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F E A T U R E The Psychopathic Brain Understanding Paranoia To Fall In Love With Someone, Maybe Do This! Mind, Brain and Music Interneuron . Volume 2, Issue 3 . February 2015 INTERNEURON

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Page 1: Interneuron - Issue 2.3

FEATURE

The Psychopathic BrainUnderstanding Paranoia

To Fall In Love WithSomeone,Maybe Do This!

Mind, Brain and Music

Interneuron . Volume 2, Issue 3 . February 2015

INTERNEURON

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TABLE OF CONTENTS1236

15

1213

78

171820

Understanding Paranoia

Letter from the Editors

The Psychopathic Brain

Mind, Brain and Music

ARTWORK

Lost In Music

FEATURE

To Fall In Love With Someone,Maybe Do This!

Oxytocin and Neurobiologyof Storytelling

ARTWORKScrawling In the Night

Faculty Profile: An AfternoonWith Dr. Melissa Holmes

OPINION

Profile: Alina Guna

Fear and Forgetting

Get Involved!

10

ARTWORK

Erasing Fear Memories

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Contributors

Cover ArtLouise Escuban

AuthorsAnn Sheng

Danitsa Vasiteva

Alexandra Mogadam

Sawayra Owais

Alina Guna

Stefan Jevtic

Alex Ghali

Nancy Diaz

ArtworkLouise EscubanAnn Sheng

Sarah Crawley

LayoutYasmine Abdelaal

Aileen ZhouOshien LekhwaniLouise Escuban

Executive TeamOmar BitarTheo BruunSteven Meas

Yasmine AbdelaalAlex JacobToni DaynoSarah PetersSusmita Sarkar

Editors-in-Chief

Letter from the Editors

Welcome back from Reading Week! We hope you were able to spend theweek finding warmth and refuge from Toronto’s bitter cold, whether bydipping your toes in an ocean or cozying up at a coffee shop.

We are glad to present Issue 2.3, featuring emotion. During our most recentcall for submissions, the Editorial Team was ecstatic to receive so manymessages from eager authors! Our submissions editors were happy to workwith you to present some (hopefully!) interesting topics.

Before you delve into this quarter’s magazine, we would like to briefly revisitthe Interneuron’s mission. As a student-led publication, we aim to provide aplatform for students to build scientific communication skills - a key asset forthose of you who aspire to research, graduate school, and professionalprograms. Even further, we hope that having access to a compilation of yourpeers’ writing will inspire you to strengthen your passion for neuroscience -even if you’re in another program! As you read, please keep in mind thatarticles represent the author’s personal interest, research, and opinions.

Next, we have a few exciting announcements! First, Interneuron has beenofficially certified by the Co-Curricular Record (CCR). What does this meanfor you? During the next school year, Editorial Team members will have theopportunity to gain recognition for their dedication to Interneuron;contributing authors and artists can also receive recognition if they fulfillsubmission and meeting attendance requirements.

We would also like to invite all readers to our next General Meeting onMarch 13th. Meetings are informal, drop-in, and a great way to connect withthe team, contributors, and other readers. In each meeting, we spend sometime casually brainstorming ideas for the upcoming issue, so we’d love tosee you there!

Lastly, we plan to host a year-end event in recognition and appreciation ofall of the contributors and readers who have helped grow Interneuron in ourfirst year as a UTSU-recognized publication. In honor of how far we havecome, don’t miss a special opinion piece on graduate studies from AlinaGuna, one of Interneuron’s founders, featured in this issue!

As always, please feel welcome to send us any questions, ideas, orfeedback. Enjoy the issue!

Regards,

Dear Readers,

Sarah & Susmita

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We see them in crime shows and horror movies—cold-

blooded serial killers that attack their victims without feeling

guilt, empathy, or remorse: psychopaths. Yet this “classic”

psychopath seldom appears in its most infamous form in real

life; more common are encounters with individuals suffering

from Antisocial Personality Disorder (ASPD). According to a

study in southern Wisconsin using a sample of nearly 2,000

participants, 8% of adult malesmet criteria for ASPD [1]. This

prevalence is even higher among male prisoners, as

demonstrated in a large study in England and Wales with

ASPD rates exceeding 63% [2]. Most of the individuals with

ASPD can be found in youth detention centers and prison;

however, wemay often see them in high corporate positions.

According to the DSM5, ASPD is

characterized by deceitfulness, aggression,

and lack of remorse and empathy [3]. Does

this sound familiar? As you may have

guessed, this description seems to fit the

typical CEO profile. The trendy term

Corporate Psychopath [4] seems to be

appropriate because in addition to engaging

in antisocial behavior, CEOs are often

callous and unemotional, impulsive, and

highly narcissistic [5]. A recent study

suggests that antisocial behavior is related to

deficits in emotional processing [6].Themost

prominent and striking emotional deficit in

psychopathy is the lack of empathy and

remorse. Indeed, it sometimes seems that

upon arrest, criminals only regret being

caught and punished for their actions—not

for committing the crime itself. This largely

reflects discrepancies in their emotional

regulation processes particularly associated

with a lack of empathy. Studies demonstrate

that the amygdala is often active when experiencing a variety

of emotions such as rage, fear, and pleasure; its role within

the perception and expression of empathy has also beenwell

documented [7]. Empathy is a strong emotion and a strong

motivator that is triggered when the observation of the

emotional states of others creates a shared state in

ourselves. The experience of empathy—for example, when

we see others suffering or in pain—has been linked to mirror

neurons which some scientists believe activate brain regions

based on observation of an emotion in others [8]. This ability

to experience a similar emotionmerely by observing others is

arguably one of the many characteristics that make us

human.

Nancy DiazThe Psychopathic Brain

2 Interneuron . Volume 2, Issue 3 . February 2015

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So how does the antisocial brain differ from ours? Although

the answer to this question is certainly complex, current

research indicates that individuals with ASPD demonstrate

significant reductions in gray and white matter in the

prefrontal cortex and limbic system [6][9]. Both of these

structures are associated with higher cognitive processes

and emotional processing: two functions that seem to be

implicated in ASPD and psychopathy. A recent fMRI study

revealed that psychopaths tend to perform poorly in facial

expression recognition and are less likely to correctly and

rapidly identify happy and fearful faces; this was associated

with dysfunctional neural networks between the amygdala

and visual and prefrontal cortices [10]. Other studies have

suggested that the orbitofrontal cortex and ventromedial

prefrontal cortex are implicated in the neuropathology of

ASPD, particularly regarding emotion regulation [7]. While

these prefrontal and limbic areas have been associated with

ASPD, it is likely that other brain regions are also involved.

The evidence across the research reminds us that despite

their superficial simplicity, emotions play an imperative role in

guiding our thoughts and behaviors. While many of us often

deem criminal behavior to be entirely under the perpetrator’s

control, we must ask ourselves whether the structural

differences in the brain are enough to justify behaviors.

References1. Barry, K. L., Copeland, L. A., Fleming, M. F., & Manwell, L. B. (1997).Conduct disorder and antisocial personality in adult primary care patients.Journal of Family Practice, 45(2), 151+. Retrieved from

2. Singleton N, Meltzer H, Gatward R. Psychiatric morbidity among youngoffenders in England andWales. London: Office for National Statistics; 20003. Diagnostic and statistical manual of mental disorders : DSM-5. (2013). InAmerican Psychiatric Association., American Psychiatric Association.(Eds.), (5th ed. ed.). Arlington, Va.: American Psychiatric Association.4. Boddy, C., Ladyshewsky, R., & Galvin, P. (2010). The influence ofcorporate psychopaths on corporate social responsibility and organizationalcommitment to employees. Journal of Business Ethics, 97(1), 1-19.doi:10.1007/s10551-010-0492-35. Henning, J. B., Wygant, D. B., & Barnes, P. W. (2014). Mapping thedarkness and finding the light: DSM-5 and assessment of the “Corporatepsychopath”. Industrial and Organizational Psychology, 7(1), 144-148.doi:10.1111/iops.121236. Aoki, Y., Inokuchi, R., Nakao, T., & Yamasue, H. (2014). Neural basesof antisocial behavior: A voxel-based meta-analysis. Social Cognitive andAffective Neuroscience, 9(8), 1223-1231. doi:10.1093/scan/nst1047. Murray, E. A. (2007). The amygdala, reward and emotion. Trends inCognitive Sciences, 11(11), 489-497. doi:10.1016/j.tics.2007.08.0138. Bernhardt, B. C., & Singer, T. (2012). The neural basis of empathy.Annual Review of Neuroscience, 35, 1-23. doi:10.1146/annurev-neuro-062111-1505369. Sundram, F., Deeley, Q., Sarkar, S., Daly, E., Latham, R., Craig, M.,Murphy, D. G. M. (2012). White matter microstructural abnormalities in thefrontal lobe of adults with antisocial personality disorder. Cortex, 48(2),216-229. doi:10.1016/j.cortex.2011.06.005

Denitsa VasilevaUnderstanding Paranoia

3

Nowadays, paranoia is considered to be excessive and

unsupported thinking that others intend to harmus. However,

for years, the very definition of the term presented a source of

controversy among psychiatrists. For years, mental health

professionals failed toagreewhetherparanoiawasadisorder

itself or merely a symptom of another illness such as

schizophrenia or even Alzheimer’s disease (1). Today, a

patient suffering fromsevere long-termparanoiaandnoother

symptoms is classified as having a personality disorder

known as Paranoid Personality Disorder (PPD)(2).

PPD usually begins to manifest in early adulthood and is

defined by a long-term pattern of suspiciousness and

mistrust, disproportionate to the circumstances (2).While it is

normal for an individual to have some paranoid or skeptical

thoughts about a person or situation, those suffering from

PPD take this distrust to an extreme as it pervades every

aspect of their daily life (1). These individuals display an

elevated sense of self-importance, frequently exhibiting self-

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self-referential thinking – the belief that everybody is talking

about them- as well as the conviction that others can read

their thoughts (3). This paranoia renders personal and social

relationships virtually impossible, causing the patients to

become isolated.

Due to the nature of the disorder and the resemblance of

its symptoms to other illnesses such as paranoid

schizophrenia, diagnosing PPD is a difficult process. As with

many other personality disorders, there is no definitive test

(1). Rather, diagnosis is based upon a psychological test and

the patient’s medical history. The consensus among experts

is that patients must display any four of the following

symptoms in order to be diagnosed with PPD: chronic

suspicionof others, constant questioningof loyalty, inability to

confide in others, continuous interpretation of benign

comments as personal attacks, hypervigilance and distrust of

significant others (3). Even then, paranoid schizophrenia

must be ruled out before a final diagnosis of PPD ismade (3).

While much promising research on the topic is currently

underway, the exact cause of PPD remains unknown.

However, researchers believe that there are a number of

contributing factors including brain chemistry, social

environment and genetics (5). In somepatients, hyperactivity

of the amygdala- the part of the brain that governs fear- has

been observed (5). [SM1] It is likely that this leads to the

elevated state of fear experienced by PPD sufferers (5) but

more research is needed before a definitive conclusion can

be reached.

While there is no universally accepted treatment for PPD,

mental health professionals consider cognitive-behavioral

therapy to be the best approach (1). However, the distrustful

4

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5

nature of the disorder makes it difficult to establish rapport

between patient and therapist and this bond is crucial for

successful treatment (1). It is best for the therapist to focus on

the patient’s day-to-day difficulties and avoid delving into the

past (3). This lack of suitable treatment means that while the

symptoms may lessen in intensity, frequency, and duration

with age, the disorder will afflict the patient throughout his

lifetime (2).

Fortunately, InstancesofPPDare relatively rareas it only

occurs in about 0.50%of the population [SM2] (2). In addition

to the possibility of paranoia as a symptom of another illness,

one of the most common causes of a paranoid state of mind

is as a side effect of mind-altering substances such as

marijuana. Understandably, the issue of marijuana

legalization has long polarized the mental health community,

one of the main concerns being, very little is actually known

about the effects of the world’s most popular illicit drug.

A large-scale experiment recently conducted by

researchers at Oxford University explored the causal

relationship between exposure to THC, the potent ingredient

of marijuana, and short-term paranoia in 121 participants

between the ages of 21 and 50, all with previous history of

marijuana use (4). Two-thirds were injected with THC while

the rest were given a placebo (4). The participants then

underwent a series of tests including real life social situations

and virtual simulations (4). Overall, one in five participants

experienced short-term paranoia as a result of THC (4). More

significantly, the results of the study suggest that increase in

negative thoughts caused by THC can lead to paranoia (4).

While the exact effect of marijuana on brain chemistry is

not yet clear, research suggests that cannabinoid receptors,

which bind to compounds in cannabis, are abundantly

present in the amygdala (6). It is likely that smokingmarijuana

may cause this part of the brain to become overly activated

and lead to an increase in anxiety and paranoia (6). By

changing our perception of the world, anxiety makes usmore

focused on a potential threat, potentially fueling paranoia (4).

However, as always, more empirical evidence is needed

before the effects of marijuana on the brain can be fully

determined.

As our understanding of the brain evolves, so too does

our paradigm of health. No longer is the absence of physical

injury or illness enough to label someone “healthy”.

Nowadays, mental health also plays an important role in

assessing a person’s well being, which is why research on

cognitive disorders such as PPD is gaining traction. The next

few decades are likely to provide more valuable insight into

these often-overlooked illnesses as well as into the effects of

controversial substances like marijuana. In recent years, the

issue of marijuana legalization has been pushed to forefront

of national politics, making good scientific research on the

topic more significant than ever.

References:(1) A.D.A.M Inc. (2012, November 10). ParanoidPersonality Disorder. Retrieved from PubMed Health:http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001934/

`````` (2) Bienenfeld, D. (2013, Jan 7). Personality Disorders.Retrieved from Medscape Reference: http://emedicine.medscape.com/article/294307-overview(3) Blais MA, Smallwood P, Groves JE, Rivas-VazquezRA. Personality and personality disorders. In: Stern TA,Rosenbaum JF, Fava M, Biederman J, Rauch SL, eds.Massachusetts General Hospital Comprehensive ClinicalPsychiatry. 1st ed. Philadelphia, Pa: MosbyElsevier;2008:chap 39(4) Freeman, D. et al.,(2014, July 16). “Cannabis reallycan trigger paranoia” Scizophrenia Bulletin. Retrieved fromThe Guardian:http://www.theguardian.com/science/2014/jul/16/cannabis-paranoia-psychoactive-thc-mood(5) Roussos, P., Giakomaki, S. G., Georgakopoulos,A., Robakis, N. K., & Bitsios, P. (2011). "The CACNA1Cand ANK3 risk alleles impact on affective personality traitsand startle reactivity but not cognition or gating in healthymales" Bipolar Disorders 13:250-259.(6) Teniel S. et al. (2014). “Multiple MechanisticallyDistinct Modes of Endocannabinoid Mobilization at CentralAmygdala Glutamatergic Synapses” Neuron 81(5): 1111 –1125.

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"Music is one of the universal mediums ofexpression for human emotion, and represents anactive area of research in cognitive psychologyand neuroscience. Although we are still in thedark about much of the brain circuits andmechanism behind musical understanding andexpertise, research is beginning to shed light onthese topics. This is represented by the radiatingcolors into the grey areas. Nevertheless, we willalways continue to appreciate music and thewonderful neurological effects it has on us."

Interneuron . Volume 2, Issue 3 . February 2015

Music is an everyday part of our lives, yet it remains

an enigma tomost. No, it doesn’t end at music theory and the

seemingly never-ending set of rules that it constitutes; the

latest set of questions on music to tickle our brains concerns

the brain itself: the mysterious, three-and-a-half pound lump

ofmeat betweenour ears.Studyingmusic’s emotional effects

serves as a gateway to understanding not only how music

makes its marks on cognition, but also what lies beneath

emotion and every other function that makes us human.

Let’s start with this: think of one of your favourite

pieces of music, whatever it may be. Now think of how often

you find yourself listening to it. You just can’t seem to get

enough of it, can you? That’s because music, like everything

else, involves the release of dopamine.

Salimpoor et. al (2010) put this notion to the test by

measuring participants’ physiological and cognitive reactions

topiecesofmusic fromanarrayof different genres (rock, jazz,

classical, etc.). Participants were given a set of

questionnaires on how they felt while listening to each

excerpt, and their responses were also measured via

neuroimaging techniques: in this experiment, functional

Magnetic Resonance Imaging (fMRI) and Positron Electron

Topography (PET) were used to measure blood flow in

different regions of the brain and neurochemical activity,

respectively.

Salimpoor andher colleagues found that that nucleus

accumbens (NAcc), the brain’s pleasure center, was

activated during the experience of pleasurable music. This

was highlighted by an increased flow of dopamine to that

region, but it doesn’t end there. The autonomic nervous

system (ANS) was also activated, hence the reports of chills,

rushes, and sweating that the participants noted during the

course of the experiment. Finally, another area of the brain,

the auditory cortical stores, was shown to be interacting with

the NAcc; the auditory stores, as you can guess, are

responsible for storing auditory information.

In my opinion, this study and others like it should

appeal to three crowds: the die-hard legions of empirically

minded neuroscience folks, the musicians and music

connoisseurs madly enamoured with the art, and those

chasing the age-old question of what makes us human. For

the neuro crowd it’s quite obvious how the data relates to the

cerebral areas in question. Those who love music can take

pride that its effects are finally being studied, and that it

presents an opportunity to be takenmore seriously instead of

being written off as a young and pointless ambition (I say this

as a musician).

The casewith the third crowd really drives this type of

research close to home: the desire to understand what it is

that makes us human. Revealing the inner workings of the

humanmind–and by extension, being – has proven to be one

of the most daunting challenges we as a species face today;

with sowide a playing field, it seems impossible to even begin

looking. But there’s no reason to give up: with the growth of

research bridging the gap between the arts and sciences, the

path is set for more to follow.

References:Salimpoor, V., Benovoy, M., Larcher, K., Dagher, A., &Zatorre, J. (2011). Anatomically distinct dopamine releaseduring anticipation and experience of peak emotion tomusic.Nature Neuroscience, 14(2), 257-262.

Alex GhaliMind, Brain and Music

6

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Ann Sheng

Lost in Music

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In the cold month of January earlier this year, The

New York Times published a warm opinion editorial in which

the author of the piece, Mandy Len Catron, recounts her

experiences recreatingawell-known relationshippsychology

experiment. The editorial piece is as a cute love story of sorts,

mixed inwithwell-chosensnippetsof science.The inspiration

for Len Catron’s experience and story is Arthur Aron et al.’s

(1997) closeness-inducing study from nearly twenty years

ago. In simple and short terms, the study reveals that a sense

of closeness or intimacy can arise between two strangers as

a result of asking each other 36 simple yet specific questions.

LenCatronwalks us through her attempt at usingAron et al.’s

(1997) procedure on a first date, revealing at the end what

happens to her and her partner after question number 36.

Aron was the principal psychologist spearheading

the experiment back in the late 90’s. In contrast to what Len

Catron implies in her piece, the experiment was not designed

to evaluate amethod bywhich people could fall in love; rather

it was intended as a tool to test the creation of temporary

closeness in a controlled and scientific manner (Aron,

Melinat, Aron, Vallone & Bator, 1997). Relationship

psychology has often been limited to correlational studies, in

which various aspects of personality or behavior are

correlated to relationship types and/or outcome (Aron, et al.,

1997). In light of this tendency in the field, studies such as

Aron et al.’s (1997) are interesting, as they set out to explore

various aspects of relationships within a controlled and

scientific setting. The 1997 paper consists of a series of

studies that try to parse out the effects of variables such as

“similarity” or “expected liking” on engendering closeness

between two individuals. The authors discuss the

effectiveness of the experimental method to test concepts in

relationship psychology, and review the effects of the various

variables on measures of closeness; interestingly, they

conclude that the 36-step method itself has the most

significant effect in creating closeness. This is quite

surprising, especially considering prior research supporting

“similarity” and “expected liking” to be key in cultivating

intimacy and closeness in relationships (Aron et al., 1997).

This result of course begs the question: is this procedure the

magical solution to making anyone fall in love with you and

vice versa?

Len Catron’s article would suggest that it is; after all,

the name of her article is “To fall in love with anyone, do this”.

Whether you find this an exciting prospect or a terrifying one,

it is perhaps not surprising that it isn’t quite that simple:

On the other hand, it seems unlikely that the

procedure produces loyalty, dependence, commitment, or

other relationship aspects that might take longer to

develop” (Aron et al., 1997).

The working definition of ‘closeness’ that Aron et al.

(1997) presents at the outset of their paper frames the

phenomenon as “an interconnectedness of self and other”, or

more simply as intimacy (Aron et al., 1997; Aron, Aron &

Smollan, 1992; Aron, Aron, Tudor & Nelson, 1991). The

authors admit that this is a narrow understanding of the

Interneuron . Volume 2, Issue 3 . February 2015

FEATURETo Fall in Love With Someone,Maybe Do This!

8

Alexandra Mogadam

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concept, which only accounts for “feeling close”, ignoring the

behavioral components of “behaving close”, which would

takemore time tocultivate (Aronetal. 1992;Aronetal., 1997).

In an earlier paper Aron et al. (1992) found both dimensions

to be equally significant in defining closeness.

In other words, the Aron et al.’s procedure

successfully creates a temporary sense of closeness, which

manages to transcend characteristics such as attachment

style or similarity. However the task does not necessarily

engender behavioral closeness, or diminish the importance

of attachment style and other psychological concepts in

creating long-term intimacy (Aron et al., 1997). Nonetheless,

these arguments do not take away from the importance and

significance of the researchers’ findings. After all, they did not

seek to cultivate long-term love, only a temporary sense of

closeness, which they accomplish successfully. One has to

be aware of this, and understand how this limits the

applicability of this procedure; it's not the magical 36-step to

love.

Theeditorialhasasomewhatbanalending (surprise,

surprise Len Catron and her partner fall in love). However, in

its defense, it is not entirely blind to method’s limitations, and

does present an interesting take on choosing to act with

deliberateness when becoming close to someone. Len

Catron suggests that theexperiment could inspire one to view

closeness or love as a process that one deliberately takes

part in, rather than something that simply befalls you.

Therefore, the next time you meet up with that special

someone you have an eye on,maybe do describe to them the

last time you went to the zoo (question 13/36) – it might just

make you closer after all.

References:(1) Aron, A., Aron, E. N., Tudor, M., & Nelson, G. (1991).Close relationships as including other in the self. Journal ofpersonality and social psychology, 60(2), 241.

(2) Aron, A., Aron, E. N., & Smollan, D. (1992). Inclusion ofOther in the Self Scale and the structure of interpersonalcloseness. Journal of personality and social psychology, 63(4), 596.

3) Aron, A., Melinat, E., Aron, E. N., Vallone, R. D., & Bator,R. J. (1997). The experimental generation of interpersonalcloseness: A procedure and some preliminary findings.Personality and Social Psychology Bulletin, 23(4), 363-377.

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Oxytocin and theNeurobiology of StorytellingAnn Sheng

10 Interneuron . Volume 2, Issue 3 . February 2015

Night is falling. Hurrying back to the eatery where her

parents have stopped to take platefuls of unattended food,

Chihiro is aghast when she finds two bloated pigs inmomand

dad'soutfits, still gorgingon thedelicacies.Shescreams–and

flees as unearthly apparitions begin to materialize into

mythical spirits of all shapes and sizes around her.

She is trapped, alone in a nightmarish, fantastical

world.

It is easy to relate to the young protagonist in Spirited

Away. As a child, who hasn't harboured the fear of getting

lost? This emotional resonance, says Paul Zak, the Director

of the Centre for Neuroeconomics Studies at Claremont

Graduate University, is "an amazing neural feat.” It allows us

to directly experience what the characters are feeling, even

though consciously, we know these personalities are nothing

more than flickering lights on a screen or squiggling lines on

paper.

How does the brain do this? According to Zak, the

hormone oxytocin is implicated. Oxytocin has been found in

non-human mammals to play a key role in pair bonding,

breastfeeding, labour, sex, and the ability to form social

attachments. In humans, oxytocin appears to exert an

influence on whether we trust a stranger, and is released

when we are engaged in an emotionally-charged story, such

as that of Spirited Away.

Inanexperiment toquantify theneurobiological effect

of storytelling, Zak's teamshowedvolunteers oneof twoshort

videos: a father's narrative of his struggles facing his 2-year-

old son with terminal brain cancer, or an emotionally-neutral

clip of the same father and son at the zoo. Compared to

control subjects, those who viewed the emotional video

experienced an increase in oxytocin levels by an average of

47%, alongside increased feelings of empathy. Empathetic

individuals were more likely to donate part of their

experimental earnings to charities supportingpatients like the

child in the video, although no direct relationship was found

between oxytocin levels and likelihood of donation.

However, oxytocinwasnot theonlymolecule keeping

meenthralled inHayaoMiyazaki'sbrilliant visual narrative.By

facilitating dopamine and serotonin release, oxytocin

activates reward circuits in the brain involved in pleasures

such as food, sex and drugs. Undeniably, as Jonathan

Gottschall noted in the preface of his book The Storytelling

Animal:HowStoriesMakeUsHuman, "[w]eare,asaspecies,

addicted to story."

Not only dobooksandmovies captivate our attention,

but we are also constantly surrounded by narratives in the

form of advertisements, news reports, biographies,

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daydreams, songs and video games. At night, our brains

conjure up fantastical scenarios while our bodies are

immobilized. Storytelling seems too pervasive in our lives to

be an evolutionary coincidence, which begs the question:

Why?

Throughout much of human history, storytelling has

been contextualized as a social event during which people

gathered to listen to tales of ancient heroes or distant lands.

In thisway, narrativemayserve to connect people together by

affecting themwith the sameemotions and forginga common

identity through shared ideas. Indeed, fMRI studies have

shown that when speakers and listeners communicate, they

display similar neural activity. Others suggest that stories

offer goodescape, as self-reflection and thedemandsof daily

life can be stressful. Gottschall, however, notes that fiction is

rarely pure pleasure fulfillment but instead full of crises and

conflicts which range from natural disasters to interpersonal

drama. Since most of the time we cannot directly learn from

experience, Gottschall tells how storytelling may "[a]llow our

brains to practice reacting to the kinds of challenges that are,

and always were, most crucial to our success as a species.”

Whatever the evolutionary advantages, storytelling is a

powerful medium to motivate, move, and sometimes

misguide people. With the knowledge of how good narrative

can influence our brains, however, we can avoid falling victim

to orchestrated marketing campaigns and inflammatory

conspiracy theories.

In Spirited Away, though, the message is

resoundingly positive. As Chihiro completes her "hero's

journey" to save her parents and find a way home, her hard

work and courage are rewarded with help from a white

dragon, an eight-legged apothecary, a gregarious co-worker

and a kind witch. We, like Chihiro, appreciate the growth she

has gained from this unforgettable adventure.With advances

incognitiveneuroscience,weare just beginning toappreciate

the mastery of storytelling from a whole new perspective.

References:

(1) Barraza, J. A., & Zak, P. J. (2009). Empathy toward

strangers triggers oxytocin release and subsequent

generosity. Annals of the New York Academy of Sciences,

1167(1), 182-189.

(2) Gottschall, J. (2012). Hell is Story-Friendly. In The

Storytelling Animal: How Stories Make Us Human (p. 67).

Boston: Houghton Mifflin Harcourt.

Insel, T. R., & Young, L. J. (2001). The neurobiology of

attachment. Nature Reviews Neuroscience, 2(2), 129-136.

(3) Kosfeld, M., Heinrichs, M., Zak, P. J., Fischbacher, U., &

Fehr, E. (2005). Oxytocin increases trust in humans. Nature,

435(7042), 673-676.

(4) Marshall, J. (2011). Gripped: why stories are so

compelling. New Scientist,209(2799), 45-47.

(5) Stephens, G. J., Silbert, L. J., & Hasson, U. (2010).

Speaker–listener neural coupling underlies successful

communication. Proceedings of the National Academy of

Sciences, 107(32), 14425-14430.

(6) Zak, P. (2013, December 17). How Stories Change the

Brain. Retrieved February 5, 2015, from http://

g r e a t e r g o o d . b e r k e l e y . e d u / a r t i c l e / i t e m /

how_stories_change_brain

11Interneuron . Volume 2, Issue 3 . February 2015

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"No great mind has ever existed without a touch of madness." Aristotle's famous quote of the"tortured genius" has been echoed in the scientific communities by findings that creativepeople are more likely to be afflicted with mood disorders such as bipolar disorder. Thisdrawing is a depiction of such an artist in the state of creative mania, frantically scribblingdown the loose associations and unsuppressed ideas that surface into his consciousness.

Scrawling in the NightAnn Sheng

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Faculty Profile:An Afternoon with Dr. Melissa Holmes

13

Sawayra Owais

As a behavioralneuroscientist with a focuson neuroendocrinology andneural plasticity, Dr. Holmes'current research focuses onthe unique eusocial mammal,the naked-mole rat.

Hard work, persistence and a little bit of luck led Dr.

Melissa Holmes, a behavioural neuroscientist at the

University of Toronto Mississauga, to a professorship and

research lab at a world renowned institute. However, Dr.

Holmes admits that as an undergraduate student at Simon

Fraser University (SFU), she was confused about which

career path to pursue. Indeed, her first year and a half at SFU

were spent toward attaining a Bachelor of Business

Administration. Dr. Holmes comments, “You have a sense of

what your abilities are and I knew I wasn’t succeeding

according to my abilities.” Contrast that remark with her

effusive description of her first year psychology class that she

chose only to complete as an elective. “I loved the professor

as he was incredibly engaging,” Dr. Holmes enthusiastically

describes. Serendipity had it that she chose biopsychology in

second year to gain admission into upper year psychology

courses and the rest, Dr. Holmes remarks, was history.

Hands-on lab work during her undergraduate degree

partnered with the excitement of working toward a common

lab goal indicated to Dr. Holmes that she should pursue

graduate school. After completing her undergraduate degree

in Psychology from SFU, Dr. Holmes did a Masters in

Biopsychology from the University of British Columbia.

Afterwards, she obtained her PhD in Neuroscience from

Michigan State University and completed a postdoctoral

fellowship at University of Massachusetts to further her

academic training.

Endemic to east Africa, naked-mole rats live in strict

social hierarchies: 2 members of the colony are socially-

dominant breeders while the rest of the members are their

subordinates fulfilling roles such as colonymaintenance and/

or pup rearing. When thinking about hormones that foster

cooperation or love, oxytocin comes to mind. Indeed,

oxytocin, often called the cuddle hormone, is secreted by the

posterior pituitary gland to modify caring behaviour. Skyler

Mooney, a graduate student in theHolmes lab, demonstrated

that subordinates have more oxytocinergic neurons than

breeders. “This finding is great because it suggests that

oxytocin is important for pro-social behaviour in this species.”

However, Dr. Holmes explains that this hormone-behaviour

relationship is not that simple. “We don’t know if oxytocin is

directly promoting affiliation and attachment because they

Page 16: Interneuron - Issue 2.3

are pro-social or if it’s acting as a buffer for stress. Currently,

that is what we’re trying to figure out,” clarifies Dr. Holmes.

The dual function of oxytocin as both a love and stress

hormone may muddle the direct relationship with a certain

behaviour but Dr. Holmes gushes that the pursuit of

knowledge is her motivation.

Surrounded by an academic and stimulating

environment, it is natural for a university student to lean

toward academia as a career. However, after getting mixed

reviews of the anticipated labour market of graduate

students, one’s hopes may be dimmed. After reading the

headline of a 2013Globe andMail article titled, “Who will hire

all the PhDs? Not Canada’s universities” Dr. Holmes

acquiesces to the article’s claims. She explains that Canada

is producing a lot of graduate students and it is not

immediately clear where they are all going to go. However,

she stresses that there are many opportunities for PhD

students outside of academia. “Maybe they go into industry,

policy or government. You can do a lot of great things with a

PhD that isn’t sitting in an office like this and running a

research lab,” Dr. Holmes remarks, gesturing to her book-

filled enclosure.

Some undergraduate science students may only

know two options that exist to them after convocation:

professional or graduate school. When asked how students

canbeexposed toother career opportunities,Dr.Holmeshad

a plethora of answers. First, she encourages students to visit

their career counselling or academic skill centres. “I think

students should capitalize on the resources that universities

provide for them...I think it’s a great opportunity to pursue.”

Indeed, a quick search of University of Toronto’s career

centre revealed ample help with resume writing, interviews

and opportunities post-graduation. Dr. Holmes also

recommends paying attention to the world around you. “Look

at people in your community and ask them what they do, if

they like their job and how they got to be where they are”. In

fact, Dr. Holmes and her colleagues anticipate networking

with university alumni so they can relay what kind of career

paths are available for their present undergraduate and

graduate students.

Dr. Holmes closed by re-emphasizing that students

pursuing graduate studies should not be despondent. “I

think there is tremendous value in getting an education.

But, there are no handouts so just work really hard and be

really good,” motivates Dr. Holmes.

We would like to sincerely thank Dr. Holmes for taking

time to lend us her insights!

References

(1) Mooney, S. J., & Holmes, M. M. (2013; 2012). Social

condition and oxytocin neuron number in the hypothalamus

of naked mole-rats (heterocephalus glaber). Neuroscience,

230, 56-61. doi:10.1016/j.neuroscience.2012.11.014

(2) Naked Mole Rats. (n.d.). Retrieved February 11, 2015,

from http://animals.nationalgeographic.com/animals/

mammals/naked-mole-rat/

14 Interneuron . Volume 2, Issue 3 . February 2015

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I started graduate school last October. It has been

interesting. For starters, I spent my entire undergraduate

degreemildly obsessed with neuroscience and all it entailed:

from classes to research to student organizations. My PhD is

in cell biology, in a primarily biochemistry heavy lab (the only

course I have taken in biochemistry being the long gone

BCH211). I also happen to be in a different country, at the

secondoldest English speakingUniversity in theworld. Is this

enough of a hook? I was hoping it would be. Basically, I want

to tell you a bit about why I ended upwhere I am. And in doing

so, I want to try to convince you that stepping outside of your

comfort zone is one of the best things you can do.

Last year at around this time, I was getting ready to

interview for PhD programs. I was a fourth year student

specializing in Neuroscience at UofT. Whenever one of my

classmates asked me where I was going next year and I

responded with ‘probably grad school’ I sometimes got a

sympathetic look and a ‘oh, yea it’s good to have a back-up

for med school but don’t worry, I’m sure you’ll get a few

interviews!’. Suffice to say I was very confused. Graduate

school was never a substitute or side road for me. Research

had always been the coolest way you could possibly spend

your time, and I was excited. I also had interviews to Harvard,

Stanford, Columbia, MIT, and Cambridge, so you can

imagine that I took these comments pretty well. To this day I

maintain that more people need to consider graduate school

as a thing in and of itself. It will be a very intellectually

challenging but rewarding period of time, and you will learn a

lot about a lot of things. I never thought too much about the

future (what I would do after my PhD). This perhaps reckless

mindset is also a very liberating one – maybe you should try

it out.

I ended up going to the University of Cambridge, to

study at the MRC Laboratory of Molecular Biology (to get a

taste for the richhistory of this place, here’s a tiny list of people

did ground breaking work at the LMB: Fred Sanger, Watson

andCrick, SydneyBrenner andAaronKlug). Apart froma few

logistical and research oriented reasons, I must admit that a

large portion of my decision-making was based on how I felt

when I camehere – I just felt good. Therewas also something

thrilling (dare I say YOLO-esque) about switching into

OPINIONProfile: Alina Guna

15

Alina's lab at Cambridge

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There was also something thrilling (dare I say YOLO-esque)

about switching into something you theoretically know little

about, for the purposes of doing a PhD (a 3-year PhD might

I add).

This being said, the first few months were objectively

not the easiest. Confronting your own incompetence on a

daily basis is at times very frustrating. The key is not to get

demoralized under any circumstance. I think it is possible to

turn this frustration into something very positive. This is one

of the things I learned during the first few months of my PhD.

I learned a few other things:

a)Despite howyoumay feel, being the least informed

and knowledgeable person in a roommeans you’re the most

privileged person in the room. Embrace the opportunity.

b)Whenever you’re tempted to think about silly things

like ‘I’m not good enough’ or ‘nothing works and I’m going to

fail’ remind yourself that these are all practically useless

thoughts. If you want something to happen, work for it. It will

happen eventually (if you’re not willing to wait 10-20 years for

it to happen that’s a different story!)

c) Other people are a wealth of

information. And if you’re likeable and not

completely annoying they will share this

information with you for FREE. FREE

KNOWLEDGE!

d) A few don’ts: don’t be afraid to be

wrong, don’t compare yourself to anyone but the

you of yesterday, don’t conflate authority with

someone who possesses supernatural

knowledge, and don’t talk so much (a simple

cost/benefit analysis will usually show you that

listening is usually a much better investment)

e) Every once in a while, remove yourself from your

daily environment. While away do some thinking. Just sit

somewhere looking at something you think is pleasing and

think. See what you come up with.

f) Stop worrying so much. Transform that energy into

movement and doing and living and listening to some good

jams at the end of the day. Trust.

I’ve been told the first few months of grad school are

rough, and that it will get better. If that’s true I can hardly wait.

It’s been sweet. I predict there will be very few times in my life

where I can sit down at the end of the day and literally list the

things I have learned (be it about research or life in general).

Iwouldneverhavebeenhere if I didn’t takea fewchancesand

though this is very anecdotal advice – I suggest you give it a

shot.

16 Interneuron . Volume 2, Issue 3 . February 2015

St. John's College, Cambridge

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Erasing Fear MemoriesSarah Crawley

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Many of us would love to be able to alter certain fears

ormemories: a bad break-up, an embarrassing presentation,

or even a phobia of spiders. Despite all our hopes of having

the neuralyzer from Men in Black, our memories are here to

stay- or are they? The field of neuroscience has seen a wave

of revolutionary research, thanks to novel genetic

manipulation techniques. Several studies in the past decade

have looked into various roles that fear plays in the formation

of memory, and whether it is possible to modify these

memories. Although there is much research yet to be done,

the current state of the field leaves us hopeful that the key to

understanding the complicated interplay of neurons in the

brain is within our grasp.

The year 1885marked a revolution in our conception

of memory with the publication of Hermann Ebbinghaus’s

Über dasGedächtnis (OnMemory)1. Despite conducting the

experiments only on himself, Ebbinghaus was able to

demonstrate many fundamental cognitive principles that

remain valid to this day: the forgetting curve, the learning

curve, and the serial position effect, among others1. Ever

since, we have gone on to classify the location of memories

in the brain, as well as their interaction with certain primal

emotions such as fear. Over the past decade, one of the

techniques that has shown a similar transformative potential

is the field of optogenetics.

Briefly, optogenetics is the use of light to control the

activation and deactivation of neurons in the brain. Realized

in 2005 by Karl Deisseroth and Ed Boyden at Stanford, the

procedure consists of inserting a protein, called

channelrhodopsin-2 (ChR2), into neurons in the brain2.

ChR2 expression is generally linked to a gene involved in

early memory consolidation, such as c-Fos, which allows it to

be integrated only into memory-related neurons. When

exposed to light, the channel undergoes a conformational

change, opening and allowing ions to enter the neuron,

subsequently causing neuron firing3. The light is usually

delivered by an optic fiber inserted into the skull of the animal

subject. This robust technique has seen a quick rise to fame,

as it allows neuroscientists greater control over the

manipulation of specific neurons in the brain, and has opened

the door to astonishing discoveries.

One such finding came fromMIT, with an experiment

ledbyXuLiuandSteveRamirez; their results demonstratean

ability to stimulate the recall of fear memories in novel

environments4. The researchers first inserted ChR2 into a

select population of neurons in the dentate gyrus (an area

within the hippocampus) of mice, under the control of a

tetracycline response element (TRE) promoter. This

promoter allows researchers to use the chemical doxycycline

to control the expression of the ChR2 gene. When the mice

were administered doxycycline, ChR2 was not expressed;

whendoxycyclinewas removed, neurons involved in learning

were labelled with ChR2 and a visible marker called YFP

(yellow fluorescent protein).

Using this method, the researchers were able to

fear condition (FC) mice in one chamber (chamber A) and

label the neurons encoding the fear memory with ChR2. As

ChR2 can be stimulated by light, the researchers were

Fear and ForgettingStefan Jevtic

18 Interneuron . Volume 2, Issue 3 . February 2015

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able to selectively activate these labelled neurons.

When placed into a novel chamber (chamber B), these

neurons were stimulated by an optic fibre implanted into

the mice’s skull, causing them to freeze. As freezing is a

reaction to fear, this demonstrated that the contextual fear

of chamber A was stimulated in chamber B, even though

the mice had no “reason” to fear the new chamber.

The same researchers who led this experiment also

managed to create a false fear memory in mice, through a

similar procedure5. When mice were exposed to a novel

context, C, the neurons were labelled with ChR2; when

these mice were later fear conditioned in a different

context, D, the previously labelled neurons were

simultaneously activated with light. This activation led to

the creation of a hybrid memory, with fear encoded into the

memory of context C, despite not having undergone fear

conditioning in this context. The result was increased

freezing in these mice when placed in context C, where

they had not been fear conditioned. This result of being

able to create a false or altered memory leaves us with

many questions, the answers to which have far-reaching

implications. For example, this study demonstrates not

only that our memories are malleable and subject to

change, but raises questions pertaining to the validity of

witness testimonials. How can we be sure that witnesses

of dangerous situations correctly remember crucial details

when they present a testimony in court?

Similar experiments have managed to go one step

further in isolating pathways for memory development,

even to the point of inactivating and reactivating a memory.

Working under the model that long-term potentiation (LTP)

is the dominant mechanism for memory formation in the

brain, Roberto Malinow and colleagues employed

optogenetics to activate LTP and its antagonist, long-term

depression (LTD), during fear conditioning6. First, the fear

condition memory was formed through optogenetic

stimulation in mice. These mice were then exposed to an

optogenetic LTD protocol, which resulted in loss of the fear

memory (no conditioned response). When subsequently

exposed to an optical LTP protocol, the mice again

demonstrated a conditioned response, indicating

reactivation of the memory. This study, in addition to

providing evidence for the mechanism of LTP/LTD in the

brain, demonstrates an ability to selectively alter the recall

of fear memories in the brain.

With the ability to selectively activate specific

neurons in the brain, we are entering a Golden Age of

neuroscience research. From false memory creation to

selective activation/reactivation, we are inching closer to

elucidating the formation of memories in the brain.

Although we won’t be sticking optic fibers into our own

skulls anytime soon, it may be that the scarring memory

from eighth grade gym class already has one foot out the

door.

References:

(1) Abbott, B. Herman Ebbinghaus. Retrieved from http://users.ipfw.edu/abbott/120/Ebbinghaus.html(2) Boyden, E. (2011). A history of optogenetics: the developmentof tools for controlling brain circuits with light. F1000 Biol Reports,3(11).(3) Guidera, J. (2014). Optogenetics: A New Frontier. HarvardScience Review. Retrieved from http://harvardsciencereview.com/2014/04/28/optogenetics/.(4) Liu, X. et al. (2012). Optogenetic stimulation of a hippocampalengram activates fear memory recall. Nature, 484, 381-5.(5) Nabavi, S. et al. (2014). Engineering a memory with LTD andLTP. Nature, 511, 348-352.Ramirez, S. et al. (2013). Creating a false memory in thehippocampus. Science, 341(6144), 387-391.

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