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Investigating the Effect of Nicotine on the Heart Rate of Daphnia Results: Table 1: Heart Rate of Daphnia with Various Amounts of Nicotine Present in Surroundings


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SBI4U Shonara Gibson

December 7, 2010 Partner: Helen Picard



Investigating the Effect of Nicotine on the Heart Rate of Daphnia
Results:
Table 1: Heart Rate of Daphnia with Various Amounts of Nicotine Present in Surroundings

Amount of Nicotine in Surroundings (drops)

Heart Rate (beats per minute)

Average

Variation

Daphnia #1

Daphnia #2

No nicotine

384

372

378

10% of 378 = 38

Variation

6

6

6

1 drop

402

414

408

10% of 408 = 41

Variation

6

6

6

2 drops

420

420

420

10% of 420 = 42

Variation

0

0

0

3 drops

510

480

495

10% of 495 = 50

Variation

15

15

15


Figure 1: Graph showing Heart Rates of Daphnia with Increasing amounts of Nicotine Present in Surroundings


Sample Calculations:

Beats per minute = beats per 10 seconds x 6



Discussion:

In this lab, the goal was to observe the effect that varying amounts of nicotine had on the heart rate of a clear-shelled crustacean, Daphnia. It was found that the more nicotine present in the water surrounding Daphnia, the higher the heart rate was. For example, Daphnia Number One had a heart rate of 640 bpm without nicotine in the water and a rate of 850 bpm with three drops of nicotine in the water (see Table 1).

Nicotine can bind to the same receptors as a chemical messenger called acetylcholine. Acetylcholine binds to various receptors, one of which is a nicotinic receptor. These receptors are located at the synapses between two neurons and at the synapses between a neuron and a muscle cell (1), and, except in the heart, are ligand-gated ion channels. When bound to acetylcholine, these receptors change shape and form ion channels, enabling an EPSP, or excitatory postsynaptic potential (1).

However, in the heart, acetylcholine receptors play a different role. Instead of being ligand-gated ion channels, the receptors are G-coupled protein receptors (1). When acetylcholine binds to these cardiac receptors, a signal transduction pathway is activated that leads to inhibitory effects rather than the excitatory ones it causes elsewhere. When activated by acetylcholine, a “decrease in the contractile force generated by the muscle (2)” results because “the G proteins in the pathway ... open potassium channels in the muscle cell membrane (1).” Potassium leaves the cell, making it more negative. This hyperpolarizes the cell, reducing the chance of action potential and therefore slowing the heart rate.



Nicotine binding to cardiac acetylcholine receptors does not have the same inhibitory effect as acetylcholine does because it does not trigger the same signal transduction pathway. Since the nicotine takes the place of acetylcholine on the receptor, effectively blocking it, acetylcholine cannot open potassium channels. Closed potassium channels mean that while ATP pumps bring potassium into the cell, very little amounts leave. This process results in a less negative charge inside the cell which leads to the cell depolarizing. Like neurons, after the cardiac cell depolarizes enough it reaches threshold. Instead of sending an electrical signal, the cell contracts. Cardiac cells contracting together more frequently results in an increased heart rate, because nicotine blocks acetylcholine from its receptors.
The results collected supported the hypothesis that nicotine would increase Daphnia’s heart rate. The data in this lab contains only two trials because time was limited and it was not possible for the experimenters to conduct three trials. Nevertheless, the two existing trials had very little variation and so the results can be considered consistent. However, the method used to track heart rate was dependent on the reflexes of the experimenters, so the accuracy of the results is questionable. Also, heart rate was measured for only 10 seconds as opposed to a full minute. Therefore, the data has been extrapolated, and the heart rate is simply assumed to be constant for the entire assumed minute. The nicotine could have decreased in concentration or the effects might have become magnified during the supposed minute, meaning the heart rate may have decreased or increased in this time. This means it is uncertain as to whether or not the heart rate remained constant for 60 seconds.
References:

  1. Campbell, Neil A., and Jane B. Reece. Biology. 8thth ed. San Francisco: Pearson Benjamin Cummings, 2009. 1060. Print.

  2. Hebert, Terry. "Re: Why do Ethanol, Acetylcholine, Adrenaline affect the heart rate of Daphnia." MadSci Network. N.p., 1 Mar. 1999. Web. 8 Dec. 2010.


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