First Biology Research in Grinnell by Su

Ketamine Reduces EPSP Amplitude and Increases Paired-pulse Facilitation in Procambarus clarkii’s Neuromuscular Junction

AN HOANG, GRACE PARK, MICHAEL SLATTERY

Department of Biology, Grinnell College, Grinnell, Iowa

ABSTRACT

Ketamine is recently found to have effects on humans’ synaptic plasticity that are similar effect antidepressant. Studying this drug’s effect on invertebrate’s synaptic plasticity can shed light into its influence on humans. Our research focused on ketamine’s role in the synaptic plasticity of crayfish dorsal extensor’s muscular junction. Specifically, we examined how ketamine affects the excitatory postsynaptic response in Procambarus clarkii. In our experiment, we applied paired-pulse stimulation on crayfish tail in 3 conditions: basic crayfish saline (control), ketamine solution (250µM and 500µM), and return to control. We examined the EPSP amplitudes and the percent change between all conditions. Our findings revealed that there was a reduction in synaptic excitation when ketamine was introduced but there was increase in facilitation of the second EPSP pulse. The difference between the two concentrations of ketamine, however, were not dramatic, revealing that 250µM of the drug may have been sufficient in blocking the receptors. We also deduced from our “return to control” data that ketamine did have a long lasting effect on the neuromuscular junction.

INTRODUCTION

Regulation of ketamine for human consumption and treatment is currently a controversial topic in the medical world since studies on how this drug affects the human nervous system, particularly synaptic plasticity, remain insufficient and inconclusive. Ketamine is known as an antagonist of N-methyl-D-aspartate (NMDA) receptors, which means that the drug blocks receptors of this type and disrupts their regular functions. It also affects other glutamate receptors, such the as α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor and the beta-adrenoceptors receptors.

Excessive consumption of ketamine causes hallucinations and dissociative mental states, both of which results in several deaths. However, numerous recent science journal articles have found ketamine’s potential as an antidepressant, since it negates the changes in synaptic plasticity caused by depression (Marsden, 2013). Significant limitations of available treatments for depression, along with rapid antidepressant effects of ketamine (Martinowich et al. 2013, Browne and Lucki 2013), have spurred renewed efforts in the scientific community to study this drug’s effect on synaptic plasticity more extensively. 

Synaptic plasticity, the ability of synapses to strengthen or weaken over time, is one of the important neurochemical foundations for human behavior. Therefore, by studying synaptic plasticity, we can understand the rationale behind cognitive processes in human, such as perception, language, memory, reasoning and emotions. NMDA receptors are the predominant molecular device for controlling synaptic plasticity. NMDA receptors were thought to exist only in vertebrates (Mayer and Westbrook 1987), but evidence suggests that this type of receptors is also present in invertebrates’ neuromuscular junction, specifically on the membrane of the presynaptic neuron (Dale and Kandel 1993).

The NMDA receptor interacts with glutamate, the most abundant excitatory neurotransmitter in the invertebrate’s nervous system. Glutamate is released from the presynaptic cell (Schramm and Dudel 1997) when an action potential occurs and binds to non-NMDA receptors on the postsynaptic cells. This binding causes excitatory postsynaptic response (EPSP) – a temporary depolarization of postsynaptic membrane potential – in the postsynaptic cell. However, when the amount of glutamate becomes excessive in the synaptic gap, these molecules bind to NMDA receptors on the presynaptic membrane, which stops the release of additional glutamate. (Feinstein et al. 1998). In human, blocking NMDA receptors and influencing synaptic plasticity can cause various effects, ranging from temporary loss of consciousness to brain damage, depending on the concentration. 

Although there are numerous studies on how ketamine affects rats’ synaptic transmission and plasticity (Kamikaya et al. 2011; Riberio et al. 2014), similar studies on invertebrates like crayfish are scarce and yield inconsistent results. This is a gap in the current body of scientific knowledge. The nervous system of crayfish features similar neurophysiological and neurochemical mechanisms to organisms of higher complexity, which allows for relevant analysis at the cellular and circuit level. Invertebrates such as crayfish have proven to be excellent models for the study of synaptic plasticity. Much of the information we now have about synaptic plasticity and glutamate receptors was discovered in work done on crayfish preparations (Dudel, et al., 1987; Shinozaki, 1988; Parnas, et al., 1994; Dudel, et al., 1997; Schramm, et al., 1997). Therefore, by studying the synaptic plasticity, and the factors that affect it, in crayfish will provide a better understanding of human’s synaptic plasticity. Furthermore, the studies of ketamine on rats lack reliability, as they yield very different results. Some researches, like Kamikaya et al. (2011) claim that ketamine induce synaptic depression, while others, such as Narimatsu et al. (2002) came to the conclusion that ketamine cause synaptic facilitation in rat hippocampal.  

Our research seeks to reconcile these findings, while giving insight on how ketamine affects the excitatory postsynaptic potential of crayfish. By examining one of ketamine’s potential mechanisms, we hope to provide a framework for future research directions aimed at developing safe and efficient antidepressants from ketamine.

In this experiment, we examined the effect of ketamine on the EPSP of the crayfish species Procambarus clarkii. We applied paired-pulse stimulation on crayfish tails that were first submerged in basic crayfish saline (control), then in two different concentrations of ketamine (500 µM and 250 µM) and finally in the control solution once again. We then examined the difference in EPSP amplitude and percent change of second-pulse facilitation of crayfish muscle cells between the four conditions. The EPSPs in the crayfish dorsal extensor muscle cell, in response from the paired-pulse stimulation were obtained using the intracellular recording method.

We hypothesized that exposure to ketamine will result in an increase in EPSP amplitude and less facilitation - lower percentage change in EPSP amplitude between the first and second EPSPs. This is because ketamine, as an NMDA antagonist, will block NMDA receptors and prevent glutamate from binding to these receptors. Since the negative feedback loop discussed earlier will be disrupted, more glutamate will be released and bind to postsynaptic receptors, which in turn results in more depolarization and EPSP amplitude. Also, ketamine will cause a lower percentage change in the two EPSPs. Most of the postsynaptic receptors will have been occupied with glutamate after the first stimulation, so additional release of glutamate will not cause a much higher second EPSP. In the end, we had to reject our hypothesis because our results showed that ketamine reduces EPSP amplitude and increases paired-pulse facilitation.

MATERIALS AND METHODS

Preparation of the crayfish specimen

In this experiment, we used the crayfish species Procambarus clarkiii. For the preparation of the crayfish specimen, we followed the instructions for dissection in “Crawdad: A Lab Manual for Neurophysiology” (Wyttenbach, Johnson and Hoy, 2012), under the subheading “Muscle Resting Potential.” We began our dissection of the tail by cutting the carapace along the ventral ridges of the shell. We then removed and discarded the superficial muscle to expose the dorsal extensor muscle. After muscle removal, both the nerves connected to the dorsal extensor muscles and the muscles themselves were accessible for observation.

Solutions

Our control condition is basic crayfish saline, consisted of 5.4 mM KCl, 200.7 mM NaCl, 12.3 mM MgCl26H2O, 5 mM Sodium Hepes Buffer, and 6.5 mM CaCl2*2H2O. Immersing the crayfish tail in this basic crayfish saline will prolong the life of the cells and preserve cell fatigue and integrity, which allow for experimentation.

To expose the crayfish dorsal extensor muscle to ketamine, we immersed the crayfish tail in ketamine solutions of either 250 or 500 µM. For the 250 µM ketamine solution, we mixed 99.5 mL of aforementioned basic crayfish saline and .5 mL of a 50 mM ketamine stock solution. For the 500 µM concentration, we mixed 99 mL stock saline with 1 mL of the same ketamine solution.

Making Microelectrodes for Intracellular Recording

We pulled two types of glass microelectrodes using the PUL-1 electrode-pulling machine, manufactured by World Precision Instruments. The recording microelectrode was filled with 3.0M of KCl and was tested for an optimal resistance of 5-10Ω using the A-M Systems Inc. Intracellular Electrometer. The suction electrode was sanded down to effectively capture the nerve that would receive the stimulation. Both microelectrodes were secured in micromanipulators to ensure stability when piercing the muscle cell or capturing the nerve.

Testing Timeline

We performed 4 trials, each with a different crayfish. In each trial, we tested 3 conditions: “control,” “with ketamine” and “return to control.” For the control, we submerged crayfish in basic saline. Then, we replaced the saline with either the 250 µM 500 µM ketamine solution. Finally, we removed the ketamine solution and submerge the crayfish tail in basic crayfish saline once again. We used the 250 µM ketamine solution for two trials, and the 500 µM for the other two. 

Recording and Analyzing Data

To begin recording data, we captured a nerve using the suction microelectrode. We then pierced a deep extensor muscle near the suctioned nerve with a recording microelectrode by using a micromanipulator. We zeroed the junction potential, which was recorded in the extracellular solution, before entering the muscle cell. A resting membrane potential was found using the program LabChart. We then applied on the captured nerve a paired pulse stimulation with a frequency of 0.55 Hz, duration of .05 ms and delay of 40 ms. The stimulation’s voltage magnitude varied from one trial to another because some nerves are more sensitive to stimulation than others. 

We took between 60-90 EPSP recordings for each condition. Whenever we change the conditions (changing the solutions), we allowed a diffusion period of 15 minutes before data recording. Using a module of DataPad, we recorded the EPSP amplitude of both EPSP that result from the paired-pulse stimulation. 

In order to analyze the data, the mean amplitude for the first and second EPSP were calculated for each trial. Then, we averaged the means for the trials that involved the same ketamine concentration. We applied the same method to the percent change in amplitude data. The percent change between the paired EPSPs were calculated using the following equation: Percent change in amplitude = 

((Second EPSP amplitude - First EPSP amplitude) /First EPSP amplitude)*100

We used bar graphs to present our data. Our first graph compares the average EPSP recorded in control condition to that recorded in 500 µM ketamine solution. Another graph compares the percent difference in the two consecutive EPSPs of paired pulse between our aforementioned conditions. The purpose of these graphs is to show the effect of ketamine on facilitation. We also had similar graphs for the 250 µM concentration trials. 

   Initially, we planned to analyze the data using t-test, comparing the EPSP amplitude and the percent change between the paired EPSPs from one condition to another. These comparisons would help us to determine whether to reject our initial hypothesis or not. If there is a significant difference between one condition to another, we can conclude that ketamine has an effect on EPSP. However, since we did only two trials for each concentration of ketamine, we cannot perform a statistical test due to insufficient data. A t-test is only meaningful when used to compare the data of three or more trials.

RESULTS

Our research aimed to test the effects of ketamine, an NMDA receptor antagonist, on the crayfish. In our experiment, we used three different saline baths. We started out with the basic crayfish saline bath to record the baseline and then replaced the solution with either the 500µM concentration of ketamine or the 250µM concentration to the crayfish environment. Finally, we returned to our original control solution to observe any changes. 

           For the average EPSP magnitude values for our first two trials was 11.670mV for the first-pulse and 13.703mV for the second-pulse (Fig. 1). Data of the other two trial revealed a first-pulse magnitude of 12.833mV and 14.258mV for second-pulse (Fig. 2). Over time, the EPSP amplitude did not change significantly in the control condition. Therefore, any changes to EPSP would be the effect of ketamine and not because of cell fatigue over time.

Ketamine reduces EPSP amplitude

When we switched to the 250µM ketamine solution, we saw a significant decrease in EPSP magnitude for both pulses when compared to control data (Fig. 2). The average magnitude for first and second pulse was 3.493mV and 4.605mV respectively. The 500µM concentration bath yielded a similar decrease in EPSP magnitude to the 250µM concentration. The average first- and second-pulse EPSPs were 3.860mV and 4.866mV (Fig. 1). In overall, 250 µM and 500 µM ketamine reduces EPSP amplitude by 65.70% and 70.23% respectively.

When we returned to the control saline bath, we saw EPSP amplitude that were smaller than that of the control data. Our first and second-pulse EPSPs were 1.913mV and 2.548mV for the 500µM concentration trials (Fig. 1) and 1.769mV and 2.179mV for 250µM trials (Fig. 2). 

(Figures are presented on the next page)

Figure 1. Average EPSP magnitude for three testing conditions. The blue bars represent control EPSP magnitudes, orange bars represent the 500µM ketamine concentration testing, and the gray bars represent the return to control data. Error bars represent the range of averages from two trials. N equals 2.

Figure 2. Average EPSP magnitude for three testing conditions. The blue bars represent control EPSP magnitudes, red bars represent the 250µM ketamine concentration testing, and the green bars represent the return to control data. Error bars represent the range of averages from two trials. N equals 2.

Ketamine increases paired-pulse facilitation

For all conditions, we observed a facilitation – an increase in amplitude – from the first EPSP to the second. Percent Change in EPSP is a way to mathematically represent facilitation. The average percent change between control pulses was 17.644% for the 500 µM trials (Fig. 3) and 11.083% for the 250 µM ones (Fig. 4). 

When we switched to the 250 µM ketamine condition, the average percent change increased to 27.303% (Fig. 3). The average percent change in 500 µM ketamine trials was 31.293 %. Both concentration of ketamine resulted in a similar increase in percent change compared to the control. 

Facilitation in the return to control test groups also occurred at a smaller level than both experimental concentrations with an average percent change of 20.056% for 500µM trial days (Fig. 3) and 21.416% for 250µM trial days (Fig. 4).

Figure 3. Average percent difference between first- and second-pulse EPSP magnitudes. Each bar represents the percent difference for a testing group: Control, 500µM Ketamine Concentration, and Return to Control. Percent difference was calculated using this formula: ((Second EPSP magnitude - First EPSP magnitude) / First EPSP magnitude)*100. Error bars represent the range of averages from two trials. N equals 2.

Figure 4. Average percent difference between first- and second-pulse EPSP magnitudes. Each bar represents the percent difference for a testing group: Control, 250µM Ketamine Concentration, and Return to Control. Percent Difference was calculated using this formula: ((Second EPSP magnitude - First EPSP magnitude) / First EPSP magnitude)*100. Error bars represent the range of averages from two trials. N equals 2.

250 µM and 500 µM ketamine solutions results in identical effects

We tested two different ketamine concentrations to determine whether different concentrations of ketamine result in significantly different changes. The effect of 250 µM and 500 µM ketamine turned out to be quite similar (Fig. 5).

(Figure 5 is presented on the next page)

Figure 5. Average EPSP magnitude for 500µM and 250µM ketamine concentration testing. This graph compares the average of the average EPSP magnitudes of each experimental group. Error bars represent range of averages. N equals 2.

DISCUSSION

We hypothesized that exposure to ketamine would increase the EPSP amplitude and cause a lower facilitation between the two EPSPs in paired pulse stimulation. The results did not support both parts of our hypothesis, since there was a decrease in EPSP amplitude and higher facilitation when ketamine was added.

Since Feinstein et. al (1998) found that the binding of NMDA to NMDA receptor decreases the release of neurotransmitter and EPSP amplitude, we would expect ketamine, as an NMDA antagonist, to increase EPSP amplitude. However, our results showed that ketamine caused a lower EPSP amplitude compared to that of the control, demanding further investigations into scientific studies on the drug ketamine. 

The research of Leong (2002) can provide a rationale behind the lower EPSP amplitude for the conditions with ketamine. Leong’s finding challenges the claim that ketamine is a selective NMDA receptor antagonist. Ketamine can also block non-NMDA receptors, such as the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA), causing EPSP amplitude to decrease (Leong 2002). The concern with this inference is the inconsistency in the research subject. Leong experimented with a vertebrate while we did research on crayfish, an invertebrate. However, Craig et. al (2006) confirms the existence of AMPA in invertebrate’s muscle membrane, and also concludes that AMPA receptors are the most prevalent type of glutamate receptor in invertebrates like crayfish. By blocking postsynaptic AMPA receptors, ketamine prevents glutamate from binding to these receptors, resulting in a low EPSP since the postsynaptic ion channels cannot open for ion transfer. Therefore, even though blocking NMDA receptors causes a higher EPSP, the decrease in EPSP caused by ketamine blocking AMPA receptors might have been so overwhelming that it resulted in an overall decrease in EPSP.

To rationalize the increase in paired-pulse facilitation, we continued to look into ketamine additional effects on receptors other than NMDA and AMPA. Besides NMDA and AMPA receptors, Ketamine also influenced other glutamate receptors. Narimatsu et. al (2002) concluded that ketamine causes a higher facilitation the second EPSP in paired-pulse stimulation by activating beta-adrenoceptors . The findings of Ishida et. al (1980) confirms that beta-adrenoceptors are present in crayfish. This study enables us to use Narimatsu’s results in an attempt to explain the higher percent change (facilitation) caused by ketamine.

In order to extensively test the effects of ketamine on the crayfish neuromuscular junction, we used two different concentrations of the drug, 250µM and 500µM. From our data we found that there was not a big difference in the result between the concentrations. The 500µM concentration yielded a slightly smaller reduction of synaptic excitation compared to that of the 250µM. Nevertheless, when we analyzed the data of the 250µM ketamine condition, all the trends discussed above are consistent with those concluded from the 500µM condition. The molecular reasoning for this phenomena could be that the 250µM concentration of ketamine was sufficient to block most of the glutamate receptors. Thus a concentration double that amount would not have made much of a difference.

We noted that Ketamine has a long lasting effect on the crayfish dorsal extensor neuromuscular junction because the EPSPs data (EPSP amplitude and percent change) recorded in the “Control” condition and “Return to control” condition are very different. We know that without ketamine, the crayfish EPSPs don’t change over time (the data is not presented in Results). This observation means that the cell does not die over time and any changes to EPSP are induced by ketamine’s neurochemical effects. Therefore, ketamine seems to have a permanent, irreversible effect on the neuromuscular junction of crayfish. An alternative explanation would be that the recovery time was not long enough. We recorded the EPSP for “Return to control” 10 minutes after replacing ketamine solution with basic crayfish saline, while other studies suggest that the minimum time for recovery is 4 to 5 hours, and may take up to 24 hours (Bioniche Pharma USA, 2009)

Initially, we wanted to examine the effect that ketamine has on NMDA receptors of crayfish. However, since ketamine also affects many other sites and receptors, our results were skewed and the effect on NMDA was not clear. Therefore, for future researches, we would block the AMPA and beta-adrenoceptors by including inhibitors of these receptors in the saline bath. Also, to determine whether Ketamine has a permanent effect on crayfish’s synaptic plasticity, we will allow a recovery period of more than 24 hours in the future.

This study offers a potential answer to the unique properties of ketamine as a non-selective antagonist that shows a direct effect on AMPA receptors. However, such research has not yet been pioneered in the science community. Thus with this reported literature of the extraordinary findings of ketamine’s effects on the neuromuscular junction of crayfish, we wanted to provide a spark for subsequent extensive research to confirm our still limited understanding of the drug and its potential to alter the very core of human behavior.

ACKNOWLEDGEMENTS

We thank our professor Rempel-Clower, Joy Becker, our class mentor, and Jason Parks, our lab assistant, for all of their help and guidance throughout the making of this project. Without their guidance and occasional assistance, we would not have been able to produce these results and this paper.

REFERENCES

Blank, V., Donahue, A.C., and Spector, G. 2000. The crayfish fast extensor muscle exhibits NMDA and non-NMDA receptor activity. Pioneering Neuroscience 1: 1-5. 

Bliss T. V. and Collingridge G. L. A. 1993. Synaptic model of memory: long-term potentiation in the hippocampus. Nature 361:31–39.

Browne, C. A. and Lucki, I. 2013. Antidepressant effects of ketamine: Mechanisms underlying fast-acting novel antidepressants. Frontiers in Pharmacology 4: 161.

Collingridge G. L. and Singer W. 1990. Excitatory amino acid receptors and synaptic plasticity. Trends Pharmacol. Sci. 11:290–296.

Dale N., Kandel E. A. 1993. l-Glutamate may be the fast excitatory transmitter of Aplysia sensory neurons. Proc. Natl. Acad. Sci. USA 90:7163–7167.

Dudel, J., Adelsberger, H., and Heckmann, M.1997. Neuromuscular glutamatergic and GABAergic channels. Invert Neurosci 3: 89-92.

Dudel, J. and Frank, C. 1987. Single glutamate-gated synaptic channels at the crayfish neuromuscular junction. Pflugers Arch 408: 307-314.

Feinstein, N., Parnas, D., Parnas, H., and Parnas, I. 1998. Functional and Immunocytochemical Identification of Glutamate NMDA Autoreceptors of an NMDA Type in Crayfish Neuromuscular Junctions. Journal of Neurophysiology 80(6): 2893-2899.

Ishida, H., Sasa, M., Takaori, S. 1980. Local anesthetic activity of beta-adrenergic blocking drugs in the Crayfish giant axon, with reference to calcium ion. The Japanese Journal of Pharmacology 30(50): 607-619.

Kamiya, H. 2012. “Photochemical inactivation analysis of temporal dynamics of postsynaptic native AMPA receptors in hippocampal slices.” The Journal of neuroscience: the official journal of the Society for Neuroscience 32.19: 6517-6524.

Kamiyama, H., Matsumoto, M., Otani, S., Kimura, S., Shimamura, K., Ishikawa, S., and Togashi, H. 2011. Mechanisms underlying ketamine-induced synaptic depression in rat hippocampus-medial prefrontal cortex pathway. Neuroscience 177: 159-169.

Leong, Darrell Andrew. Ketamine disrupts synaptic transmission by interacting at AMPA/Kainate receptor channels in neocortical neurons. 2002. University of British Columbia 1-34.

Marsden, W.N. Synaptic plasticity in depression: Molecular, cellular and functional correlates. 2012. Progress in Neuro-Psychopharmacology and Biological Psychiatry 43: 168-184.

Martinowich, K., Jimenez, D. V., Zarate, C. A., and Manji, H. K. 2013. Rapid antidepressant effects: Moving right along. Molecular Psychiatry 18(8): 856-863.

Mayer M. L. and Westbrook G. L.1987. The physiology of excitatory amino acids in the vertebrate central nervous system. Prog. Neurobiol. 28:197–276.

Mulkey R. M. and Malenka R. C. 1992. Mechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus. Neuron 9:967–975.

Narimatsu, Eichi, Kawamata, Yurie, Kawamata, Mikito, Fujimura, Naoyuki, and Namiki Akiyoshi. 2002. NMDA receptor-mediated mechanism of ketamine-induced facilitation of glutamatergic excitatory synaptic transmission. Brain Research 953: 272-275.​

Parnas, H., Parnas, I., Ravin, R., Yudelevtich, B. 1994. Glutamate and N-methyl-D-aspartate affect release from crayfish axon terminals in a voltage-dependent manner. Proc Natl Acad Sci 91: 11586-11590.

Ribeiro, P. O., Tomé, A.,R., Silva, H. B., Cunha, R. A., and Antunes, L. M. 2014. Clinically relevant concentrations of ketamine mainly affect long-term potentiation rather than basal excitatory synaptic transmission and do not change paired-pulse facilitation in mouse hippocampal slices. Brain Research 1560: 10-17.

Saitow, F., Suzuki, H., Knoishi, S. 2005. ß-Adrenoceptor-mediated long-term up-regulation of the release machinery at rat cerebellar GABAerfic synpases. J Physiol. 565(Pt 2): 487-502. 

Schramm, M. and Dudel, J. 1997. Metabotropic glutamate autoreceptors on nerve terminals of crayfish muscle depress or facilitate release. Neuroscience Letters 234(1): 31-34.

Shinozaki H. 1988. Pharmacology of the glutamate receptor. Prog Neurobiol 30: 399-435.

Walker, W.S., Brockie, P.J., Madsen, D.M., Francis, M.M., Zheng, Y., Koduri, S., Mellem, J.E. Struz-Seebohm, N., and Maricq, A.V. 2006. Reconstitution of invertebrate glutamate receptor function depends on stargazin-like proteins. Proc Natl Sci USA 103(28): 10781-10786.-311.

Portrait Essay - Who runs the world?

    Women: A simple word that has the potential to trigger numerous and endless conversations among historians, artists, writers, religious figures, most of whom are male. Women are multi-faceted and complex in nature. 

According to Christianity, Eve was the woman who listened to the snake and committed the original sin; and from that same woman, human kind was born and flourished. Taking advantage of this complexity of the other gender, James Joyce repeatedly implements the image of women in his autobiographical novel: “The Portrait of the Artist as a Young Man.” 

The life, morality and artistry of the protagonist, Stephen Dedalus, are heavily influenced by the various female figures that he encounters at each stage of his physical and mental development. By incorporating motif of several female figures that permeates throughout the kuntslerroman, Joyce illustrates the growth of Stephen as a person and as an artist. His mother’s care and affection result in Stephen’s craving for a motherly figure when he was in bed with a prostitute. Eileen, Mercedes and Emma serve as moral compasses, guiding his sense of morality and artistry as he makes decisions that shape his identity. Finally, Stephen sees parts of himself in the girl who os sunbathing on the beach when he has an epiphany about his choice of identity and his mission as an artist.

Stephen's relationship with the opposite sex begins to develop early in his life. Within the first few pages of the novel lie hints of the different roles women will play in his story. Senses are sources of inspiration for an artist, since art intensifies the sense of immediate living and accentuates what is valuable in enjoyment. 

Therefore, sensory ability is directly proportional to artistry. Stephen expresses and develops innate artistic talent as he, influenced by female figures around him, characterizes his world with senses. Betty Byrne is associated with the sour taste of lemon platt. His mother introduces him to the auditory sense when she sings him a song and plays on the piano for him to dance. As a five or six year-old boy, Stephen starts to differentiate between warm and cold, between the smell of the oil sheet and that of his mother, who “had a nicer smell than his father” (Portrait,7).  

Dante broadens his sense of color with her marron and green brushes for two different politicians in her press. She also becomes the first to give Stephen some experience of the world outside himself when she teaches him about geographical features in other countries and on the moon. This physical understanding of the exterior world may be “the impetus for Stephen’s subsequent construction of a hierarchical list that defines his place within the universe” (Coyle, 52). From the moment Stephen’s infantile conscience unfolds, female’s influence on his growth and artistry is undeniably abundant.

The various female figures that Stephen encounters throughout his life serve as his artistic inspiration. Upon listening to a song sang by his mother, Stephen creates his own version of the song, changing the lyrics into “O, the green wothe botheth” (Portrait, 7). By using incorrect, incomprehensible words, James Joyce underscores Stephen’s ability to take a common, cliqué phrase and turn it into his own. 

This is simultaneously the creative power and mission of the artist, which Stephen identifies in his epiphany later in the novel as “to recreate life out of life” (Portrait, 434). From his childhood leading up to this epiphany, many female figures, real or fictional, inspire him to generate and discover his own art. Both Dante and Stephen's own mother assert that he "will apologise" or "the eagles will come and pull out his eyes" (Portrait, 8). 

This incident results in Stephen's composition of a poem based on "apologise" and "eyes," one of his first artistic endeavors. Dante and Mrs. Dedalus, by planting these words in Stephen’s mind, are the first females to inspire him to create. Another female figure, Eileen, indirectly leads Stephen to the conclusion that "by thinking of things you could understand them" (Portrait, 287) when he sees in her hands and hair possible meanings for the terms Tower of Ivory and House of Gold. 

In the kunstlerroman, Stephen writes two poems using Emma Clery as inspiration, a super-romanticized one in his early childhood and a villanelle ten years later. Because both poem vaguely evoke Stephen’s feelings of love, desire and confusion rather than focusing on Emma’s specific characteristics, some critics argue that Stephen “devotes these poems to his poetic, idolized and ideal model of a “beloved” rather than Emma herself” (Coyle, 127). Either way, Emma is an indispensable driving force that stimulates Stephen to write poems, which are yet another indication of Stephen’s gradual but inevitable transformation into an artist. 

The key to understanding the relationship between women and creation lies in Stephen's association of himself with his mythological name, Daedalus. In Greek mythology, Daedalus (meaning “clever worker”) was a skillful craftsman and artisan. Pasiphae, wife of King Minos, provides Daedalus with the impetus to create when she asks him to construct a cow-shaped shell in which she can hide in order to have sex with a bull (Wikipedia). If the readers take this myth into consideration, there is enough evidence that this connection between female figures and invention of art goes beyond the novel and is integrated into Stephen’s identity.

Women also serve as moral compasses for Stephen to make choices that shapes his identity as a person and as an artist. Throughout his life, each of the various female figures marks a stage of mental development and artistic ideology. Young Stephen's first romantic interest in the opposite sex comes in the form of his playmate, Eileen, whom he plans to marry when they are older. Stephen adore Eileen for her physical characteristics, such as long thin cool white hands. 

This “recognition of women as sexual beings” (Coyle,132) manifests itself again when Stephen begins to have sexually-driven fantasies about Monte Cristo’s Mercedes. He expects that he will be transfigured when he encounters his Mercedes, that “weakness and timidity and inexperience would fall from him in that magic moment” (Portrait, 60) Stephen, on the metaphorical moral bridge, decides to immerse in sin, and believes that sin is needed for the creation of art. His desire draws him toward the prostitute, who calls Stephen “Willie dear” and “a little rascal” (Portrait, 101). 

These terms of motherly endearment, along with the repetition of “his lips would not bend to kiss her” capture the protagonist’s disillusionment when his poetic ideal shatters against harsh reality. Stephen feels awkward and is conscious that the sexual experience is “too much for him” (Portrait, 101). The emotion is similar to when he has to play football or endure math classes in highschool. At this point, the woman beauty perceived by Stephen is purely sexual. It induces in him what he would later call “kinectic emotions”. 

From then, Stephen temporarily loses his moral and artistry direction. Being overwhelmed with guilt from his sins that clouds his mind from creating art, the young artist seeks refuge in piety and in mortifying his senses. However, his art – reflected in the narrative in the beginning of chapter IV – becomes extremely dry, lacking the usual rich details that overflow in earlier section:

Sunday was dedicated to the mystery of the Holy Trinity, Monday to the Holy Ghost, Tuesday to the Guardian Angels, Wednesday to saint Joseph, Thursday to the Most Blessed Sacrament of the Altar, Friday to the Suffering Jesus, Saturday to the Blessed Virgin Mary. (Portrait, 140)

It is not until Stephen encounters the girl sunbathing that he stops wandering hither and thither between absolute piety and sin, between whores and priests. Upon the sight of this female figure, Stephen epiphanised his mission as an artist and the path he must walk to establish his identity. He sees and admires the girl’s beauty with the “esthetic motion,” which is static and “raised above desire and loathing” (Portrait, 203).  

Dedalus becomes aware that he can neither be hither or thither, but must invent a new religion and become “the priest of eternal imagination” (Portrait, 204). The girl sunbathing on the beach, an angel of youth and beauty, is a secular version of the Virgin Mary. She reveals to Stephen the possibility of achieving heaven and producing great art without the church by not conforming to the norm and choosing his own ideal of artistry. 

Once again, a female figure exerts a driving force and provides inspiration for Stephen’s biggest epiphany, a catalyst for his decision of "encounter for the millionth time the reality of experience and forge in [his] soul" (Portrait, 253).  

There is enough evidence to claim that Stephen owns his inspiration for artistry, art creation and identity to the various female figures that he encounters throughout the kuntslerroman.  Stephen, or Joyce himself, attempts to deny this reliance on and attachment to women by incorporating reoccuring images such as birth in the scene of Stephen and the prostitute, and the image of birds flying away from the net and soar high in the scene of the sunbathing girl. 

The author even includes the details of Stephen’s mom “putting [his] new secondhand clothes in order”(Portrait, 252) and praying before Dedalus leaves Ireland to live his own life, with the possible intention of showing the protagonist’s independence from the care of his mother. 

However, when one examines the passage where Stephen encounters the sunbathing girl, one can find small but essential details, such as the parallel phrases “He was alone” – “She was alone” and “a faint flame on her cheek” (Portrait, 166),  a flame that is similar to that on Stephen’s cheek when the Director of Studies mentioned “le jupes.” These details may imply not only the great extent to which Stephen depends on women, but also the idea that Stephen sees himself in the girl, and that the process of creation has a feminine characteristic.

A Lie That Stupefies

(A Research Paper of US History course done by Su in Pomfret.)

Humans have an inclination to overgeneralize and oversimplify. This psychological tendency is the root of many significant problems in the world, such as stereotyping and prejudice.

Oversimplifying history, however, can result in severely misinformed understandings and interpretations of historical events. Nowadays, there is a popular and unchallenged misconception that the Civil War occurred because slavery was practiced in the South, and that the determination to abolish such an immoral practice as slavery left the United States with no option other than a resort to arms. 

This is a view which cannot be rectified by many historical facts. The aftermath of the Civil War, specifically the Emancipation Proclamation, proved that slaves - though being an integral force that helped the Union win the Civil War - did not achieve their goal of total freedom and abolition of slavery. 

This suggests that the North did not fight to end slavery. In fact, the proclamation and Lincoln’s tactics in the war serve as evidence to reveal how the North used the idea of slavery to gain military support from the slaves, to prevent foreign intervention, and to change the focus of the war.

There is a popular but inaccurate notion that eliminating slavery was the North’s prime motivation to enter and fight the Civil War. Historians such as Allen Guelzo [1] and James Oakes [2] argued that Lincoln and the Union in general viewed slavery as a cruel, inhumane laboring system that needed to be eradicated. 

According to them, the North was no longer willing to tolerate slavery as being part of the fabric of US society and that Lincoln was planning to abolish slavery from the first day of his presidency. 

This is what we are all taught in school; and the idea is strongly entrenched today. Most of post-1965 texts define the motivation of Northern soldiers in the war to be emancipation and freeing of slaves, rather than the saving of the Union. 

According to Henry Bragdon, Samuel McCuthen, and Donald Ritchie (1992) [3], the Northern population could never justify the war by mere restoration of the Union; another text suggests that the Emancipation Proclamation "aroused a renewed spirit in the North" and strengthened the will to win the war (Downey and Metcalf 1997:375, 461-62) [4]. 

These historical criticisms and textbooks all share the same point of view: that the major goal of the North was not preserving Union but "the movement to free the slaves and an enduring commitment to racial justice" (Boyer, Todd, and Curtis 1995:379-80) [5]. 

More radical historians insist that “since slavery was the war's moral issue, Emancipation was the cement that only held the North together (Buggey et al. 1987:391) [6]. This understanding and interpretation oversimplifies a complex issue, and even cause some distortions of the truth. 

Historical record and evidence – some of them provided by distinguished historians such as Foner, McPherson, and Gallagher – revealed that slavery was only used as an instrument to ensure victory of the Union.Many historians argued that freeing slaves from cruel bondage was the sole purpose of Union soldiers; in reality, few Union soldiers professed to fight for racial equality. 

The majority of soldiers was either apathetic about the issue of slavery or oppose emancipation and the freeing of slaves. Even if there was an antislavery sentiment, it was not necessarily an abolitionist position resulting from humanitarian concerns for the slaves. Rather, it stemmed from the mindset that portrays the South as underdeveloped and barbaric compared to the North. 

In a letter to his to his wife from Tennesse in 1862, the colonel of the 53^rd Indiana unit described his belief and how backwards the South is:

“I am no abolitionist, but the more I see of slavery in all its enormity the more I am satisfied that it is a curse to our country…Outside the towns in the South the people are a century behind the free states.” [7] 

As Northern armies invaded the South, they hid fugitives in camps and prevent their masters from reclaiming them back [8]. Some historians identify this as an abolitionist movement. Nevertheless, these soldiers were more pragmatic than altruistic. They understood that every slave laborer who emancipated himself by coming into the Union lines weakened the Confederate war effort and strengthen the Union army. 

An indisputable proof for this counterargument was the way Union soldiers treated slaves. One lieutenant could not be more blunt in his letter when he said that “I don’t care a damn for the darkies…I have 11 negroes in my company now. They do every particle of the dirty work. Two women among them do the washing for the company.” [9] The soldiers viewed slaves as property and exploited slave’s labor, identical to what Confederates and slave owners did. 

This illustrate that Union soldiers were not genuinely concerned for the human rights and well-being of slaves.  Furthermore, many Union soldiers strongly opposed the idea of freeing the slaves. Numerous soldiers said that if Lincoln caved in to “these ‘black Republicans’” and made it “an abolition war… I for one shall be sorry that I ever lent a hand to it.” [10] 

Their resistance to any notion of turning a war for Union into a war against slavery has been one reason for Lincoln’s hesitancy to embrace emancipation. 

Lincoln addressed this issue of a divided Union in a letter to his friend Joshua Speed in 1855: “But you say that sooner than yield your legal right to the slave -- especially at the bidding of those who are not themselves interested, you would see the Union dissolved.” [11]  

Some Union soldiers feel betrayed because of the Emancipation Proclamation. This proves that they were willing to risk their lives for Union, but not for black freedom. Lieutenant colonel of the 3rd New York was enraged, stating that “I did not come out to fight for the nigger or abolition of Slavery…Lincoln ought to be lashed up to 4 big fat niggers & left to wander about with them the balance of his life” [12]. 

The Emancipation Proclamation intensified a morale crisis in Union armies during the winter of 1862-1863, especially in the Army of the Potomac, resulting in a sharp rise in Desertion rates. The cause of Union united Northern soldiers; the cause of emancipation divided them.

How could the Union have aimed to fight for racial equality when their leader, President Abraham Lincoln, did not believe in equal social and political rights between whites and blacks? The contemporary perception of Lincoln is a flawed and misinformed one, inconsistent with historical evidence.  

In a survey carried out by Knowledge Networks between July 13 and July 17,2001, approximately 1,000 American adults were asked the question:  "Suppose a nephew or niece about 12 years old had just heard some mention of Abraham Lincoln and asked you to explain what Abraham Lincoln had done. What would you say?” 

The results show that 66.3% of those adults mentioned Lincoln as “The Great Emancipator” – who fought to abolish slavery, who freed and gave slaves social and political rights – while only 14.2% of respondents have any mentions of Lincoln as the savior of the Union [13]. 

Clearly, the image of Lincoln as a man who abhorred slavery and racial discrimination is ingrained in the public’s opinion. Supporters of this view will be disillusioned had they known that eliminating slavery was the last thing on the president’s mind.  

On September 18, 1858, in his fourth debate with Stephen Douglas during the Illinois race for U.S. Senate, Lincoln was straightforward about his view: ““I will say then that I am not, nor ever have been, in favor of bringing about in any way the social and political equality of the white and black races,” [14] he began, going on to say that he opposed blacks having the right to vote, to serve on juries, to hold office and to intermarry with whites. 

Even as President, his belief did not change. “I have no I have no purpose, directly or indirectly, to interfere with the institution of slavery in the States where it exists. I believe I have no lawful right to do so, and I have no inclination to do so,” [15] the “Great Emancipator” declared in his Inauguration speech. 

Some historians are not convinced by these evidence, saying that Lincoln was compelled to tell the public statements that contradicts his true belief in order to win popular support. 

His letter to Horace Greeley in 1862, which reaffirms the President’s real motive behind the war, invalidates this interpretation:

“My paramount object in this struggle is to save the Union, and is not either to save or to destroy slavery. If I could save the Union without freeing any slave I would do it, and if I could save it by freeing all the slaves I would do it; and if I could save it by freeing some and leaving others alone I would also do that.” [16]

Contrary to popular belief, Lincoln was not an abolitionist; he was not concerned about slaves and the cruelty of slavery. Because he was the leader of the Union troops, the person who gives the army a common cause to fight the war, eradicating slavery could not have been the intention for the North to fight the Civil War.

The Emancipation Proclamation is one of the most misunderstood documents in American history; its purpose was not to free slaves, but to weaken the South while enforcing the North with black soldiers, to prohibit foreign intervention and to justify the war. 

Historians like Guelzo and Oakes refer to the Emancipation Proclamation as the most convincing evidence that conflict over slavery is at the heart of the Civil War, arguing that it freed a significant number of slaves. This is a confusion between the means and the ends.  

The reason that Emancipation Proclamation was issued did not involve slaves. Continuing lack of military success make emancipation necessary, since emancipated slaves might help meet the army’s growing manpower needs. 

Lincoln knew that the South was using enslaved people to aid the war effort, that black men and women were forced to build fortifications, work as blacksmiths, nurses, boatmen, and laundresses, and to work in factories, hospitals, and armories. 

The president was therefore forced to release the proclamation to stop this military aid and weaken the South.  Another similar legislature by Lincoln to punish the South was the First Confiscation Act on August 6, 1861. 

According to this act, fugitive slaves were declared to be "contraband of war" if their labor had been used to aid the Confederacy in any way; and if found to be contraband, they were declared free [17]. 

Indeed, the Emancipation Proclamation and the First Confiscation Act were devastating to the South’s army.  A Confederate general stated in 1862 that North Carolina was losing approximately a million dollars every week because of the fleeing slaves [18]. Slaves were merely manipulated as an instrument to ensure the North’s victory.

Emancipation Proclamation helped the North win the war and preserve the Union more than bettering the conditions of slaves. Lincoln’s action made the war no longer merely a contest between North and South; but a contest between human rights and human liberty on one side and eternal bondage on the other. 

After  Lincoln’s Proclamation “foreign nations will now have to come out flat-footed and take sides; they dare not go with the South for slavery, and consequently they will all be ranged on our side.”[19] Britain, along with other European countries that had abolished slavery, could not become diplomatically hypocritical and aid the South during the war. This morality switch in the purpose of the war also diminished the South soldiers’ fighting willpower. Confederates began to accept a defeat that would rid themselves of the moral burden of slavery. 

The Emancipation Proclamation made many white Southerner “even more uneasy about their isolation in a world in which the great powers of Europe, now joined by the US, sought to extirpate slavery.” [20] Unable to bear the weight of world moral disapproval, many Confederates abandoned their commitment to slavery – and with it a major reason to strive for an independent southern nation.  

On the other hand, the Emancipation Proclamation also enabled blacks to enlist in Northern armies. By the end of the war more than 186,000 black soldiers had joined the Union army; 93,000 from the Confederate states, 40,000 from the border slave states, and 53,000 from the free states. [21] 

The racism and discrimination was evident in the North’s army, however. Black soldiers therefore received $7 per month, plus a $3 clothing allowance, while white soldiers received $13 per month, plus $3.50 for clothes. “Are we soldiers, or are we laborers?” James Henry Gooding, a black soldier, wrote directly to President Lincoln. “We are fully armed and equipped, and have… done a soldier’s duty. Why can’t we have a soldier’s pay?” [22] 

Of course, it would be extremely biased to overlook the fact that Emancipation Proclamation freed slaves. Nonetheless, Lincoln did not free slaves with a stroke of his pen. The Proclamation applied almost exclusively to areas under Confederate control. Thus, it had no bearing on the nearly half a million slaves in the border slave states that had never seceded from the Union, or on more than three hundred thousand slaves in areas of the Confederacy occupied by Union soldiers and exempted by Lincoln from its coverage – the entire state of Tennessee and parts of Virginia and Louisiana. [23]

Therefore, putting over-emphasis on the Proclamation’s freeing of slaves rather than the advantages it provided for the Union is an incorrect and distorted interpretation of the abundant historical evidence. Emancipation was an afterthought, a last resort, a means, not an end.    

The North did not fight for racial justice nor freedom of slaves; they fought to preserve the Union. Now that the misconception has been dismantled, one cannot help but wonder why the oversimplified and inaccurate representation of the Civil War is so prevalent in public opinion. One possible explanation for this phenomenon is that abolishing slavery was an excuse for Americans, both common people and the authority, to justify this gory war. 

Contrary to popular belief, the war was unnecessary and was avoidable. If intense desires to end slavery of the North and to preserve slavery in the South were truly the central conflict of the war, Americans could probably have reconciled the conflict without shedding a drop of blood. 

The author of The Right and Wrong in Our Civil War suggests a very plausible theory that a sum of money equal to one fifth of the loss caused by the Civil War would be sufficient to pay their masters more than twice the average market value of every black man, woman and child [24]. 

However, the war ended with both the North and South devastated. Historians, textbook writers and educators – while striving to remain neutral and unbiased in their interpretation of the Civil War – made the war seem unavoidable, that it was an all glorious birth of true democracy, and that no one was to blame. 

Today, American youth simply boast about how big and brave their ancestors were. Too often, the moral element is ignored and the vital truth is unrecognized. Americans need to build up courage and view the Civil War under an earnest lens in order to see how unnecessary and unjustifiable the war was, and how befogged and gullible their mind were to think otherwise. 

[1] Allen C. Guelzo, Lincoln's Emancipation Proclamation: The End of Slavery in America (New York: Simon & Schuster, 2004)

[2] James Oakes, The Ruling Race: A History of American Slaveholders (New York: Alfred A. Knopf, 1982).

[3] Bragdon, Henry W., Samuel Proctor McCutchen, and Donald A. Ritchie. History of a Free Nation. New York: Glencoe/McGraw-Hill, 1998. Print. As appeared in History, Commemoration, and Belief: Abraham Lincoln in American Memory, 1945-2001 Barry Schwartz and Howard Schuman American Sociological Review Vol. 70, No. 2 (Apr., 2005) , pp. 183-203 . Published by: American Sociological Association

Stable URL: http://www.jstor.org/stable/4145367

[4] Downey, M.T.G. Jr. and E. D. Metcalf. 1997. United States History: In the Course of Human Events. St. Paul, MN: West Publishing.

[5] Boyer, Paul, Lewis P. Todd, and Merle Curti. 1995. TheAmerican Nation. Austin, TX: Holt, Rinehart, and Winston.

[6] Buggey, Joanne, Gerald A. Danzer, Charles L. Mitsakos, and Fredrick Risinger. 1987. America! America! Glenview, IL: Scott, Foresman and Company

[7] Walter Q. Gresham to Tillie Gresham, March 24, 1862, Gresham Papers, LC , as appeared in McPherson, James M. For cause & Comrades. Oxford, Newyork: Oxford University Press, 1997.

[8] McPherson, 118

[9] Charles Wills to family, April 16, 1862 in Army Life of an Illinois Soldier: Letters and Diary of the late Charles Wills (Washington,1906), 83,158

[10] Charles S. Wainwright, Diary, entries of Jan. 15 and May 29, 1862, HEH.

[11] Abraham Lincoln to Joshua Speed, August 24, 1855 as appeared in Lincoln, Abraham, and Roy P. Basler. The Collected Works of Abraham Lincoln. New Brunswick, NJ: Rutgers UP, 1953. Print.

[12] Henry P. Hubbell to Walter Hubbell, Jan. 26, Feb.7, 1863, Hubbell Papers, FLPU as appeared in McPherson, 125

[13] Survey of Knowledge Networks and Maryland, as appeared in Schwartz and Schuman, 189

[14] Pruitt, Sarah. "5 Things You May Not Know About Lincoln, Slavery and Emancipation."History.com. A&E Television Networks, 21 Sept. 2012. Web. 01 Mar. 2014.

[15] Abraham Lincoln's First Inaugural Address". Abraham Lincoln's Classroom. Retrieved 2010-04-12.

[16] Abraham Lincoln’s letter to Horace Greely, 1862, as appeared in Lincoln and Basler

[17] "Confiscation Acts." Encyclopaedia Britannica. Encyclopaedia Britannica Online Academic Edition. Encyclopædia Britannica Inc., 2014. Web. 02 Mar. 2014.

[18] Gallagher, Gary W. The Confederate War. Cambridge, MA: Harvard University Press, 1997. 

[19] George W. Biedelman to father, Oct. 1, 1862, in The Civil War Letters of George Washington Beidelman, ed. Catherine H. Vanderslice (New York, 1978), 116

[20] Gallagher, 26

[21] Gallagher, 30

[22] Foner, Eric. Forever Free. Illustrated by Joshua Brown. Edited by Christine Doudna. N.p.: Afred A. Knoff - Borzoi Book, 2005, 55

[23] Foner, 57

[24] The Right and the Wrong in Our Civil War AN OLD SOLDIER and H. B. S. The Advocate of Peace (1894-1920)

Vol. 65, No. 9 (SEPTEMBER 1903) , pp. 160-164 Published by: World Affairs Institute Stable URL: http://www.jstor.org/stable/25752194

Su's Chapel Speech, Monday Dec 16, 2013

Good morning,

12-year-old me was playing tag with my friends in my middle school’s playground and I was “It”. I remembered the wind rushing against my face as I took big strides, running in circles to tag another person. 

The moment I found my target, I accelerated. My mouth was wide open as I tried to breathe and laugh at the same time. I was about 3 feet away from my target when I saw HIM standing in my way. In a fraction of a second, the following things happened: I tried to steer away from him, he put his leg out, his leg tripped me and I fell.

I face-planted to the ground and slid a few inches forward with my mouth still opened. My teeth scraped the hard cement that was heated by the scorching sun. The impact caused my right incisor to fracture, as you can see here (Points to tooth) and influenced how my teeth are arranged. Although the taste of blood and dirt overwhelmed my senses, I could still see his smirk in the corner of my eyes.

He was a bully. He bullied me because I “look fat and clumsy,” and that irritated his eyes. Yes, I was overweight back then. After tripping me, he walked away and pretended like nothing happened as teachers rushed in to help me stand up. 

Those who I called friends, the only ones who witnessed the whole thing, told the teachers that I fell on myself. They were scared that he would beat them up.

After that day I went on fasts. I asked my parents to eat meals in my room just so I can throw the food away. The scale kept slipping downward, the number shrank like my dying stomach. The measuring tape became reins and I became the horse of weight-obsession. It directed my life, told me where to go. That incident also put the lens of cynicism onto my eyes. 

Growing up, I had numerous acquaintances but no friends. I pushed away whoever tried to be close to me because I did not want to get hurt again. This cynicism has diminished a lot during my time at Pomfret, but I don’t think it will disappear anytime soon.

But it was not all negative. That bully taught me how to fend for myself, how to fight back or die trying. He was my first and last bully. He also motivated me to work hard, to improve and broaden my knowledge everyday so that no one can bully me physically or intellectually. I am sure that I would have given up several times without this motivation. 

Being a victim of bullying also made me strive to do everything I can to help people around me, because I understand how significant an impact one individual can have on another. Something as simple as a hello, a smile or “how has your day been” can do wonders. So, Pomfret, be conscious of everything you say, everything you do to others. Challenge yourself to reach out to those around you, even if you’re too busy minding your own life.

Some people will think it’s bad to have my life influenced too much by another person. But it’s hard not to. I am reminded of him every morning when I brush my teeth and every time I grin. My parents told me I should go to the dentist to get the fracture fixed, but I refused. I like to keep it as a reminder of the incident, so that I continue to work hard and not treat anyone badly. It’s like a battle scar, just cooler. I realize that the fractured tooth may chase girls away, but I don’t need those superficial girls anyways. Those who matter don’t care and those who care don’t matter.

I recently learned that the bully dropped out of high school and is currently in rehab. Sometimes I wonder, what will I do to him were we to meet? I thought about spitting on his face to get revenge. But then I thought, if I do that, I’ll be equal to him and I don’t want that. The years I spend working so hard, my education in America will be wasted, meaningless. I guess I will tell him: “Thank you, thank you for shaping me to who I am today.”

I will forgive but never forget.

Thank you for listening.