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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
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
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
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
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-
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
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.
"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
Ann Sheng
Lost in Music
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
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.
9
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,
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
"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
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
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
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
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
Erasing Fear MemoriesSarah Crawley
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
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.
19
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