Genetic Mutagenesis Screen

Genetic Mutagenesis Screen
Question 1
(1A) Design a forward genetic mutagenesis screen, in a fly or rodent model, that would allow you to
identify genes required for proper axon guidance. Discuss the main steps involved in this approach.
Question: Which genes are required for proper axonal guidance of the mesolimbic and/or
nigrostriatal dopamine pathways in the mouse?
Brief background: In mice, the first DA neuron neurites appear at E11.5. These neurites extend
towards the striatum, forming the medial forebrain bundle (MFB), the main neural tract connecting
ventral tegmental area (VTA) and the substantia nigra (SNc) to the striatum. At E14.5 the DA
neurites approach the border of ventrolateral ganglionic eminence (VM). These neurites then
multiply without further ... Show more content on Helpwriting.net ...
Perform complementation analysis to determine if the generated mutation is unique or has been
previously described. To perform the analysis, I would mate the mutants I produced with known
mouse lines which have null mutations in genes known to be important for DA neuron axon
guidance (DCC–/–, Nkx2.1–/–, Pax6–/–, Slit1–/–, Robo1–/– ). If WT phenotype is produced by the
cross, the mutations are in 2 different genes. If the offspring shows mutant phenotype, the mutation
might occur in the same gene (Hegarty, Sullivan et al. 2013).
5. Perform linkage analysis to map the gene. This technique is used to relatively position gene of
interest in relationship to the known gene. For this analysis I would have to pick genes which
produce different phenotype from the one seen in the mutants generated in my experiment. The
mutants generated are then mated with this known mutant of a different phenotype and both traits
are examined in the offspring. In the offspring produce both phenotypes, the genes may be near each
other and are inherited together.
6. One the location of the gene is determined, the gene is then cloned (design primers and PCR the
gene, insert gene into a vector). Cloning of the gene will allow for future experiments in which the
gene can be manipulated in vitro or in
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The Neurobiology of Parkinson's Disease Essay
The Neurobiology of Parkinson's Disease
In neuroscience it is assumed that the central nervous system governs and defines all aspects of
behavior (Grobstein, 1998). Therefore, the brain, the hub of the central nervous system, is
responsible for integrating all sensory and motor patterning. To understand the mechanisms of
neurobiology it is often useful to observe the nervous system at the level of the neuron. Integration
and communication between neurons is facilitated by neurotransmitters, chemicals which act as
intermediaries at the synaptic gap (Delcomyn, 1998). Many behavioral disorders have a
neurochemical basis, oftentimes associated with abnormal neurotransmitter activity. These
abnormalities are thought to stem from ... Show more content on Helpwriting.net ...
The National Parkinson's Foundation estimates that each PD patient pays $2500 a year on medicines
alone. When accounting for Social Security and nursing home payments, Parkinson's Disease costs
over $5.6 billion annually to the nation (PD Web, 1998). Despite the high occurrence of Parkinson's,
it is still not always recognized as a significant medical problem. The symptoms are often ignored in
the elderly because they are thought to be part of the natural process of aging (PD Web, 1998).
Symptoms include tremors in hands, arms, legs, jaw, and face; slowness of movement, or
bradykinesia, and difficulties in balance and coordination. As the chronic disease progresses, PD
patients may have difficulty with simple tasks, such as walking and talking (PD Web, 1998). Much
of the oversight of PD in medical research, and of other neurodegnerative diseases associated with
elderly populations, like Alzheimers, could be a reflection of a dismissive attitude towards the aging
process in the medical community and American culture.
The primary symptoms of Parkinson's Disease stem from the deterioration of the part of the brain
that controls motor functioning (NHGRI, 1998). This region is the substantia nigra which is found
deep within the brain stem and contains neuronomelanin, pigment cells, which synapse to cells of
the striatum. The striatum is responsible for balance, control of movements, and

The Cerebellum Research Paper
The Cerebellum
The "little brain," or cerebellum, in many ways resembles a smaller version of the cerebral cortex
(e.g., it contains two distinct hemispheres) and is located just behind and underneath it. The
cerebellum works as an integrator, allowing us to control and process our perceptions and motor
movements. Many neural pathways link the cerebellum with both the cerebral cortex and the spinal
cord. The cerebellum smoothly integrates these pathways, receiving feedback about body's position
and using this information to direct our movement.
Because the cerebellum modifies motor movement rather than producing it, damage to the
cerebellum causes movement–related difficulties rather than paralysis. These difficulties tend to be
most obvious

Goal Directed Behavior
There are two main components involved in goal–directed behavior, which is defined as the
behavior directed towards accomplishing a specific goal. The first is to select a proper course of
action and the second is to learn to adjust the behavior depending on the surrounding conditions.
Studies have shown that the basal ganglia is the brain region largely responsible for the selection
and initiation of these 'willed' movements. That is to say, the main function of the basal ganglia is in
controlling voluntary movements. Within the basal ganglia of the brain, there is an important input
structure called the dorsal striatum, which plays a vital role in the reward system of the brain.
Moreover, the dorsal striatum is made up of 2 opponent pathways ... Show more content on
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For instance, when the researchers activated the population of neurons in the direct pathway
(dMSNs), it caused the mice to accelerate and push the joystick at a faster rate on future movements.
In contrast, when the researchers activated the population of neurons in the indirect pathway
(iMSNs), it caused the mice to decelerate and push the joystick at a slower rate on future
movements. These results were consistent with the wide–held belief that separate population of
neurons in the basal ganglia promote and suppress movement. However, contrary to popular belief,
Yttril and Dudman found that this is not always the case as they discovered that stimulation of
dMSNs of the direct pathway can also slow movement, while stimulation of iMSNs of the indirect
pathway can also speed movement. Interestingly, this result only seemed to occur in situations
where the researchers activated a population of neurons at a moment the mouse was making a slow
movement of the joystick. This was different from the first case, in which researchers activated a
population of neurons at a moment the mouse was making a fast movement of the joystick.
Additionally, the researchers discovered that stimulation of either population of neurons did not
have any impact on the rate of movement initiation or on the rate of water licking by the mice, thus
indicating that movement initiation and motivation are not affected by activation of the neurons.
Lastly, Yttril and Dudman attempted to stimulate the loss of the chemical dopamine in mice in order
to help determine the effect of dopamine on the movement speed of the mice pushing the joystick.
Dopamine is a neurotransmitter, a chemical messanger released by neurons in the brain, that plays a
vital role in reward–motivated

Parkinson 's Disease : Disease
Parkinson 's disease Twanda H. Lewis North Carolina Wesleyan Dr. Quinan Parkinson 's Disease
Twanda H. Lewis North Carolina Wesleyan Dr. Quinan Outline
Abstract...................................................................................................5
Introduction........................................................................................... 6
Symptoms.............................................................................................. 6
Tremor.................................................................................................... 6 Slow
Movement.................................................................................... 6 Rigid
Muscles......................................................................................... 7 Disfigured
Posture................................................................................ 7 Loss of Automatic
Movements........................................................... 7 Changes in the Speech
Pattern........................................................... 7 Changes in
Handwriting........................................................................8
Constipation........................................................................................... 8 A Quite
Voice......................................................................................... 8 Masked ... Show more content on
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This paper examines the symptoms, the causes and the treatment options for the Parkinson 's
disease. Introduction Parkinson 's disease is a neurodegenerative disorder and a movement disorder.
Parkinson's is the gradual loss of the ability to control muscle movement thereby, resulting in the
trembling of the limbs and the head even during rest. Other characteristics include slowness,
stiffness and impaired balance. As the Parkinson 's disease progress it becomes hard for the patient
to move, to talk and even fulfill simple tasks (Berg et al., 201,4). Parkinson's disease varies from one
patient to the next patient reason being that the rate of impairment for an individual patient is faster,
for others, they tend to live many more years. The premature death is often brought about by
complications to do injuries such as falling or pneumonia. Symptoms Tremor In this case, there is
the presence of shaking which typically beings in the limb such, has the hand or the fingers.
Additionally, there is a back and forth, rubbing the thumb & forefinger, a condition known as a pill–
rolling tremor. The hand usually experiences tremors even when relaxed for Parkinson's disease.
Slow Movement Slow movements are also known as bradykinesia. Over a duration of being affected
by Parkinson 's disease, the ability of movement reduces, and the movement becomes slow instead
thereby rendering the simple tasks to be challenging and time–consuming. As

What Makes Us Human Research Paper
There is evidence to suggest that humans have been around for 200,000 years. Even the earliest of
humans were able to make good decisions which contributed to their survival. But what helped them
make those decisions? The answer lies in their circumstances and the emotions that came with them.
Growing up, we as humans are taught right from wrong, but our lives still have a great impact on
our actions. Circumstances dictate how we feel emotionally and what we do as a reaction. Just as
Jenna Fox faced adversity through her accident, we all face challenges in our lives. It is how we
recover from these harmful situations makes us human. Unlike other mammals, we stand our ground
and accomplish our goals. You may say that some people do go into fight or flight mode, but, we are
still able to survive the situation and make our lives better. For example, Jenna survives a terrible car
accident and her life is forever changed. After coping with the changes, she is able to return to a life
that is as normal as she could make it. ... Show more content on Helpwriting.net ...
When there have been trying tribulations, more people will understand what it is like for emotions to
take a toll mentally. When there is the constant hum of worry in their head, some will understand
what it is like to be overcome with anxiety. Emotions are high and you feel out of place. When there
is the prickling of happiness, people will know how hard it is not to act impulsively. Emotions
influence the decisions humans make. When there is anxiety, some may decide to drink water or
take a nap. When there is excitement, some may make bad choices because of the adrenaline rush.
These feelings let humans know what would be the best thing to do. When there is danger, emotions
let people know to be on high alert and watch for

Alcohol Addiction Is The High Risk Of Relapse
Alcoholic beverages are served in many restaurants, sold in many stores, and acceptably consumed
in many populations. Although alcohol can become a drug of abuse, not many view it that way.
According to the National Institute of Alcohol Abuse and Alcoholism (2014), about 7.2% of adults
in the United States ages 18 and over have an alcohol use disorder. A variety of environmental and
genetic factors contribute to the development of alcohol addiction. The variability in the causes of
alcohol addiction generates variability in the response to treatment. However, what is common
among all alcohol addictions is the high risk of relapse. This risk is potentially caused by the lasting
changes in the brain that occur when voluntary alcohol use becomes an addiction. The neural
changes that are a result of an alcohol addiction potentially put a recovered alcoholic at high risk of
relapse until these circuits can be erased and replaced with healthier circuits. Not enough is known
about the nature of alcohol addiction to provide a clear cut way to replace addiction circuitry with
healthier wiring, however, new research on the neural mechanisms of addiction are creating a better
understanding of the effects of alcoholism. This new insight is leading to suggestions for more
effective treatments. One new treatment, called cue exposure therapy, might be a significant new
development because it addresses the neural changes caused by alcohol addiction and focuses on
using conditioning to

Huntington's Disease Research Paper
Huntington's disease (HD) is a rare and fatal disease known as a polyglutamine neurodegenerative
disorder effecting only 4–10 per 100,000 people of European decent (Driver–Dunckly et. Al 2007).
This means there is a problem with the trinucleotide that codes for glutamine, cytosine–adenine–
guanine (CAG). In the case of HD there is an extreme overproduction of the CAG repeats in the
protein huntingtin. Accumulation of this mutated form of the protein in neurons causes cell atrophy
which in turn causes the brain to malfunction. The disease was first described by Dr. George
Huntington in 1872, however it wasn't until 1993 that the cause of the disease was actually
discovered (Bertram et. Al 2005).HD is characterized by symptoms effecting the afflicted ... Show
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The dorsal striatum is composed of the caudate nucleus and the putamen. The striatal cells appear to
be the most vulnerable to the inclusion bodies formed by the aggregates of mutant huntingtin. As the
disease progresses and more inclusion bodies are accumulated the striatal cells begin to die at a
faster rate than they are reproduced. The death of these cells cause the striatum to degrade. The
exact mechanisms by which the striatal cells function is disrupted is still being researched, however
it is theorized that the damage to the mitochondria from mutant huntingtin or toxic glutamine
segments is one of the culprits (Turner, et. Al 2010). The basal ganglia allows one to start and stop
movement, controls cognition and comprehension, and also controls mood. The degradation of the
striatum interrupts all of these function which attributes to the clinical manifestations of the disease.
The disease is fatal because eventually the striatum of the basal ganglia becomes so damaged that
the individual can no longer swallow. Mutant huntingtin may also affect certain layers of the
cerebral cortex, the hypothalamus, thalamus, and parts of the cerebellum (Purves et. Al,

The Effects Of Drug Addiction
Drug addiction is a chronic brain disorder that affects millions of people around the world. It is
characterized by compulsive drug seeking and use despite the harmful consequences that may occur.
Surprisingly, drugs affect people in different ways. One person may habitually take a drug and never
become addicted, while another person can have only a single experience with a drug and become
iammediately addicted. To be clear, addicts are habitual drug users who continue to use a drug
despite its unfavorable effects on their health and social life. It is also worthy of noting, that
addiction does not solely occur with drugs, ambling, food, shopping and video games also can
become an addiction. There are three stages in drug addiction that should be known, initial drug
taking, habitual drug taking, and lastly, drug craving and addiction relapse.
The first stage in drug addiction is the initial drug taking. In other words, how does a person begin
taking the drug in the first place. It should first be noted, that not everyone who has access to a drug
will take it and not every who takes the drug will continue to do so after that first use. To begin with
there are various environmental factors that play a role in whether or not a drug is taken by a person.
The first factor is drug availability and price. This may include how easily a drug can be accessed
and how expensive is it to buy. The second factor is social pressures. This depends on what type of
people a person is

Psychopaths In Prison
Generally defined, psychopathy is a personality disorder that is characterized by a combination of
superficial charm, strong antisocial behavior, and extreme sensation–seeking and impulsivity.
Psychopaths make up approximately 15% of the prison population while between 50% – 80% of
that prison population could be diagnosed more broadly with antisocial personality disorder (Ogloff,
2006). While the percentage of those diagnosed with antisocial personality disorder is high, the
percentage of psychopaths in prison is extremely overrepresented compared to the average
population which hovers between 1% – 4% (Ogloff, 2006). While it would be disingenuous to say
that all psychopaths are dangerous, their overrepresentation in the population of violent ... Show
In prison, they figured out that the best way to leave was to operate at the best behavior possible.
From there, once they were outside again, they were able to operate the same way they were before.
This aspect emphasizes the effect that the striatum and the amygdala play. The amygdala acted in
complete disregard for previous punishment once the subject was out of prison; meanwhile, the
striatum drives the constant desire for stimulation. This drives the thought that there may be
psychopaths in existence who are caught less frequently and how that may influence their

Essay about The Dopamine Hypothesis of Schizophrenia
The Dopamine Hypothesis of Schizophrenia
Schizophrenia is a disease that has plagued societies around the world for centuries, although it was
not given its formal name until 1911. It is characterized by the presence of positive and negative
symptoms. Positive symptoms are so named because of the presence of altered behaviors, such as
delusions, hallucinations (usually auditory), extreme emotions, excited motor activity, and
incoherent thoughts and speech. (1,2) In contrast, negative symptoms are described as a lack of
behaviors, such as emotion, speech, social interaction, and action. (1,2) These symptoms are by no
means concrete. Not all schizophrenic patients will exhibit all or even a majority of these symptoms,
and there is some ... Show more content on Helpwriting.net ...
(2) However, there are some problems with this evidense. Amphetamines only mimic the positive
symptoms of schizophrenia. They do not produce any of the negative symptoms. Likewise, anti–
psychotic drugs are only affective on the positive symptoms of the disease. There is still some
evidense that schizophrenics do posess higher levels of dopamine, however, these increases are only
found in the striatum of the brain (7). The striatum is a region of the brain that receives its inputs
from and outputs to the cortex. Injury to the striatum results in problems with intiation and control
of motor behavior. (9) Also, there is evidence that the prefrontal cortex produces lower levels of
dopamine. (4) The prefrontal cortex is involved in the organization and coordination of information
to and from the cortex. (7)
The major support and refutation of the dopamine hypothesis has come from the examination of
dopamine receptors in these regions of the brain. There are two main types of dopamine receptors,
D1 and D2. However, within the category of D2 receptors, there are three subtypes, D2, D3, and D4.
(5) Through PET scan analysis of dopamine usage in the brain and post–mordum molecular analysis
of brain tissue, researcher were able to determine relative levels of dopamine receptors in patients
with schizophrenia compared to non–schizophrenics. Overall analysis of dopamine

Alcl3 Lipid Case Study
Results Lipid Peroxidation and nitric oxide: The present findings showed that the daily oral
administration of AlCl3 induced a significant increase in the levels of cortical, hippocampal and
striatal lipid peroxidation marker MDA recording +55.20%, +128.32% and +427.39%, respectively
above the control values. In addition, NO level increased significantly by +100%, +72.22% and
+57.14%, in the cortex, hippocampus and striatum respectively of AlCl3–treated rats. Protection of
AlCl3–intoxicated rats with caffeine attenuated the increased values of MDA and NO in the studied
brain regions to non significant changes from the control (Figure 1). Reduced glutathione: In AlCl3–
intoxicated rats, the GSH levels showed a significant increase in the cortex (+10.41%) and a
significant decrease in both hippocampus (–27.03%) and striatum (–12.04%) as compared to control
group. In the cortex the increased GSH level continued after caffeine protection. In addition,
caffeine maintained the decreased level of striatal GSH. However, caffeine protection improved the
significant decrease induced by AlCl3 in hippocampal GSH level (Figure 1). ... Show more content
on Helpwriting.net ...
The protection of AlCl3–intoxicated rats with caffeine prevented the recorded increase in
hippocampal and striatal TNF–α level. However, caffeine protection failed to normalize the
significant increase induced by AlCl3 administration in cortical TNF–α

Comparing ParkinsonÂ´s Disease And Huntington's Disease
Two Diseases, One Hope: Fetal Neural Transplantation in the Treatment of Parkinson's and
Huntington's Disease
Parkinson's Disease (PD) and Huntington's Disease (HD) are neurodegenerative diseases that are
caused by malfunctions within the motor sector of the nervous system. These malfunctions, which
are caused either by the surplus (as in HD) or absence (as in PD) of hormones, are a direct result of
neural cell deterioration within the brain. PD and HD illustrate two very different behavioral
patterns that are subsequently caused by two opposite and extreme biological abnormalities. Yet the
common thread between the two conditions is that there are major mechanical predicaments arising
between cellular connections within the brain. ... Show more content on Helpwriting.net ...
Information from the nigra cells passes through the synapses with the aid of a specific hormone,
dopamine, which is a significant chemical transmitter in the brain. Because the existence of
dopamine is essential to the function of the substania nigra, it is also essential for the various
muscular activities controlled by the striatum, such as walking, balance, etc. (16).
In Parkinson's Disease and Huntington's disease the nigra–striatum neural communication
assemblage is severely hampered. PD results from a depletion in the amount of dopamine produced
by the brain. At the onset of the disease, dopamine–secreting cells of the substania nigra, either
because of genetic factors or environmental toxins, experience mass cell death. Thus, the nigra cells
are unable to form synapses through which they secrete and relay dopamine to the striatum in a
neural circuit within the basal ganglia (18).
HD, in contrast, is not a condition offset by the environment, as PD is thought to be. It is indeed a
condition due to cell death in the brain (basal ganglia) but is caused by an abnormal gene that codes
for a mutant protein called huntingtin. Huntingtin, thus, interferes with normal brain cell functions
by causing a depletion in neural cellular energy and neural death (12)(9).
Another example of how HD can be described as being the opposite condition to PD, has to do with
both behavioral and biological symptoms of the neurodegenerative

The Virtues Of Isolation Summary
Annotated Bibliography
AGAINST:
Crane, Brent. "The Virtues of Isolation." The Atlantic, Atlantic Media Company, 30 Mar. 2017,
www.theatlantic.com/health/archive/2017/03/the–virtues–of–isolation/521100/.
"The Virtues of Isolation", written by Brent Crane, states that under the right circumstances being
alone can provide significant psychological help. The article stated that scientists often associate
isolation with negative outcomes due to it having adverse effects on the minds of children. However,
when it is voluntarily pursued, it can be shown to have significant befits–some would even say its
therapeutic. That temporarily isolating yourself gives you a chance to take a step back and take a
good look at yourself. It alleviates the stress on our everyday lives and lets us relax. That the
difference between solitude as therapy and solitude as misery depends on the quality of self–
reflection that a person experiences, and the ability to reintegrate into social groups when their
ready.
Edmonds, Molly. "What are the effects of isolation in the mind?" HowStuffWorks Science,
HowStuffWorks, 6 Apr. 2010, science.howstuffworks.com/life/inside–the–mind/emotions/isolation–
effects.htm.
"What are the effects of isolation in the mind?" discusses the scientific aspect of what transpires in
our brains when we are lonely vs non–lonely. Writer Molly Edmonds tells us how The University of
Chicago researchers conducted an experiment to see how lonely people's brains react to certain
stimuli as opposed to that of a non–lonely person. Both the lonely and non–lonely subjects were
shown photographs of people in both pleasant and unpleasant settings. When viewing the pleasant
pictures, the non–lonely subjects showed much more activity in a section of the brain known as the
ventral striatum than the lonely subjects. The ventral striatum is a part of the brain that deals with
learning and part of the brain's reward center. The lonely subjects showed less activity in this region
of the brain while viewing the pleasant pictures and unpleasant pictures. The results left researchers
wondering whether loneliness rewires the brain to function differently or if the brain inclines certain
people to feel isolated.
Khullar, Dhruv. "How

Primary Theories Of Schizophrenia Essay
There are three primary theories for schizophrenia that need to be considered:
The first theory being, the Genetic Theory. This theory proposes that schizophrenia is inherited and
passed through genes. An initial study shows, one in eight children of a schizophrenic parental
background develop this disorder, similarly another study concludes 75% of children will be
mentally healthy. Research also states, the illness occurs in 10% of persons with a first degree
relation to a family member with schizophrenia. Statistics are even high for an identical twin of a
person with schizophrenia, with a probability of 40–65% of developing the disorder.
Next is the Environmental/ Interpersonal Theory. This theory proposes that schizophrenia and
emotional disorders are directly correlated to a person's young upbringing in the home and parental
figures. It also proposes the idea that stress is a pivotal cause. A strong ... Show more content on
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The initial indication of schizophrenia being a factor of dopamine was amphetamine consumers.
Amphetamine causes several symptoms of schizophrenia including: delusions and hallucinations. In
schizophrenics there is an unsteady, high amount of dopamine in the brain. Antipsychotic drugs
work to lower the presence of dopamine on the brain by impeding dopamine receptors. There are
two primary dopamine receptors, D1 and D2. In schizophrenic patients the latter is split into D2, D3
and D4 subtypes. Dopamine activators are found in the striatum, prefrontal cortex and limbic system
of the brain. Clinical research has observed an increase of dopamine in the emotion controlling
striatum through PET and SPECT brain scans. Unfortunately there is no one pinpointed cause of
high dopamine levels. Many of these causes are: Agitation, anxiety, cognitive acuity, feeling of
pleasure, hedonism, high energy, high libido, insomnia, paranoia and

Different Structures Of The Brain Essay
Structures of the Brain
The Brain Stem
The brain stem or the medulla is the closest to the spinal cord. The brainstem is responsible for most
of the human bodily functions. The brain stem is critical for human survival and normal human
functions. The brain stem is also responsible for information of pain and touch from the head and
neck; it is also responsible for the inputs from the face and the mouth. Reticular formation is a group
of neurons, nuclei, that are important for sleep and wakefulness. In reticular formation there is
nuclei that are a major source of neurotransmitter serotonin. Serotonin is important for regulating
mood and activities.
The Pons
The pons is the region above the brainstem. The pons contains the locus coeruleus, a region of cells
that belong to the reticular formation. The neurotransmitter norepinephrine are necessary for arousal
and attention. These neurons are found in the brain and spinal cord.
The Cerebellum
Connected to the brain stem and is located in the back of the brain is the cerebellum. The cerebellum
is responsible for motor coordination and also some learning involving movement. Once someone
learns a new motor action that information is held in the cerebellum.
The Midbrain
The midbrain is located above the pons. The midbrain has an area called the substantia nigra which
holds different nuclei. The midbrain is responsible for the body 's movement that is not covered by
the cerebellum. The neurotransmitter dopamine, that produced by

Essay On Endogenous Modulation Of Pain
Second, this study also provides supporting evidence for endogenous modulation of pain based on fc
changes compared cLBP in different pain condition with HC and within cLBP. Substantial evidence
is accumulating to show that the striatum plays an important role in the endogenous modulation of
pain.
Published data provide evidence that the limbic system is essential to chronic pain processing59.
The NAc is a critical node in this network. Functional interactions between component structures in
the limbic system are wide–ranging. Previous studies show that the nucleus accumbens (NAc) is
extensively anatomically connected with cortical areas including cingulate, prefrontal cortex,
parahippocampal gyrus, and insula 60–63 and subcortical areas ... Show more content on
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Therefore, some previous studies hypothesized that these brain regions, especially within the
emotional corticolimbic system, acted as the bridge of pain modulation and stress regulation5.
In practice, research on the emotional brain has often focused on a few structures thought to be
central to this type of processing – hypothalamus, amygdala, insula, and so on. However, chronic
pain frequently coexists with other disorders such as anxiety, depression, or learning and memory
deficits. This co–occurrence might manifest if chronic pain were to precipitate neuroplastic changes
in supra– spinal structures, such as amygdala, that lead to these pain–related disorders.
We also found the bilateral VSs, DC, DCP and DRP had significantly overlay increased connectivity
with the right DLPFC in cLBP in HP compared with cLBP in LP.
The bilateral DCP and DRP had significantly overlay increased connectivity with the right insular
cortex and ACC in cLBP in HP compared with cLBP in LP.
The above–mentioned dorsal and ventral striatum, amygdala, anterior cingulate cortex (ACC), the
anterior insular and the orbitofrontal cortex are all implicated in reward as well as pain processing.
Recent experimental data suggest that basal ganglia may also be involved in various dimensions of
pain sensation and pain experience 69. So far, there

How Does Our Brain Communicate? Essay
Love
According to Merriam–Webster dictionary, it defines love as "A feeling of strong or constant
affection for a person." (Love, 2015). In order to have the feeling of other person, we need social
connection to support it and it is the foundation of all social activities. How does our brain respond
to the love of other person? Will external factors change the way our brain responds to love or do
our brain actually ignore these outside things and only focus on the inside activities only? I would
like to start the discussion with Dr. Lieberman's perspective. According to Lieberman, we human
has both the ability to connect to the social world, and it is the basic needs for us to survive
(Lieberman, 2013). Dr. Lieberman explained everything in the society at neurological perspective–
the brain activity. Since social connection can be explained by the brain activities, love can be
explained the same way. Because love is based on the social connection, in order to love someone,
we need to know them first. The process of "getting to know someone" require social skill. There
are serval different ways to look at our brain activities and it will explain the relationship between
our brain and love. The department of neurology of Harvard University did an experiment on
college students. They showed pictures of someone special to them and by using the fMRI to scan
their brain compare to the time they look at the picture and the time they did not. The fMRI scan
shows two parts

Nature Vs. Nurture : Addiction
Nature vs. Nurture: Addiction Introduction Psychology is a developing science which studies the
mental functions, processes, and behaviors of an individual. In the science of psychology, many
debates arise; nature vs. nurture is one of the most popular ones. These psychological debates are
followed by research, backing up either nature or nurture or both. Nature suggest heredity impacts
human psychological development; nurture suggests the environment impacts our psychological
development. Addiction plays a large role in nature vs. nurture. Addiction is defined as a person
being attached to a certain activity or item; an addict is one who has a dependency on particular
substances or activity. There are many debates on whether addiction is caused by genes or the
environment. Many researchers believe if they had the answer of addiction being a genetic condition
or an environmental factor, they would be able to resolve the problem of addicts, or so they believe.
Nature Aspect on Addiction Addiction has been proven to be in the genes of humans. "Addiction is a
notorious treatment–resistant psychiatric disorder characterized by the impairment of self–
monitoring, loss of interest in other targets of pleasure, and uncorrectable impulsive/compulsive
drug–seeking behaviors"(Todo, 2012,para.1).
Susan Ferguson stated that the basal ganglia system and the striatum are thought to create positive
and negative

Research Paper On Parkinson's Disease
Parkinson's disease (PD) is a chronic, progressive neurodegenerative disorder affecting
approximately 1% of the population over age 60 [1]. It is the second most common
neurodegenerative disorder after Alzheimer's disease and is predicted to increase in prevalence as
the population ages, imposing a social and economic burden on society [2]. PD is classically
characterized by a loss of mesencephalic dopaminergic neurons and the development of Lewy
Bodies within the substantia nigra pars compacta (SNpc) [3]. Neurons originating in the SNpc
project to the striatum where they activate D1 or D2 receptors to stimulate the direct or indirect
pathway of the basal ganglia, respectively. Activation of the direct pathway by dopamine (DA)
results in

Basal Ganglia Model
The term "basal ganglia" describes a band of subcortical nuclei that is made up of two different
input structures known as the striatum and the subthalamic nucleus. Its role is associated with
behavioral, emotional, executive, and learning motor control, which includes cognition, and is
embedded deep within the brain hemisphere. The striatum and the subthalamic nucleus are able to
be further divided into subdivisions in accordance to cortical connectivity. The classical basal
ganglia model demonstrates the transfer of information to the cortex by the use of two pathways
with opposing effects that mediate motor movement. This model is utilized to demonstrate,
compare, and contrast the transfer of information from a healthy person to that of ... Show more
content on Helpwriting.net ...
Locomotion is essential to human existence and every animal, and it is something that you decide to
do like moving, without really having to think about it. When it comes to movement there are two
pathways that occur: the indirect basal ganglia pathway and the direct basal ganglia pathway. The
basal ganglion is responsible for movement by using a variety of signals. When a person moves, the
frontal lobes send a signal through the glutamate neurotransmitters which end up in the striatum.
The excitatory signal ends up in those neurons which converts the signal from excitatory to
inhibitory and leads to the globus pallidus internus and the substantia nigra pars reticulata. The GPi
and the SNr to do not inhibit the thalamus; the thalamus is where the function rests. Instead, it sends
messages to the cortex allowing for the movement that is desired to occur. The motor cortex finally
sends that processed message to the spinal cord where activation of the movement becomes active.
Dopamine is said to initiate the striatum and in turn inhibits the globus pallidus. The thalamus
stimulates the cortex because the GPi does not inhibit the thalamus. In the indirect basal ganglia
pathway, inhibitory signals are sent through the neurotransmitter GABA to the external portion of
the GP which differs from the direct pathway because in the direct pathway the signal is sent to the
internal segment of the GP. The internal GP sends the inhibitory signals to the thalamus and the
motor cortex no longer sends excitatory signals. Therefore, there is no signal sent to the spinal cord
and a decrease in movement occurs. Dopamine, in the indirect pathway, binds to D2 receptors unlike
the D1 receptors in the direct pathway in the striatum. The external GP does not have the burden of
receiving inhibitory messages, so it suppresses excitatory signals and this causes less inhibition of
the thalamus,

The Teenage Brain In Shakespeare's Romeo And Juliet
"It's important to remember that even though their brains are learning at peak efficiency, much else
is inefficient, including attention, self–discipline, task completion, and emotions. So the mantra 'one
thing at a time' is useful to repeat to yourself. Try not to overwhelm your teenagers with
instructions." ― Frances E. Jensen. Noting that teens are in the process of having a fully mature and
self–disciplined brain, there is always a step by step procedure that leads to the right path. No matter
how dangerous the situation is, teenagers do almost anything from jumping off of rooftops to under
age drinking and smoking. However, on this account, the teenage brain is very confident about
learning new things. During the teenage years, it is best ... Show more content on Helpwriting.net ...
Because of this, It seeks out rewards through immediate gratification, impulsivity, and risk–taking.
For example, In the play Romeo and Juliet, Romeo begins to love Juliet so much that he hides in the
bushes and sees what Juliet does. After Juliet finds out Romeo had been watching her, Romeo says
"I have night's cloak to hide me from their eyes; And but thou love me, let them find me here. My
life were better ended by their hate than death proroguéd, wanting of thy love" (2.2.75). From this
excerpt, one can acknowledge that Romeo is risking his life to get Juliet to love him. Romeo loves
Juliet so much that he explains that he has Juliet as a shield to protect him from death. Romeo also
would rather die with the Capulets hate between the Montague feud than the wanting of his love
between Juliet. This implies that the high pleasure and risk Romeo is taking proves how the
adolescent brain seeks out rewards. Additionally, Romeo also adds more impulsivity to his feelings
and thought with being with Juliet. For instance, Romeo says to Juliet that "Lady, by yonder blesséd
moon I vow, that tips with silver all these fruit–tree tops" (2.2.109). From this excerpt, it can reveal
how the satisfaction Romeo has by swearing to the moon for Juliet can have a sudden seeking
reward. However, even though Romeo's words of swearing might seem positive, to Juliet it is
contrasting that the moon is inconstant because of its monthly orbit in a circle. This makes Romeo
concede to make Juliet forgive him and that he shall never swear to the moon again. Mindless
thoughts that Romeo had made led to an outrage of how swearing to a specific thing isn't always the
right decision and at times can be disturbing or harmful to someone or something. Moreover,
"Insight into the Teenage Brain", a TED Talk by Adriana Galván states in the striatum that "So when
you receive something that you think is rewarding, your striatum is very responsive and it

Technology And Cancer
Many people have asked if technology affects people's bodies in negative ways, and many studies
have researched this question. It turns out that thousands of studies have discovered that too much
screen time and using too much technology is directly linked to multiple diseases and even cancer.
Many of these diseases are fatal and cause major damage to your body, if we don't limit our use of
technology we could all contract these terrible diseases.
One of multiple causes of anxiety and depression other than trauma, stress, genetics, etc, is actually
proven to be cell phones, but not only are cell phones proven to cause anxiety, depression,
moodiness, and short attention spans, it can also cause brain damage (Dunckley). Although some
screen ... Show more content on Helpwriting.net ...
The type of radiation cell phones give off is called radio frequency (RF) radiation. This radiation can
go through your body and cause major damage to your tissues and cells. In fact, the World Health
Organization (WHO) even classified this type of radiation as a possible 2B carcinogen (Burrell).
There are also thousands of studies saying cell phones cause cancer, one study is the Interphone
Study, this study concluded that "regular use of a cell phone by adults can significantly increase the
risk of gilomas by 40% with 1640 hours or more of use" (Burrell). This equals out to about 30
minutes per day for ten years. Another study done by the Hardell Research Group concluded that
using cell phones gives you an increased risk of developing gilomas or acoustic neuromas (Burrell).
Another study done in the UK in 2013 studied 790,000 women and found that women using cell
phones at least 10 hours a day are 2 1/2 times more likely to acquire an acoustic neuroma (Burrell).
In the 1990s, at the University of Washington, Professor Lai linked cell phone radiation exposure
directly to single–stranded DNA breaks. "This is important because, micronuclei proliferation
indicates a type of DNA damage strongly associated with cancer" (Burrell). Not only can cell
phones give you two different types of deadly brain tumors, but it can also give you eye cancer,
lymph node cancer, breast cancer, thyroid cancer, stem cell cancer, leukemia, paratoid malignant
tumors, cancer of the pituitary gland, melanomas, and it can damage your DNA, which in turn can
lead to cancer (Burrell). To conclude, major damage can be done to your brain and whole body if
too much time is spent

What Are Huntington's Disease?
It is estimated that approximately one in every four American adults suffer from a mental disorder
today. Within this subset of Americans, about six percent experience serious disabilities from their
mental disorder. One of the more devastating mental disorders today is known as Huntington's
disease (Huntington's chorea). Huntington's largely affects people of European ancestry the most, an
estimated three to seven out of every 100,000 of this decent suffer from it. Named after George
Huntington who first characterized the effects of adult onset Huntington's at the age of 22. In 1872,
in the newspaper The Medical and Surgical Reporter, he described a disease that exhibited; loss of
motor control, altered personality and a decline in cognitive ... Show more content on
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The exact answer to this question has yet to be discovered, but steps to explain why it affects the
brain have been made. The Huntingtin protein (HTT) is known to be a necessary protein for
development and is found throughout the whole body. However, it only kills the selective nerve
cells; this suggest that the HTT protein only interacts with proteins associated with the brain.
Various experiments revealed that HTT protein interacts with two other proteins (HIP–1 and HAP–
1) which are both only present in the brain. This could explain how the HTT only affects the

Pramipexole Research Paper
Pramipexole is a medication indicated for treating Parkinson's disease and restless legs syndrome
(RLS). It is also used in treatment for cluster headache or to counteract the problems with low libido
experienced by some users of SSRI antidepressant drugs. Pramipexole has shown robust effects on
pilot studies in bipolar disorder. Pramipexole is classified as a non–ergoline dopamine agonist.
Chemical name: (S)–N6–Propyl–4,5,6,7–tetrahydrobenzo[d]thiazole–2,6–diamine dihydrochloride
Molecular formula : C10H19Cl2N3S Molecular weight : 284.243 g/mol Solubility : Freely soluble
in water Colour : white to yellowish white Protein binding : 15% Half life : 8 hours Dose : 0.125,
0.25, 0.5, 0.75, 1, 1.5, 3 and 4 mg. Phrmacodynamics: Pramipexole is a nonergot dopamine agonist
with high relative in vitro specificity and full intrinsic activity at the D2 subfamily of dopamine
receptors, binding with higher affinity to D3 than to D2 or D4 receptor subtypes. The relevance of
D3 receptor binding in Parkinson's disease is unknown. The precise mechanism of action of
Pramipexole as a treatment for Parkinson's disease is unknown, although it is believed to be related
to its ability to stimulate dopamine receptors in the striatum. This conclusion is supported by
electrophysiologic studies in animals that have demonstrated that Pramipexole ... Show more
Urinary excretion is the major route of pramipexole elimination, with 90% of a pramipexole dose
recovered in urine, almost all as unchanged drug. Nonrenal routes may contribute to a small extent
to pramipexole elimination, although no metabolites have been identified in plasma or urine. The
renal clearance of pramipexole is approximately 400 mL/min (CV=25%), approximately three times
higher than the glomerular filtration rate. Thus, pramipexole is secreted by the renal tubules,
probably by the organic cation transport

Synthesis Of Basal Ganglia
In terms of motor control, the basal ganglia is composed of interconnected nuclei located in the
telencephalon, diencephalon, and midbrain which include the striatum, globus pallidus (GP),
entopeduncular nucleus (globus pallidus internal in humans), subthalamic nucleus, and the
substantia nigra (figure1) (6,8). Although there are multiple structures that partake in the modulation
of movement, the basal ganglia serves to integrate information deriving from the parietal, frontal,
and temporal cortex. In particular, electrical stimulation from the cortex to the striatum derive from
regions implicated in the planning and execution of motor movement (6). All of this information
converges and activates GABAergic medium spiny neurons (9). Of note, ... Show more content on
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It has been demonstrated that altered activity of pallidal neurons evoke irregular signaling patterns
of dopaminergic neurons, which in turn may cause a shift in signaling rates to the stiatum and its
activating role of the indirect pathway (7). Interestingly, axonal collaterals from the substantia nigra
pars compacta also provide innervation to the globus pallidus through dopaminergic signaling
(5,1,13). The literature suggests that activation of dopamionergic receptors in the globus pallidus
play an important regulatory role of GABAergic activity. Therefore, stimulation of dopaminergic
receptors is also involved in the modulation of pallidal firing. The depletion of dopaminergic
stimulation in the pallidus suggests a potential role in PD motor deficits and correlation with
symptoms such as tremors and dyskenisia (1,2) .Interestingly, experiments conducted in non–human
primates have demonstrated that a decrease in dopaminergic inputs to the globus pallidus, due to
degeneration of dopaminergic neurons in the substantia nigra pars compacta, triggered irregular
firing patterns (1,4); however, the precise role of these dopaminergic projections that cross and
directly innervate the GP in parkinsonian physiopathology is not clear

Understanding Huntington's Disease Essay
Understanding Huntington's Disease
Diagnosis of Huntington's Disease
Today, a blood test is available to diagnose a person displaying suspected Huntington's symptoms.
The test analyzes DNA in the blood sample and counts the number of times the genetic code for the
mutated Huntington's gene is repeated. Individuals with Huntington's Disease usually have 40 or
more such "repeats;" those without it, 28 or fewer. If the number of repeats falls somewhere in
between then more extensive neurological and diagnostic testing are called for. Tests of the patients
hearing, eye movements, strength, feeling, reflexes, balance, movement and mental condition will
follow. The patient may also be asked about any recent intellectual or emotional ... Show more
Most often, symptoms begin between the ages of 35 and 50, although onset may occur at any time
from childhood to old age. Research continues to progress rapidly, but up to this point no cure has
been found.
Huntington's disease is inherited in an autosomal dominant fashion. The child of an affected parent
has a 50% chance of inheriting the disease. The discovery of the HD gene in 1993 has made it
possible to test at–risk individuals for Huntington's disease before symptoms occur.
Clinical Features
The clinical features of Huntington's disease can be thought of as a triad of emotional, cognitive and
motor disturbances. Symptoms include chorea (dance–like involuntary movements), clumsiness,
slurred speech, depression, irritability, and apathy. Cognitive losses may include attention,
intellectual speed, and short–term memory.
Huntington's disease affects people in different ways. One member of a family may have more
trouble with clumsiness while another may have emotional outbursts. Moreover, symptoms of
Huntington's disease in the same individual change over time.
Neuropathology
Huntington's disease is characterized by atrophy of the caudate nucleus and putamen. There are two
populations of GABAergic striatal efferent neurons that are involved and this is evident based on

their projection targets and neuropeptide content. In the very early stages of the disease there is a
major loss of

Pallidal Striatal Pathway
Proposal – Part A
Organize your proposal using this outline. Use 1.5 line spacing and the reference style appropriate
for the area of study.
I. Background Research
Understanding what others have done in the field is essential to pursuing an inquiry question. Write
a coherent and credible narrative in response to the question: "What do you and others know that
academically grounds and supports your proposal?" Develop your research both in terms of the
broader topic area and with sources more specific to your focusing question. Draw from appropriate,
credible sources, using a minimum of five. You may include a brief paragraph about your personal
interest in this investigation and what led you to it. It is expected that the length of this section ...
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al) is the process used to detect antigens, like proteins, in cells inside the brain in our case. Staining
is helpful in our experiment so that we can trace the rabies virus. Through this method,
monosynaptically connected cells can now be labeled without much effort. This helps us better see
which parvalbumin (PV) cells are infected by the virus. PV is one of the best striatal GABAergic
interneurons (Tepper, Koós, & Wilson). In our experiment we stain with Red Fluorescent Proteins
(RFPs) (Shen, Lai, & Campbell) because of their lower photo toxicity, auto fluorescence, and can go
into deeper tissue. This allows us to more clearly see which cells were at

Dopaminergic Observation
Though it is believed that the loss of dopaminergic innervation is the cardinal neurotransmitter
system involving in PD, other systems of innervation such as serotonergic, cholinergic and
glutamatergic innervations are also involved in the pathogenesis of PD16. The serotonergic
transmission is thought to be heavily affected due to the non–physiological administration of L–
DOPA during the treatment of PD17.After exogenous administration of L–DOPA, it is meant to be
converted by the nigrostriatal dopaminergic neurons that contain a large amount of DA converting
decarboxylase enzyme. However, as dopaminergic neurons are heavilydenervatedin PD, 5–HT
neurons are then primarily responsible for the conversion and the release of DA after the
exogenously ... Show more content on Helpwriting.net ...
Dampening serotonergic activity with 5–HT1A can prevent the exocytotic release of dopamine from
serotonergic terminals17,26.Though it is thought that DA is released from serotonergic innervations
from all the brain areas including the hippocampus, prefrontal cortex, substantia nigraand striatum,
the striatum is believed to be responsible for LID because of the source of the major release of DA
from L–DOPA from the abundant serotonergic innervation24,25.Therefore, my proposal includes
reducing dysregulated serotonergic activity specifically in the striatum with local striatal
administration of 5–HT1A agonist in a PD mouse model. Whereas most of the other studies focus
on treating dyskinesia with 5–HT1A agonist when LID is already developed in PD17,20,my
research proposal will target on the prevention of dyskinesia while giving a L–DOPA treatment for
PD. For this purpose, I hypothesize that co–administration of a specific5–HT1Aagonist with L–
DOPA may reduce the dysregulation of dopamine and could potentially produce the effectsof L–
DOPA treatment for PD without the appearance of

Huntington's Disease Study
Huntington's disease, or HD, is a genetic neuro–generative condition that is characterized by
progressive dysfunction in motor, cognitive and behavioral abilities. There are about 4–10 cases per
100,000 throughout the world, which makes it one of the most prevalent genetic neuro–generative
disorders. Huntington's disease is a dominant gene mutation that occurs in the huntingtin gene. The
result is an excessive repeat of the nucleotide triad cytosine–adenine–guanine (CAG) and causes
damage to neurons. The striatum of the brain and the cerebral cortex are most affected by the gene
but other parts of the brain atrophy as well. Typically, onset begins around the 4th decade of life
although an early onset form can occur before the age of 20. ... Show more content on
Helpwriting.net ...
compared the metabolic profiles of pre–manifest, manifest HD and control groups. The results
showed that amylin and ghrelin levels were significantly increased in all HD subjects compared to
the control group. The increase in ghrelin, an appetite stimulant, and amylin, an appetite
suppressant, demonstrates the numerous abnormalities regarding regulation of food ingestion and
absorption (Wang et al., 2014).
Another abnormality observed was a significant decrease in glucagon in the manifest HD group
compared to the control group. Glucagon plays a major role in upholding normal metabolism in the
body. It also acts as a protective agent by reducing the neurotoxic glutamate. Therefore, a decrease
in glucagon can play a significant part in the pathogenesis of Huntington's disease (Wang et al.,
2014).
Adiponectin is a hormone that is released from adipose tissue and is negatively correlated with Body
Mass Index. In HD subjects, this correlation was not significant. Decreased adiponectin levels is
usually linked with obesity and insulin resistance. These changes suggest that irregular adipocyte
function is associated with the metabolic changes in the pathophysiology of Huntington's disease.
Prolactin and total cholesterol levels were also decreased in all HD subjects and showed erratic
levels of leptin. This is likely due to impaired food digestion and absorption, which is also supported
by the increased amylin levels. Essentially, the study's findings show that HD patients have a
decreased ability to maintain metabolic homeostasis and abnormal hormone levels (Wang et al.,

The Brain, The Hippocampus And The Striatum ( Jacobsen &...
There are two essential learning sections in the brain, the hippocampus and the striatum (Jacobsen &
Forste, 2011). Focused learners are individuals who pay full attention in class and are not easily
distracted by their mobile devices. These individuals utilize the hippocampus which is typically the
heart of the memory and the learning center of the brain. These students have the ability of thinking
in high level scenarios and typically end up with higher paying jobs than those that are categorized
as multitaskers (Jacobsen & Forste, 2011). Multitaskers are those that do two or three things at once
and are therefore not focusing on getting one task accomplished (Boyd, 2014). Such students use the
area of the brain known as the striatum. This manner of learning is not an adverse learning
approach; however, this area of the brain is for learning habits. Multitasking is usually right for
those that want to work on assembly lines. Students that graduate with degrees typically aim for
high paying jobs and in order to achieve this they must shut down their laptops and phones and pay
attention in their classes. A startling fact is just how dependent and almost fixated college students
are when it comes to accessing the internet. A few studies such as that of Jacobsen & Forste, (2011)
have highlighted that most students consider the Internet as fundamental as food, shelter, water and
air. These thoughts are highly astonishing. Most of these students find that the internet is more

Essay on Parkinson’s Disease
Parkinson's Disease
Parkinson's disease is a disease with a wide variety of disabilities recognizable as changes in
appearance, posture, walking, and balance. In 1817, the English physician James Parkinson
described these symptoms in his patients and has had his name become synonymous with the
disease. In 1893 the substantia nigra of the basal ganglia was identified as an area of disease for
Parkinson's. Examination with the naked eye reveals a lack of black pigment in this portion of the
brainstem. Subsequent follow up with the microscope showed a deterioration of the nerve cells in
this area. The circuitous relationship between the substantia nigra and the basal ganglia explains
many of the symptoms of Parkinson's disease. Today the ... Show more content on Helpwriting.net
...
Consequently, both the basal ganglia and the cerebellum are influenced by and return influence to
the descending motor pathways (pyramidal and extrapyramidal), which affect the activity of the
lower motoneurons.
The substantia nigra is a subcortical nucleus that is closely related to basal ganglia. It is reciprocally
connected with the striatum and sends efferents to the ventral anterior and dorsomedial thalamic
nuclei and, to some extent, to the ventral lateral thalamic nuclei. The substantia nigra pars reticulata
also projects to the superior colliculus. Neurons that originate in the striatum and project to the
substantia nigra are inhibitory and utilize the neurotransmitters GABA and substance P. Fibers that
arise in the pars compacta of the substantia nigra use the neurotransmitter dopamine and synapse in
the striatum, while GABAminergic cells in the pars reticulata receive striatal input and project to the
thalamus.
Recordings from neurons in the basal ganglia of monkeys during various motor tasks reveal that the
discharge of single cells in the neostriatum show a direct correlation with movements of the
contralateral arm or leg, and that the discharge of substantial percentage of neurons precedes the
onset of a movement. These studies suggest that the basal ganglia participate in movements at a high
level, including the planning of movement synergy's. Lesions of the basal ganglia resulting from
disease in humans cause: disorders of the

Parkinson 's Disease And The Disease Of The Nervous System
Definition: "Parkinson's disease is a chronic, progressive disease of the nervous system
characterized by the cardinal features of rigidity, bradykinesia, tremor, and postural instability"
(O'Sullivan and Schmitz, 2007). The condition can develop between age group 60 and 80 years and
symptoms mostly appear around 60 years of age (O'Sullivan and Schmitz, 2007).
Parkinson's disease or PD is classified into idiopathic Parkinson's disease, parkinsonism due to
identifiable causes and parkinsonism in other neurodegenerative disorders. True Parkinson disease is
classified into two subclinical groups. One group demonstrates postural instability and gait
disturbances as dominant symptoms whereas the other group exhibits tremor as the prominent
feature (O'Sullivan and Schmitz, 2007).
Pathophysiology:
Parkinson's disease is affected by the degeneration of dopaminergic neurons which is responsible to
produce dopamine. Dopaminergic neurons have their cell bodies in substantia nigra pars compacta
(SNpc) in basal ganglia (O'Sullivan and Schmitz, 2007). Basal ganglia are a collection of
interconnected gray matter nuclear masses deep within the brain". These gray matter masses are
caudate, putamen, globus pallidus, subthalamic nucleus and the substantia nigra. Basal ganglia
receive its input through striatum (O'Sullivan and Schmitz, 2007).
Clinical Presentation:
1. Rigidity: Rigidity is defined as increased resistance to passive movement. Parkinson patients
complain of "heaviness" or

Tourette Syndrome Case Study
Ashley Batra Neurology 699
May 16, 2018
How does dysfunction in the cortico–striato–thalamic circuit contribute to the pathophysiology of
Tourette syndrome?
Tourette syndrome (TS) is a neuropsychiatric disorder involving motor and vocal tics. Typical onset
occurs around 5–7 years and it is associated with comorbid conditions such as OCD or ADHD.
There is evidence that TS is an inherited disorder as shown in familial and twin studies, but the exact
genetic pathology or etiology is still unknown. The neurobiology of TS appears to be involved in
cortico–striatal–thalamo cortical (CSTC) circuits, which connect parts of the frontal cortex to
subcortical structures. Tics are caused by focal excitatory abnormalities in the striatum that lead to
inhibition ... Show more content on Helpwriting.net ...
There were no differences in glial cells in terms of number, density, or morphology, nor were there
differences in the volume of the GPe or GPi. For TS patients, the density of PV+ cells was greater
by 122% in the GPi while a lower density of PV+ cells were found in all other components of the
basal ganglia, most notably the caudate, with a 51% reduction (Kalanithi et al, 2005). The total
number of PV+ cells was 31% smaller in the GPe, and 129% greater in the GPi of TS patients. In
the caudate and putamen, the number of PV+ neurons were 54% and 40% fewer

Food Rewards
The OFC function has been implicated in the devaluation of food rewards by satiety (Gremel and
Costa, 2013). It has been implicated in various cue related behaviors modulated by changes in
expected value. Furthermore, the OFC neurons hold value based information 'online' to guide future
decision–making and therefore estimate the likelihood of specific outcomes to guide future
responses (Wilson et al, 2014). Given that the OFC receives significant sensory information, the
OFC likely integrates signals about sensory properties with expected outcomes (Thompson et al,
2017). Thus, the OFC registers the current value of foods and updates actions based on this
information. However, several studies have indicated that obese humans and rats fed a ... Show
Studies show that an inability to shift between habits and goal directed actions (break habits) might
underlie distorted behaviours observed in obsessive–compulsive disorder addiction, and other
decision–making disorders. Goal directed and habitual actions are controlled by different parts of
the striatum, which lies posterior to the orbitofrontal cortex (Figure 1). Through lever pressing
experiments done on mice, it has been determined that the dorsal medial striatum (DMS) is
necessary for goal directed actions (Thompson et al, 2017), while the dorsal lateral striatum (DLS)
is necessary for habitual actions. The OFC modulate medial striatum through direct projections and
indirectly through connexions with striatal projecting cortical areas, basolateral amygdala and
ventral tegmental/substantia nigra. Through lesions of the lateral OFC, which did not affect
neighbouring cortices, it has been discovered that mice do not reduce lever pressing following
outcome revaluation. Conversely, Sham mice, which are mice used as a control through fake
surgical intervention, shifted between habitual and goal directed actions. OFC lesioned mice showed
intact habitual actions but disrupted goal directed actions. This suggests that the OFC is critical in
modifying outcome value, and that obese mice may have similar disruptions in the OFC, causing
them to eat in a habit–like fashion. Overall, it seems that the execution of daily life tasks, such as
transitioning between goal

The Effects Of Gambling On The Brain
Gambling and the Effects on the Brain
Gambling is the act of risking an object of personal value, usually money, for the chance of winning
a greater reward. A gambling disorder, previously known as pathological gambling, is when
gambling begins to take over all aspects of life affecting relationships, and work. The category that a
gambling disorder should be classified under in the Diagnostic and Statistical Manual of Mental
Disorders, Fifth edition (DSM–5) has been debated. Gambling disorder previously was classified as
an Impulse Control Disorder, but in the new edition, DSM–5, it is classified as a Substance–Related
and Addictive Disorder (Clark, 2014). The reason for debate on the topic was because of the
characteristics of the disorder, ... Show more content on Helpwriting.net ...
Of the people that use dopamine agonist medication for Parkinson's disease, 4.4% reported that
gambling became a problem for them after using the medication (Grosset et al., 2006). Some of the
respondents initially did not admit to having a gambling problem, but later did admit to the problem,
which indicates the results possibly are underestimated at 4.4% (Grosset et al., 2006). At 4.4%, the
statistic is relatively high and should be explained to patients using a dopamine agonist as their
medication to try to decrease the chances of developing a gambling disorder. The study noted
patients who had a gambling disorder normally were on a higher dosage of the dopamine agonist,
but patients on lower doses also reported developing gambling problems (Grosset et al., 2006).
Another disorder in which patients may use dopamine agonist medication is for restless legs
syndrome (RLS). RLS patients are also at a higher risk for developing a gambling disorder (Stone,
2007). Three patients at the Mayo Clinic Sleep Disorders Centers reported having a gambling
disorder after approximately nine months of using the medication. With increased amounts of
medication, the gambling problem got worse (Stone,

Suffering With Food Poisoning Caused By Salmonella Sp Essay
Scenario C
The patient in this scenario C was suffering with food poisoning caused by Salmonella sp.
Non–typhoid Salmonella sp. causes inflammation of the digestive tract (enterocolitis). Common
symptoms such as abdominal pain, fever, myalgia and watery non–bloody diarrhoea usually appear
between 8 and 72 h after the ingestion of a pathogen (D 'Aoust, 1994). Human salmonellosis is self–
limiting infection, nevertheless patients are advised to replace fluid and electrolytes (D 'Aoust,
1994). Sometimes the progression of enterocolitis into local infections via blood stream can occur
(D 'Aoust, 1994; D 'Aoust, 1991).
The infection process is very complex due to numerous virulent factors of the pathogen. In order to
enter the small intestine a bacterium must first overcome the antimicrobial activity of saliva enzyme,
lactoperoxidase and the low pH of digestive fluid in the (D 'Aoust, 1991). Cytotoxin present on the
bacterial cell wall disturb membrane integrity of the host cells which contribute to bacterium
attachment and to cell invasion (D 'Aoust, 1991). Salmonella attaches itself to the intestinal
epithelial cells by fimbriae. Pathogens enter epithelial cells by membrane–bound vesicle, this
process is known as bacteria–mediated endocytosis (D 'Aoust, 1991). Bacterium then divide and
invade mucosa layer. Diarrheagenic enterotoxin is released in the intestinal lumen and into the
lumen of epithelial cells. Effect of enterotoxin and local inflammation cause water and

The Effects Of Caffeine On Oxidative Stress
In the present study, the MDA level was measured as an index of lipid peroxidation in order to
observe the effect of caffeine on the oxidative stress induced by AlCl3 in cortex, hippocampus and
striatum brain areas. Brain tissues are more vulnerable to oxidative stress other than tissues for many
reasons such as high oxygen consumption (more than 20% of the total inspired oxygen), the
presence of abundant amount of polyunsaturated fatty acids which are susceptible to free radicals
attack, low antioxidant levels, high iron content in addition to the non–regenerative nature of
neurons (Nehru and Anand, 2005; Kim et al., 2015). All these reasons may explain why brain is
more susceptible to aluminum toxicity than other organs. In the present ... Show more content on
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The present results showed that daily protection with caffeine attenuated the increase in MDA levels
in AlCl3–intoxicated rats. Supporting the present finding, previous studies have revealed the
antioxidant potential of caffeine against lipid peroxidation in various animal models of neurologic
diseases, including Alzheimer's disease (Prasanthi et al., 2010), epilepsy (Souza et al., 2013) and
Parkinson's disease (Khadrawy et al., 2017). It has been demonstrated that caffeine has the ability to
scavenge reactive oxygen species (Devasagayam et al., 1996) and modulated the brain antioxidant
system through increasing the content of GSH and activities of antioxidant enzymes like glutathione
reductase and superoxide dismutase (Abreu et al., 2011). Generally, the antioxidant capacity of
caffeine was similar to that of the established biological antioxidant GSH and significantly higher
than ascorbic acid (Devasagayam et al., 1996). Accordingly, this may explain the ability of caffeine
to attenuate lipid peroxidation induced by AlCl3 in the current study via direct scavenging of
reactive oxygen species or by increasing GSH content and antioxidant enzymes activities.
The present data revealed that daily oral administration of AlCl3 resulted in a significant increase in
NO levels in the cortex, hippocampus and striatum. NO is the smallest signalling molecule within

Autism Spectrum Disorder Essay
Introduction Autism spectrum disorders Autism Spectrum Disorders (ASDs) are a collection of
heterogeneous disorders that share the characteristics of social and communicative deficits, highly
focused and restricted interests, and repetitive behaviors (American Psychiatric Association, 2013).
The estimated prevalence of the disorder in 2014 was 1 in 45 (2.24%) children and adolescents age
3 to 17 (Zablotsky et al., 2015). Behavioral symptoms typically become evident in the first 2 years
of life and involve abnormalities in language development, social attention, and emotional reactivity
(Landa & Garret–Mayer, 2006; Dawson et al., 2004). The symptoms of this disorder often have a
negative impact on the quality of life of the individual, ... Show more content on Helpwriting.net ...
The overfunctioning of primary perceptual regions may explain this atypical perceptual processing.
We also see of enhanced feedforward, but reduced feedback connectivity in ASD, based on MEG
findings. One study found a locally generated cortical response in the primary motor cortex (S1) and
secondary somatosensory cortex (S2) to be reduced in adolescents with ASD. Feedforward
functional connectivity between S1 and S2 was also investigated, which was increased in the ASD
group. This study also reported significantly reduced mu–β rhythm, a measure associated feedback
connectivity (Khan et al., 2015b). Functional studies have found that activity from sensorimotor
tasks 'invade' association cortices (Müller et al., 2004; Müller et al., 2003), and overconnectivity
between sensorimotor cortices and supramodal cortices (Carper et al., 2015). This developmental
hypothesis is yet to be tested between the basal ganglia and the cerebral cortex, and could likely lend
insight to the symptoms we see in the ASDs. Striatum Anatomy, function, and connections of the
striatum The striatum works in conjunction with the cortex to execute and control motor functions
(Raz et al., 1995). The striatum is also crucial to higher order functioning, such as action planning,
decision making, motivation and reward perception (Hollander et al., 2005). This structure has been
associated with symptomatic behaviors in a number of other disorders, including

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