Brain Matters Vol. 8 No. 1


Interview with Two Professors 
Written by Brianna Mae Huner

Introduction
While psychology and neuroscience have a long history, this
knowledge is not set in stone, nor is it all-encompassing.
New findings are always being presented, sometimes
disproving generally accepted principles. The scientific
method allows scientists to constantly be testing and
retesting hypotheses, and if these hypotheses are wrong,
then sometimes the solution is questioning the foundation
on which these hypotheses are built upon. Asking questions
is the entire foundation of science. The scientific model
requires questioning what is known. The importance of
asking these questions cannot be overstated, as
investigation into these hypotheses can benefit the field and
humanity at large. At the university level, professors have
the opportunity to choose what they teach, including their
own hypotheses. At the Psychology department at the
University of Illinois, a variety of perspectives and
hypotheses can be observed, coloring the general
understanding of the topic of psychology and its
concentrations, such as Neuroscience and Clinical
Psychology.

Professor Justin Rhodes
Professor Justin Rhodes is a Professor at the Beckman
Institute for Advanced Science and Technology and an
Affiliate at the Carl R. Woese Institute for Genomic Biology.
He earned his bachelor's degree in biology from Stanford  
and his PhD in zoology from the University of Wisconsin-
Madison.

Madison. Professor Rhodes has a research focus in
cognitiveneuroscience and is researching how genes and the
environment can affect behavior. His current lab research
investigates how exercise can affect neurogenesis (the
creation of new neurons) in the hippocampus. Rhodes
frequently discusses these concepts in the classes he
teaches, which are PSYC/NEUR 302 (Applied Neuroscience)
and PSYC/NEUR/PHIL 433 (Evolutionary Neuroscience),
which is also cross coded as IB 436.

Prof. Rhodes often collaborates with colleagues and wrote a
chapter in the book of his doctoral advisor, Dr. Theodore
Garland Jr., on behavior and neurobiology. Rhodes described
the importance of splitting duties based on expertise when
collaborating on academic writing, writing sections of
papers dedicated to concepts he has the most experience in,
and leaving space for collaborators with more experience in
other topics. Recently, he wrote a paper with Dr. Ki Yun Lee
and Dr. Taher Saif about the involvement of astrocytes in
the muscle fiber contraction-hippocampal development
network, which showed that astrocytes may mediate this
relationship. Prof. Rhodes expressed his interest in the
unknown roles of glia in the brain, highlighting how
microglia are seen to have specific responses to different
levels of an organism engaging in physical activity.
Cumulatively, the function of microglia is altered by the
effect of an organism running.  He would like to see an
investigation into the role of signaling in the blood in this
effect.  Rhodes has conducted an abundance of research on  36



Interview with Two Professors

the hippocampus and has some of his own propositions to
its functions. 

During intense physical activity, it has been observed that
the hippocampus, typically associated with learning and
memory, becomes activated. The level of activation in the
hippocampus appears to have a positive relationship with
the level of intensity of the activity, further indicating that
these two are related. This phenomenon is a subject of
curiosity and debate among neuroscientists, as the current
understanding of the hippocampus and intense physical
activity seem to be independent processes. There is
evidence to show that physical activity could encourage
neurogenesis in the hippocampus. But this evidence is not
sufficient to explain how the level of intensity seems to
correlate with the level of activation in the hippocampus.

The classic interpretation behind this activation is that the
hippocampus is acting as a part of the sensory system. This
hypothesis assumes that the hippocampus activates in
response to speed, because if the animal is moving through
space faster, they will need to sample their environment
faster to keep their spatial map up to date. The spatial map
is the brain’s representation of the spatial environment
surrounding it, which is used to support functioning in the
environment and relating to the space one is in. The
mechanism used to explain this activation is that during
hippocampal activation, the hippocampus creates waves of
activity, with the most salient, or powerful and effective,
learning occurring at the peaks and troughs of these waves.
This supposes that to increase the rate of learning, the
hippocampus would need to increase the frequency of
these waves to maximize learning potential. 

Prof. Rhodes believes that the hippocampus is serving a
different purpose in this intense activity system, acting as
a motivator of this system, instead of serving as a
reactionary sensory organ. He hypothesizes that the
hippocampus acts as an intensity generator, allowing the
animal to move at intense speeds by motivating the body
to move. It should be noted that this form of motivation is
not of the higher order of consciousness, where people
choose to move intensely because of their understanding
of the health benefits of such activity or because they want
to escape something. Instead, Prof. Rhodes and his
colleagues believe that the hippocampus is the organ
needed to allow the body to move at such intense speeds
when necessary. There have been several studies
conducted testing this hypothesis, and a wealth of
evidence collected to support it. 

Recordings taken in the entorhinal cortex reveal that
hippocampal activity precedes intense movement. This
evidence could not be explained by the popular hypothesis
of the hippocampus acting as a reaction to the activity, as
this movement could not cause neural activity that
precedes it. 

The sensory hypothesis also does not explain why this
hippocampal activation does not occur when a subject is
being moved through an environment at high speeds
whenthey are not running. In a study where test mice were
placed in transportation carts (analogous to a car for a
human) and moved at a rapid rate, the level of activation
seen in intense activity is not observed in the hippocampus,
despite the need to rapidly update the spatial map still being
present. However, this is a potential side effect of human
evolution adjusting far slower than human technological
development. This lack of activation when moving quickly
through technological means could be explained by human
evolution not progressing past the stage where the only way
to get around quickly was through intense activity such as
running. These recordings of neural activity support the
hypothesis that Prof. Rhodes believes. Stimulating these
areas, instead of simply observing them, could also generate
evidence to support this theory. 

Figure 1. Positive correlation of GCaMP5 fluorescence
slope and velocity.

Prof. Rhodes cited a study conducted with Dr. Stefan Remy, a
professor at the University of Bonn in Germany. This study
was conducted in mice using optogenetics, a revolutionary
new technique that allows for the stimulation of specific
cells using light. The study used optogenetics to stimulate
the hippocampus of mice while on a treadmill. When the
hippocampus was stimulated, the mice began to move
around and run at an intensity that matched the level of
activation in the hippocampus. This evidence supports the
idea that the hippocampus supports motivation and ability
to move quickly. 

This theory has its detractors, however, who call on the
current understanding of the motor system and clinical
history. The hippocampus is not traditionally connected to
the movement system in the field of neuroscience. Patient
H.M., a famous patient in the history of psychology, was
known for having large portions of his temporal lobe
removed from his brain, including his hippocampus. While
Patient H.M. is widely known to have lost many of the
abilities traditionally associated with the hippocampus, such
as the ability to form new memories, he was able to move
quickly or engage in intense movement after his operation.

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Brain Matters Vol. 8 2025

Though, this possibility was not officially studied with HM.
The hypothesis believed by Prof. Rhodes of hippocampal
involvement provides evidence for why this may have been.
This data has also been seen in studies, as the loss of the
ability for intense movement when the hippocampus is
lesioned has also been observed in experiments where rats
have their hippocampus suppressed via anesthetics. The
combination of evidence discussed, through studies of
recording and stimulation in the hippocampus as well as
lesion studies, supports Rhodes’s motivator hypothesis. If
hippocampal activation precedes intense movement, then it
cannot be caused by intense movement, nor can it explain
why similar hippocampal activation in response to non-
neural-motor forms of rapid movement is not seen. In
addition, his idea supports why directly stimulating the
hippocampus induces intense motor activity. Finally, while
removal of the hippocampus does not have all-encompassing
effects on the motor system, it seems to remove the
organism’s ability to engage in intense movement. The
commonly held sensory hypothesis of the relationship
between hippocampal activation and intense physical
activity does not explain this evidence. Discussions such as
these encourage neuroscientists to look deeper into the
validity of these hypotheses.

Prof. Rhodes’s research and hypotheses of the hippocampus
can aid in growing the scientific understanding of the brain
region associated with some of the most damaging effects of
aging. The hippocampus is the first part of the brain to begin
deteriorating as humans age, losing about 1% of it every year
after the age of 20. The hippocampus is the brain region
most associated with dementia, but it is also one of only two
brain regions that is able to create new neurons throughout
the human lifetime. Studies have shown that hippocampal
exercise may be beneficial for retaining hippocampal mass
as humans age as regular strenuous exercise can promote
neurogenesis in the hippocampus. Evaluating the current
knowledge of the hippocampus, especially in relation to
exercise, could grant a revolutionary tool in the treatment of
neurodegenerative diseases, as well as the regular struggles
of aging and memory impairment.

Professor Thomas Kwapli
Professor Thomas Kwapil is the Director of Clinical Training
and an Associate Head of the Psychology Department at the
University of Illinois. He describes his role as being
responsible for ensuring that the Clinical-Community
program runs smoothly, as well as acting as a liaison with
the department head. The Clinical-Community program
comes with extra responsibilities, as it requires
accreditation, which requires reporting to outside agencies.
He received his bachelor's degree in psychology from
Louisiana State University, and his M.S. in psychology and
PhD in clinical psychology from the University of Wisconsin-
Madison. Prof. Kwapil is the current supervising professor
for PSYC 238 (Psychopathology and Problems in Living) and
PSYC 239 (Community Psych). 

This is a role that rotates among different professors in the
department. Instead of being the instructor for the course,
the supervising professor supports and supervises the
graduate students who teach the course. Professor Kwapil
also regularly teaches a PSYC 496 (Adv Current Topics in
Psych) course on schizophrenia-spectrum disorders, which
is his area of interest.

Schizophrenia-spectrum disorders include schizophrenia
and other psychotic disorders, including schizophreniform
disorder and brief psychotic disorder, as well as schizotypal
personality disorder. It is seen through abnormalities in
“positive” symptoms (including delusions and
hallucinations), disorganized symptoms (such as
disorganized thinking, speech, and behavior), and “negative”
symptoms (such as avolition and diminished emotional
expression). An estimated 3-4% of the population suffers
from schizophrenia spectrum disorders. Many
psychologists, especially those whose perceptions are
colored by the categorical nature of the Diagnostic and
Statistical Manual of Mental Disorders (DSM), would see
these as categorical disorders, following a yes/no binary.
Prof. Kwapil disagrees with this notion.

Figure 2. SEQ Figure \* ARABIC 2. Schizophrenia
Spectrum Disorders. Giovanni, V. (2015).

 It is widely believed that other disorders, such as depression
and anxiety, exist on a spectrum of intensity and subclinical
presentations, yet this line of thinking is not often extended
to schizophrenia-spectrum disorders. Many people report
experiencing anxiety or depression. With some, a more
clinical expression is seen. With others, these symptoms are
less intense, do not last as long, and/or cause less
impairment. All are experiencing these symptoms; some are
simply experiencing them on a subclinical level. The same
can be true for schizophrenia-spectrum psychopathology.
Even when it comes to clinical schizophrenia-spectrum
disorder presentations, categorical measures fall short to
dimensional measures. Those with schizophrenia may
experience psychotic episodes, which remit and return,
similar to depressive episodes seen in Major Depressive
Disorder. An all-or-none categorical form of thinking, in
which a subject is either in or out of an episode, may be
easier to conceptualize, but is not entirely accurate to
describe this phenomenon. Often when people remit from
episodes, their expression of symptoms doesn’t go from
disordered to regularly functioning, but rather a less intense
symptomology or degree of impairment. Where the
categorical model fails to encapsulate these observations,
Prof. Kwapil has a more fitting explanation.

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Interview with Two Professors

Prof. Kwapil and his colleagues support a dimensional
model, in which schizophrenia-spectrum disorders and
subclinical presentations of schizophrenia exist on a
continuum, called schizotypy. Prof. Kwapil and his
colleagues are pursuing an effort to reconceptualize
schizophrenia and related disorders as not simply extreme
and rare disorders, but also milder presentations. Often
conceptualized as extreme manifestations in clinical cases,  
milder forms of positive, disorganized, and negative
symptoms can also be seen. These subclinical symptoms can
develop and change in a variety of ways, if at all. Some of
these milder symptoms go on to develop into a clinical,
disordered presentation. Some continue to have these
symptoms, but they do not get worse or interfere with
functioning. Others will have these symptoms come and go,
sometimes never appearing again. A key difference between
milder symptoms and clinical symptoms when it comes to,
for example, delusional thinking, is in conviction. Someone
with a clinical expression of delusional thinking may be
convinced that someone is stealing their thoughts or
threatening them, whereas someone with a subclinical
expression of delusional thinking may wonder or suspect if
it may be possible but are unsure.
 
Prof. Kwapil’s method for studying the dimensional model
involves a complex process that he has implemented into his
research. First, development of a conceptual model for
understanding the dimensions of schizotypy is needed.
Models have been developed to measure the dimensions of
positive, disorganized, and negative schizotypy in order to
identify people who exist on this scale and how their
symptoms should present. When observed in subclinical
expressions, which do not cause impairment, those being
studied are not seen as patients, but rather personality
traits. People can be elevated on one, two, or all three
dimensions. For example, someone who may be high in the
positive dimension, experiencing magical beliefs or strange
perceptual experiences, may be low in negative and
disorganized dimensions, such that they would not be
experiencing the symptoms such as flattened affect,
anhedonia, or difficulty organizing and executing thoughts
and emotions. Participants for a study of subclinical
presentations of schizotypy are typically found through
extensive interview studies or questionnaire studies
focusing on schizotypal traits, personality, and emotion. One
of the testing methods favored by Prof. Kwapil is Experience
Sampling Methodology, or ESM. ESM is a measurement that
uses a system of daily surveys sent out multiple times each
day that assesses the dynamic system of emotional and
psychological phenomena throughout the day. This is a more
effective measurement system for seeing a larger picture of
a participant’s life by measuring them over a larger period of
time than a single lab interview session, making it a fitting
choice for studying subclinical presentations of
psychological disorders. 

Schizotypy, like many dimensional models of clinical
disorders, offers a useful conceptual model of schizophrenia
spectrum disorders that has advantages over traditional
categorical models. Human behavior and emotions have a
complexity and nuance that cannot be entirely captured
through a yes/no binary. Similar to anxiety and depression,
which are generally accepted to be experienced both
clinically and subclinically, symptoms of schizophrenia
spectrum disorder can be observed on a lower impairment
level among those who do not fit the criteria for
schizophrenia spectrum disorders. Prof. Kwapil has been
studying schizotypy for years and has developed an effective
model of study of the dimensions of schizotypy. With  
models such as these, the scientific community can move on
to a better understanding of the truly dimensional model of
psychological disorders and their subclinical presentations.

Prof. Kwapil’s proposed model of schizotypy can advance the
understanding of schizotypy, allowing for an improved early
detection system and potentially negating some of the
stigma associated with these disorders. An estimated 10% of
people experience subclinical expressions of schizotypy,
which is a large portion of the population and merits
investigating the presentation and mechanism behind these
symptoms. Identifying these individuals could be
instrumental in instituting early intervention services for
those who will eventually develop a clinical presentation of
schizotypy. However, those with schizophrenia spectrum
disorders have a heavy stigma against them among the
general public, and it is important to acknowledge this
during research. When trying to identify potential
prodromal symptoms, which can help with preventing these
symptoms from developing to a clinical level, those
identified with subclinical symptoms could put at risk of
losing social support systems, losing their jobs, and
potentially being prevented from being covered by
insurance because of the association with these disorders.
Being identified as being at risk of developing heavily
stigmatized disorders such as schizophrenia or its related
disorders carries a much difference social weight than those
identified as being at risk for the development of less
stigmatized illnesses, such as breast cancer. As those with
schizophrenia are often mischaracterized as dangerous or
violent. However, as the understanding of schizotypy grows
through research, it is possible for education about
schizotypy to be spread outside of the scientific community,
placing logic and understanding in place of fear.

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Brain Matters Vol. 8 2025

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About the Author
Brianna Mae is a Junior at the University of Illinois majoring in
Clinical/Community Psychology. She became involved in Brain Matters to
gain more experience researching and writing about the current research in
Neuroscience. When she is not writing for Brain Matters, she is also
involved in Dr. Kwapil's Project on Life Experiences Lab, and is the
Treasurer for the Psychology Research and Community Club (PRACC).
Brianna Mae is hoping to pursue a PhD in Clinical Neuropsychology and
conduct research about the neurological basis behind different clinical
disorders. 



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