction. The light of the dissection microscope may have inhibited this reduction. Every time the light was turned on, its intensity accelerated the heart rate of the D. magna. The D. magna was unable to cope with this light change because it was constantly turned on and off during the experiment. The increase in heart rate may have over-powered the effect of acetylcholine. As a result, the heart rate seemed to increase as an effect of acetylcholine, but in actuality, it was a result of the