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Shivam Khatri
Mentor: George Gescheider

In the twentieth century, neuroscientists believed in the idea of biological materialism,

which fundamentally articulated that life could be reduced to only a physical dimension
(Summerhays, 2010). The idea stated that brain was hardwired, and unlike plastic, could
not change (Summerhays, 2010). As a result of such notions, parents were given the
responsibility of placing greater emphasis on child development so that the youth could
thrive in society and within the economic world (Summerhays, 2010). However, since the
advent of the understanding of neuroplasticity, these spurious concepts have been
replaced. Neuroplasticity is the ability of the human brain to reorganize itself during
normal development and during times of illness or injury (Summerhays, 2010; Kong,
Gibb, Tate 2016). Furthermore, neuroplasticity is crucial for the optimization of neuronal
signaling, which is the transfer of information from the external environment through
neurons back to the external enviornment (Kong, et al., 2016).

The current understanding of brain reorganization comes from the theory of axonal
sprouting, which is when undamaged axons grow new nerve endings to reconnect the
neurons whose links have been weakened (Liou, 2010). The theory points out that
undamaged axons sprout nerve endings and connect undamaged nerve cells at great
speeds (Liou, 2010).

Moreover, an influx of research has revealed that brain activity can also promote brain
reorganization (Liou, 2010). Such activity includes simple brain exercises, interactions in
social situations, and getting involved in physcial activity (Liou, 2010). Another example
is rehabiliation therapy which simulates particular neurons that have not been active for a
certain duration (Liou, 2010). It is important to note that such neuroplasticity can only
occur when the brain is not too damaged since neuroplasticity holds limits as well. For
instance, if certain highly specialized brain cicuitry is destroyed, some mental functions
are lost as well (Liou, 2010). However, in a select few cases, new research suggests that
the brain can sometimes generate new neurons in a process known as neurogenesis (Liou,
2010). During this process, neurons migrate to damaged areas, forming connection and
restoring some lost functions (Liou, 2010). When a person has the most severe stages of
illness, the highest rate of neurogenesis is exhibited in the hippocampal region of the
brain (Liou, 2010). Though the concepts of neuroplasticity and neurogenesis have gained
proponents in the last few years. The concepts of neurogenesis have largely been due to
the new techniques of testing neuroplasticity that are available nowadays. The major
modality used today to study neuroplasticity is the Direct Electrocortial Stimulation
(DES), which identifies critical function areas in the brain (Kong, et al., 2016). The
normal procedure involves local anesthesia and cranioanatomy to people who are awake.
DES then maps epicenters of functional brain networks and uses those to study areas that
cannot be resected (Kong, et al., 2016). However, like all modalities, there are
disadvantages to such techniques. The one of greatest concern is the invasiveness of such
procedures and that such testing requires patients to have a lesion (a region that has
suffered damage) that requires surgery (Kong, et al., 2016).

Another technique that has been widely used in order to understand neuroplasticity has
been Functional Magnetic Resonance Imaging (fMRI) which is a noninvasive method for
mapping the brain (Kong, et al., 2016). It provides a way to know how the brian adapts to
injury and can be used to study the activation patterns of the brain of patients who cannot
be examined though DES; however, it can often have inconsistent results (Kong, et al.,
2016). As a result, it is often not a direct measurement of neural function or activity
(Kong, et al., 2016). Moreover, it frequently requires the use of low resolution images
and temporal resolution, which in effect means that scientists can only study features on a
time scale equal to or slower than the change in blood flow (Kong, et al., 2016).
As is seen, the study of neuroplasticity has progressed greatly in the last few
decades and has been influential in studying common syndromes and illnesses that affect
millions of people today, one of which is depression. Clinical depression, which
constitutes more than three million U.S cases per year, is a very common illness, yet one
that is treatable today due to the vast amount of research that has gone into identifying its
root causes (Reynolds, 2002). The World Health Organization has labeled depression as
the fourth leading cause of illness related to disabilities and death, and it would seem to
be more important than ever to give patients the right treatment (Reynolds, 2002).
Depression is a stress related disorder often associated with low mood, lack of
interest in everyday life, anxiety, social awkwardness, suicidal thoughts, anorexia, and
difficulties concentrating during tasks that require the use of memory (Sapolsky, 2001,
Reynolds, 2002). These symptoms can often be chronic in patients while other times only
present during certain intervals; however, to be diagnosed as a patient suffering from
depressive disorder, he/she must display any of the core symptoms for an extended
duration of time (Reynolds, 2002). An excess of cholinergic activity, cholinergic being a
neurotransmitter substance, over serotonin or norepinephrine activity can indicate signs
of depression (Reynolds, 2002). Neurologically, depression is associated with atrophy,
the degeneration of cells, in the Central Nervous System (CNS), which is centered in the
hippocampus, located in the brains medial temporal lobe, and is responsible for learning
and memory retention (Sapolsky, 2001).
Figure 5 and 6: Image of the Nervous System of humans today. The Nervous System can be broken down into
two parts: the CNS and PNS. The CNS consists of the brain and spinal cord. The PNS consist of the autonomic
and somatic nervous system. (Image from ChewFat, 2006) Figure 6: Image of the human hippocampus. The
hippocampus is located in the medial temporal lobe and is responsible for many of our daily functions, most
notable of which is learning and memory retention. (Image from Anderson, 2015 Medscape)

Depression can cause the retraction of the dendritic process in hippocampal neurons
(Sapolsky, 2001). Not only does the hippocampus lose dendrites, there is an impairment
of neurogenesis and a reduction in hippocampal volume (Andrade, Kumar-Rao, 2010).
The reduction in hippocampal volume can also affect the function of other downstream
areas, since the hippocampus has projections to the dorsolateral prefrontal cortex and the
hypothalamus (Andrade, et al., 2010). In such cases, stress can negatively act on the
prefrontal cortex, which may actually experience loss of dendritic spines similar to its
counterpart, atrophy of the dendritic tree, and a loss of synapse (Andrade, et al., 2010).
Moreover, depression is caused by changes in brain chemistry, genetics, hormone levels,
and as previously mentioned, the persons social lifestyle (Reynolds, 2002). Cortisol is a
stress hormone stimulates hippocampal neurons and facilitates learning and memory;
however, during stress, depression and other stress related disorders, cortisol may over
stimulate the hippocampal neurons and cause loss of synapses (Andrade, et al., 2010). In
most cases, such overstimulation is reversible, but in pathological overstimulation by
cortisol, the result can indicate neuronal apoptosis (Andrade, et al., 2010). Yet, one may
think that cortisol excess may be a possible explanation for the degeneration of cells in
the hippocampus and the volume shrinkage that take place, but studies indicate such
behavior from taking place are largely inconclusive (Varghese, Brown, 2001). Some
studies may suggest that cortisol may damage the hippocampus in depressed patients, yet
an alternate explanation suggests that a dysfunctioning hippocampus exists prior to the
onset of depression (Varghese, et al., 2001).
In order to combat the effects of an atrophic brain, physicians examine medical
history and past family records in order to diagnose patients (Reynolds, 2002). Though
depressive disorder does disrupt the daily functions in life, there is currently a vast array
of treatments. Medications include Serotonin Reuptake Inhibitors, which affect the nerves
that chemicals use to communicate to one another and concurrently block the reuptake of
serotonin (Sapolsky, 2001; Reynolds, 2002). In effect, this leads to greater cell
proliferation in the hippocampus (Sapolsky, 2001). Other antidepressant medicines are
also often prescribed and psychotherapy may be initiated depending on the severity of
symptoms (Reynolds, 2002).
On the other hand, anxiety disorders, from which three million people per year
suffer in the United States, leads to marked distress and inhibition of functions (Stein,
Carey, 2014). Anxiety can be broken up into multiple disorders, the most prevalent of
which is Generalized Anxiety Disorder (GAD) in which patients show marked signs of
extreme worry, tension and anxiety during even the pettiest of tasks (Stein, 2014).
Genetically, more common in women, GAD begins in ones teenage years and often
continues till one reaches the age of forty (Stein, et al., 2014). The pathophysiology of
this disorder can be traced to the amygdala, a structure located in the anterior part of the
temporal lobes, and plays a pivotal role in fear and anxiety (Stein, et al., 2014).
During the fight or flight responses, a response that is triggered during situations that
can be stress inducing mentally or physically due to the release of hormones, humans
tends to have increased heart and respiration rate (Stein, et al., 2014). Similarly, in GAD,
various neurochemical systems such as glutamate and gamma-aminobutyic acid (GABA)
are present when resolving communication between the connected regions in the brain
(Stein, et al., 2014). In addition to the bodys own mechanism in order to bring the body
to a stable condition, Benzodiazepines and Serotonin reuptake inhibitors are effective in
treating anxiety disorders (Stein, 2014). Many of these medications are similar to those
used in treating chronic depression. Serotonin reuptake inhibitors are usually the first
course of action since they are safer than many other drugs; however, in some cases
cognitive behavioral psychotherapy which focuses on behavioral techniques may be used
in order to threat GAD (Stein, et al., 2014).
Though depression and stress-related disorders come with a lot of psychological
and neurological damage, the advancement in neurotechnology has brought us closer to
finding solutions, most notably antidepressants. The name antidepressants is really a
misnomer, since these drug do not actually completely remove depressions, but rather
protect against the neurohistological and neurocognitive changes that come with stress
(Andrade, et al., 2010).
Furthermore, antidepressants may restore functional neuroplasticity (Andrade, et al.,
2010). It has long been disputed how antidepressants act and conventional explanations
have given us the framework to develop extended explanations. The first of three
conventional explanations holds that antidepressant drugs inhibit the reuptake of
monoamines, which include dopamine, serotonin, etc. into the presynaptic neuron. If
there are monoamines, there is an increase in postsynaptic receptor stimulation and an
increased postsynaptic neurotransmission (Andrade, et al., 2010). Such drugs include
serotonine-norepinphrine reuptake inhibitors (Andrade, et al., 2010). The second
explanation states that antidepressant drugs inhibit the breakdown of monoamines in the
storage vesicles of the presynaptic neuron (Andrade, et al., 2010). Such drugs include
monoamine oxidase inhibitors (Andrade, et al., 2010). The third explanation is that
antidepressant drugs increase the reuptake of serotonin and increase the release of
serotonin since they act directly on serotonin receptors (Andrade, et al., 2010). However,
the problem with all these explanations is that the antidepressant response is delayed
while these explanations are immediate (Andrade, et al., 2010). So an extended
explanation has been offered, which adds on that a greater availability of
neurotransmitters in the synapses can result in downregulation of monoamine receptors
(Andrade, et al., 2010). Downregulation of postsynaptic receptors decreases the activity
of such neurons, and downregulation of presynaptic receptors increase the activity of
these neurons (Andrade, et al., 2010). But some of these explanations have also been
incomplete, so the neuroplasticity hypothesis suggests that depression is really a disorder
involving the hardwiring of the brain and antidepressants act to protect or reverse such
changes (Andrade, et al., 2010). This hypothesis further states that neurogenesis occurs in
the hippocampus in such treatments; however, neurogenesis does not occur outside of the
hippocampus (Andrade, et al., 2010). However, both the hippocampus and the prefrontal
cortex may exhibit an increase in glial cells increase in richness and complexity of
dendritic branching and in the formation of new synaptic connections (Andrade, et al.,
As previously discussed, antidepressant drugs are the most common solution to
treating depressions, but they are only one solution to the treatment for depression and
not the only way that induces neuroplasticity. Electroconclusive therapy may induce
similar change, and physical exercise may also reduce the symptoms of depression;
however, in the United States, antidepressants seem to be quick fix that people wish for
and which respond more successfully than previous drugs (Andrade, et al., 2010).
The study of depression seems very basic to a normal observer; however, at its
core, it possesses greater mysteries and neurological pathways and connections, and
scientists have no idea what function they may serve. One such pathway or connection is
known as the HPA axis, which consists of a loop including the hypothalamus, pituitary
and adrenal glands (Varghese, et al., 2001).

The axis also receives important regulation from the hippocampus, amygdala, bed
nucleus of the stria terminalis (BNST), and paraventricular nuclei (PVN) (Varghese, et
al., 2001). Mainly, the HPA Axis is activated when people start to experience high levels
of physical and mental pressure (Varghese, et al., 2001). In this case, the hypothalamus
secretes two hormones, which are known as the corticotrophin-releasing hormone (CRH)
and arginine vasopressin (AVP) (Varghese, et al., 2001). The CRH is a 41-amino acid
peptide, which is scattered in various parts of the central nervous system (CNS)
(Varghese, et al., 2001). These hormones act on the pituitary to increase
adrenocorticotrophic hormone (ACTH) release (Varghese, et al., 2001). ATCH is carried
in the blood to the adrenal cortex and when it interacts with receptors on the
adrenocortical cells, it starts the production and release of the stress hormone mentioned
above: cortisol (Varghese, et al., 2001). Cortisol binds to two types of receptors, which
are known as type 1 (mineralcorticoid receptor) and type II (glucorticoid receptor)
(Varghese, et al., 2001). The type 1 receptor has the most attraction to cortisol. The whole
loop is complete when negative feedback of cortisol is given to the pituitary and the
hypothalamus (Varghese, et al., 2001). The negative feedback is dependent on the
concentration of cortisol. Fast feedback, another type of negative feedback identified,
depends on the rate in concentration and interactions with receptors in the hypothalamus
and hippocampus (Varghese, et al., 2001). The HPA axis is largely a mystery to
neuroscientists as current interest focuses on the three aspects (Varghese, 2001). The first
of these aspects is the long-term consequences on the HPA axis abnormalities on the
brain and other organ systems (Varghese, 2001). The second area is the role of early life
experiences in the ethiology of the HPA axis findings. The third area of interest focuses
on the use of medication that act on the HPA axis in the treatment of depression
(Varghese, 2001).
This research focuses on the Gut-brain axis (GBA) and its relationship to stress
caused disorders such as depression and anxiety. However, it is important to note that the
study of the GBA has just recently come into consideration by the scientific community
and only in the past decade have scientists realized that a diverse microbiota in the human
gut may be essential to avoiding disorders that agonize peoples everyday mental life.
The objective of this study is to examine how the gut microbiota and the connections
between the human gut and the powerhouse known as the brain in our body form
connections that influence depression. The human intestine is home for countless
numbers of microbes that are essential in maintaining our health (Foster, 2013). The
GBA is really the bidirectional signaling between the gastrointestinal tract, which harbors
these microbes, and the brain (Cryan, Mahoney, 2011 Carabotti, Scirocco, Maselli,
Sevari, 2015). This bidirectional communication network includes the CNS, the
autonomic nervous system (ANS), the enteric nervous system (ENS), the neuroendocrine
system and the HPA axis (Carabotti, et al., 2015).

So how do these microbes actually communicate with our brain? One way is that
the immune cells in the gut can sense bacteria in the lumen, an open space in the
gastrointestinal tract, and can release immune signaling molecules known as cytokines
(Cyran, et al., 2011). The changes in these signaling molecules can lead to changes in the
brain (Cryan, et al., 2011). Another way this communication can occur is when gut
microbes can activate cells in the intestinal walls that produce peptides, and concurrently,
this can activate nerve endings (Cyran, et al., 2011). Lastly, microbes have the ability to
send direct messages by the production of neurotransmitters (Cryan, et al., 2011). By
using neurotransmitters, they are signaling the molecules that the CNS uses (Cryan, et al.,
2011). However, the reverse may be true where the brain and CNS may communicate
with these gut microbes. Studies have show that during stressful conditions, the brain will
simulate the release of corticosteroids, which affect immune cells in the gut (Cryan, et al.,
2011). This means that microbes may leak out into your bloodstream and have diverse
effects in the human body (Cryan, et al., 2011). Furthermore, this complex
communication system is known to be essential to the maintenance of gastrointestinal
homeostasis (Cyran, et al., 2011; Carbotti, et al., 2015).
In order to understand this complex communication, it is important to grasp the
role of microbes in our body. Bacteria can be pathogenic, meaning that they cause harm
to our body; commensal, meaning that they are present in our bodies, but cause no harm
or benefit our bodies; and mutualistic, meaning that these bacteria are in a symbiotic
relationship with the human body where the environment in the body helps these
microbes survive while these microbes in effect are beneficial to our wellbeing and
perhaps even essential to our wellbeing (Foster, Neufield, 2013). Several bacteria phyla
are present in the gut, but the two most prominent phyla are firmicutes and bacterioides,
which account for about 70% of the microbiome (Foster, et al., 2013; Carbotti, et al.,
2015). Over the past few years, it has become clear that these microbes in the gut play a
role in the workings of the HPA axis (Foster, et al., 2013). For instance, exaggerated
CORT levels and ATCH response are shown in germ free mice when compared to
house-specific-pathogen-free mice (Foster, et al., 2013). Signs point to the fact that stress
is known to increase intestinal permeability, which give bacteria an opportunity to access
both immune and neuronal cells on the ENS (Foster, et al., 2013). In addition to
sustaining the function of the HPA axis, microbes have been show to influence the CNS
function using neuronal activation in stress circuits (Foster, et al., 2013). This is possible
through the activation of vagal pathways (Foster, et al., 2013). There is limited evidence
in understanding the relationship between the GBA and stress; however, growing
evidence in the scientific community has led many organizations to support such studies.
This study sets out to present empirical evidence that the gut brain axis is connected to
depression and anxiety. Though the science community has developed firm evidence that
there is some type of bidirectional communication between the gut and brain, there is
insufficient evidence that having a healthier gut can lead to reduced symptoms of
depression. It basically sets out to prove that the gut microbiota may be helpful in
lowering the symptoms of depression and altering the neuroplasticity of the brain. Thus,
this study sets out to scientifically prove the notion that You are what you eat. Due to
limited resources and the risks involved with tests on humans, this study will involve the
use of specific mice altered with the apparatus of the study in mind. The general
prediction made in this proposed study is that mice with a more diverse and possibly
healthier gut microbiome will have reduced symptoms of depression while those mice
who are fed an unhealthier diet will have a microbiome that is not as diverse and which
may rather may contribute negatively to the onset of depression. It is important to note
that clinical studies on mice are not directly applicable to humans since the brain
structure of these two animals differ. However, such studies will provide compelling
evidence that perhaps a healthier microbiome is an alternate cure to what plagues
millions of people in the United States who have depressive disorders. In order to
perform this study, two types of mice will be used: Germ Free Mice (GF) and the House
Mice (Household Mice).
Germ Free Mice (GF)
In order to study the microbiome gut brain axis, the use of germ free mice has
been a common practice. Germ Free Mice are animals that are devoid of any bacterial
contamination and offer scientists the possibility of studying the impact of the absence of
any gut microbes on behavior (Cryan, et al., 2011). Many times, these mice are used in
order to test how specific diets alter the gut brain axis (Cryan, et al., 2011). These animals
are born through a caesarian section and specific techniques are performed at their birth
in order to keep newborns free from any pathogens present (Cyran, et al., 2011).
Additionally, they are placed in special isolation units and as a result have an altered
immune system as well as other parts of their body (Cyran, et al., 2011).
House Mice
The household mouse is an animal that we have all seen in our homes and belongs
to the genus Mus (Vandebergh, 2000). It has a normal gut microbiome that is not
modified for lab use. Today, household mice are the most widely used model organisms
in medicine and in the practice of genetically engineered models (Vandenbergh, 2000).
Some common features include a pointed snout and light brown hair color (Vandebergh,

The research will use two techniques that are most widely used to test for depression in
mice. These two tests are the Forced Swim Test (FST) and the Tail Suspension Test
Forced Swim Test
The Forced Swim Test is a rodent behavioral test that is used in order to test for
the efficacy of antidepressants and to test the state of depression in mice (Can, Dao, Arad,
Terrillion, Piantadosi, Gould, 2012). In order to perform this test, cylindrical water tanks
are required (Can, et al., 2012). These waters tanks are constructed of transparent
plexiglass and are able to withstand animal movement (Can, 2012). Additionally, these
water tanks are filled with consistent amounts of water and the dimensions of the tanks
are designed so that the mice do not escape from the tank (Can, et al., 2012). Moreover,
the test involves the used of a thermometer and video recording device (Can, et al.,
2012). Dividers are also included in the test to prevent mice from seeing each during the
test and altering their behavior (Can, et al., 2012). A white noise generator, a device that
masks disturbing sounds that may startle the animals, is also used and is adjusted to the
unique environment and circumstances (Can, et al., 2012). The general procedure of the
forced swim test starts by placing the camera and dividers in position; cameras are placed
in order to obtain a high-resolution image of the mice (Can, et al., 2012). The tanks are
then utilized and filled with room temperature water (Can, et al., 2012). After setting up
the main apparatus, the white noise generator is turned on in order to mask external
noises (Can, et al., 2012). The mice are then introduced to the apparatus and held by their
tail and gently placed in the water so their head is not submerged (Can, et al., 2012). The
video recording is used to record the behavior of the mice and the stopwatch is used in
order to track the timing of the test, which usually lasts around six minutes (Can, et al.,
2012). After the procedure is finished, the mice are wiped with paper and placed back in
their designated location (Can, et al., 2012).
Tail Suspension Tests (TST)
The tail suspension test is another behavior despair tests used to screen for
potential antidepressant drugs and to test the state of the depression in mice (Can, Dao,
Terillion, Piantadosi, Bhat, Gould, 2012). The test revolves around using a suspension
box that is made of plastic and supplied by a rectangular compartment (Can, et al., 2012).
In addition, the test involves the use of tape, a video recording device, and a white noise
generator (Can, et al., 2012). The general procedure of this test involves placing the
camera in position to capture the best possible image of the mice. Next, the white noise
generator is used to mask external noises (Can, et al., 2012). The tape is then used to
adhere to the tails of mice and the middle portion of the tape is used to stick to the inner
wall of the cage to prevent tangling of tape pieces (Can, et al., 2012). The mice are then
suspended by placing free ends of the tape to the suspension and the test is recorded
(Can, et al., 2012). Finally, the mice are cleaned up and returned to their respective
locations (Can, 2012).
The Procedure
In order to perform this study and to identify the relationships of the microbial
content of the gut with effects of depression, twenty germ free mice and twenty
household mice will be used. This will be sufficient for statistical analysis between the
different groups of mice and within groups. The gender of the mice will vary. There will
be ten males and ten females per group, which will allow for the evaluation of the impact
of the sex of an animal. Since mice do not become naturally depressed, corticosterone,
the animal hormone that is involved in energy regulation and the onset of stress and
depression, will be administered to the mice. Countless studies have shown that
corticosterone injections stimulate stress and depression in mice. However, only ten germ
free mice and ten household mice will be given these injections in order to stimulate
stress and perhaps the onset of depression. The other ten germ free and household mice
(twenty in total) will be left as a control group, without the stimulation of depression. The
mice that are given corticosterone injections will then undergo the forced swim test and
the tail suspension test while the mice that do not get this injection will not undergo these
tests. However, to move to the next steps, the results of the forced swim test will need to
be analyzed. The results of forced swim tests indicate that when normal mice are placed
in the room temperature water, they usually spend about three minutes trying to stay
afloat before giving up. On the other hand, a depressed mouse gives up after one minute.
The results of the tail suspension test usually show that when a healthy mouse undergoes
the test, it struggles to latch on while a depressed mouse gives up very quickly. The
results can be analyzed in greater detail. However, these basic principles are used in order
to verify the state of the mice. Continuing with the procedure, all mice will undergo fMRI
scanning, which will give knowledge about the overall brain in these mice. Five germ
free depressed mice and five household depressed mice will then be given a probiotic diet
for a certain period of time. Five germ free depressed mice and five household depressed
mice will be give a high fat diet for a certain period of time. Additionally, five
non-depressed germ free mice and five non-depressed household mice will be given a
probiotic diet while the other five non-depressed germ free mice and five non-depressed
household mice will be given a high fat diet. The study will conclude by performing the
forced swim test and tail suspension test after a certain period of time. The results will
then be analyzed using the general guidelines mentioned above to interpret the meaning
of the tests. It is important to note that the age of the animals will be in the mature range
so maturation effects do not play any role. The general prediction of this study is that the
depressed mice given a probiotic diet will have reduced anxiety like symptoms while the
depressed mice given a high fat diet should still have stress/depression symptoms. The
non-depressed mice, given a high fat diet may have greater risks of depression or they
may not. The probiotic diet may provide a healthier microbiota and less risk for
depression since probiotic diet will offer the mice a more diverse number of microbes
that their body will be able to use to keep a diverse gut. The only way to interpret and
analyze the results is to perform the study.

The bidirectional communication between the brain and the gut has is in its early stages
of research; however, new research is uncovering the vast connections that our body
holds and the possibility that a healthier diet may be the start to a healthier brain. If this
study proves that probiotic diets reduce anxiety like symptoms, it may allow researchers
new ways to threat depression such as modification of diet. Although the conventional
approach to treating depression has been the use of antidepressant drugs, specifically
serotonin reuptake inhibitors, if scientists provide compelling evidence that diet may
reduce levels of depression associated with stress, psychologists may be able to help
patients in ways unimagined before. However, such studies as these should not be applied
directly to humans as the brain of humans and rodents differs neurologically on many
different levels. However, significant progress has been made in recognizing that gut
microbiota contribute to certain brain functions. Perhaps the statement that you are what
you eat may become applicable due to new scientific breakthroughs.

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Citations, Quotes & Annotations

Anderson, P. (2015). Human Hippocampus.

"Image" (Anderson, 2015)

Ballantyne, S. (2015). The HPA Axis. Retrieved 2016, from

"Image" (Ballantyne, 2015)

Devlin, H. (2016). FMRI Scan. Retrieved 2016, from

"Image" (Devlin, 2016)

France-Presse, A. (2015). Human Amygdala. Retrieved 2016, from

"Image" (France-Presse, 2015)

Freudenrich, C. (n.d.). Common Depressants. Retrieved 2016, from

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