Wearing on Her Nerves: Exploring the Interrelation between the Nervous and

Muscular Systems
May 2, 2018
Faryal Ahmad, ​Amanda Floyd, Amber McCool, Allison Werner, Natalie Williams
Heritage High School
Anatomy and Physiology Honors
B. Beauman
 1. What components of the nervous system are involved in physical sensation?
How does sensory impulse move throughout the body? (Allison)
The nervous system is divided into two main categories, the Central Nervous
System and the Peripheral Nervous System. The word Peripheral means “beyond the
brain and spinal cord” (Anatomy and Physiology N.D). The central nervous system is
composed the spinal cord and the brain, while the Peripheral Nervous System is
composed of all the nerves that expand from the Central Nervous System into the
limbs and other regions around the body. The Central Nervous System is most
commonly
known as
the main
control
center of
the body’s
nervous
system. The
Peripheral
Nervous
System’s
function is
to allow the
Central
Nervous
System to

communicate with the rest of the body. The Peripheral Nervous System divides into
two parts: the Sensory or Afferent Neurons, and the Motor or Efferent Neurons.
Afferent means conducting information, which is what the Afferent Neuron function is
responsible for, which is to absorb sensory stimulus materials and rushes the
information to the brain or spinal cord. Efferent means to be conducted away from
something, which explains why the Efferent Neuron sends directions from the brain,
located in the Central Nervous System, to the muscles, glands, and organs that are in
your body picking up the sensory material. The Motor or Efferent Neuron function is
divided into the Somatic Nervous System and Autonomic Nervous Systems. The
Somatic Nervous System is also known as the voluntary nervous system because it
controls the movement of muscles and the skeleton. The Autonomic Nervous System
is also known as the involuntary nervous system because it controls parts of the body
with having to think about doing the action. Some examples of the Autonomic
Nervous System is keeping the heart beating, lungs breathing and keeping the stomach
breaking down nourishment (Crash Course 2015).

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 The Autonomic Nervous
System is separated into
two divisions: Sympathetic
Division and the
Parasympathetic Division.
The Sympathetic Nervous
System fires up the nervous
system during a fight or
flight situation. Pupils
dilate to open clear vision,
heartbeats accelerate to
keep blood, which has
oxygen, pumping to the
muscles, halts digestion,
and stimulates glucose
release by the from liver to
produce immediate energy.
The Parasympathetic
Nervous System is used to
calm the body by
contracting pupils, slowing
heart rate, stimulating
digestion, and contracts the
bladder which is the
opposite of the Sympathetic
Nervous System (Crash
Course 2015).
The Nervous System is
made up nervous tissue
which is a densely packed
with cells and 20% of that tissue has extracellular space. Extracellular space is the
space between cells.
Neurons are cells that transmit nerve impulses to communicate with the body
to move or stop moving. Each part of the neuron does a different and special job for
communication in the body.
An axon is a nerve fiber
that is able to rapidly
conduct nerve impulses
away from the neuron cell
body to communicate with
other cells. A dendrite is a
lengthy extension of a
neuron that carries

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electrical signals and information from cells. Myelin Sheath is a fatty (lipids) covering
that forms a protective sheath around nerve fibers and accelerates the transmission of
nerve signals. An axon terminal is an area at the end of an axon that contains
neurotransmitters (PubMed Health N.D). A soma is the cell body that contains the
nucleus. The node of Ranvier is a periodic gap in the insulating sheath (myelin) on the
axon of certain neurons that serves to facilitate the rapid conduction of nerve impulses.
A Schwann cell is any cells in the peripheral nervous system that produce the myelin
sheath around neuronal axons (Britannica N.D).
Neurons vary in shape depending on their function and the location of the
neuron. 99% of the neurons in the body are multipolar neurons that have three or more
processes, which is one axon with many dendrites, that is sticking out from the soma
(Crash Course 2015). Bipolar neurons have two processes with an axon and many
dendrites on both sides of the soma. Unipolar neurons have one process and they make
up the sensory
receptors. Motor
neurons, which
are efferent
neurons that
impulses move
from the Central
Nervous System
to the rest of the
body, is made of
multipolar
neurons.
Interneurons, or
association
neurons that are
the impulses that
occur between
the sensory
neurons and motor neurons. Sensory Neurons, afferent neurons, are the neurons that
transport impulses from the sensory receptors towards the Central Nervous System.
Due to the unipolar sensory receptor neurons on the skin, they would detect a
stimulus on the skin which would send a signal up to the axon and into the spinal cord.
At the spinal cord, the signal gets transmitted onto several interneurons. Some of the
interneurons will send a signal down a bunch of multipolar neurons to the muscle
where the sensory receptors first detected the signal. The other interneurons will pass
that signal to neurons interpret and split the signal so that you can have a choice of
what you do.

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 2. What components of the nervous system are involved in skeletal muscle
movement? How does motor impulse move throughout the body? What is a
“motor unit”? (Faryal)
The part of the nervous system involved with skeletal muscle movement is the
somatic nervous system which is a part of the peripheral nervous system. This system
is responsible for carrying both motor and sensory information to the central nervous
system which then sends it out
to the rest of the body. It is also
in charge of voluntary muscle
movements which is done
through two major types of
neurons that carry messages to
other parts of the body; sensory
neurons and motor neurons.
Sensory neurons, which are also
known as afferent nerves, carry
stimuli from places such as your
ears or eyes to the brain or spinal
cord where it can be processed.
These type of neurons tell your brain what you are sensing and are activated solely by
sensory input. (Biology Dictionary 2017)
The sensory neurons contain a long dendrite which is used to transmit
messages and receptors to other parts of the body. The dendrites are like long branch
like extensions and they are the first part of the neuron to receive an electrical
message. It is then carried towards the soma, which is also known as the cell body, and
this part of the neuron controls the function of the entire neuron since it contains the
nucleus. The message is then carried to the ends of the axon, where a release of
chemicals occur allowing the message to travel through the synapse. The synapse is a
gap between two neurons that allows one to transfer a chemical message to the other.
This allows these electrical impulses to be transmitted to other parts of the body and
helps in the process of skeletal muscle movement. (Wheeling Jesuit University 1999)
Motor neurons, or efferent nerves, are also a key factor in skeletal muscle
movement, but perform completely opposite functions. Instead of carrying information
to the central nervous system, these neurons carry information from the brain and
spinal cord to muscle fibers
throughout the entire body. They
are located directly in the central
nervous system, where the axon
protrudes out to the muscle fibers
in order to control them. The
normal structure for this type of
neuron contains only one axon,
which is usually long and stretched
out so it can reach the muscle
fibers, and multiple dendrites that

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are thick and branched out. The motor neurons can then be broken down into two main
categories; upper motor neurons and lower motor neurons. (Farabee 1992)
Upper motor neurons are found along a bump on the frontal lobe known as the
precentral gyrus, and their main job is to pass down fibers to the lower motor neurons
to cause movement. This is done by passing its axons
through the corticospinal tract and the corticobulbar tract.
The upper motor neurons travel along the corticobulbar
tract which is a pathway that runs along the cerebral cortex
in the brain. From there on, they synapse with the
corticospinal tract which is where the lower motor neurons
are located, and connect the brain to the spinal cord. Once
the upper motor neurons reach the spinal cord through the
corticospinal tract, they form synapses with the lower motor
neurons and release glutamate which is a neurotransmitter.
This enables the transferral of an action potential necessary
for skeletal movement (Biology Dictionary 2017). At this
point, the lower motor neurons take the fibers they received
from the upper motor neurons and begin to supply muscle
fibers with nerves to cause their contraction. There are three
different types of lower motor neurons that help complete
this job; alpha, beta, and gamma motor neurons. The alpha
motor neurons are the main type of lower motor neurons
that cause movement, and they are the part that receives
signals from the upper motor neurons. Gamma neurons
support the job of the alpha motor neurons by helping keep
the muscle spindles tight and stretched back (Sampson
2017).

A motor unit consists of

only one motor neuron,
more specifically an
alpha motor neuron, and
all of the muscle fibers it
innervates. Groups of
these motor units can
work together to control
the contractions of
different muscles. Large
muscles that require more
energy or are used more
than other muscles, like
the calf, require hundreds
of these motor units to
control them, whereas

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smaller muscles may only require one motor unit. It differs on the power of the
muscle. Motor units can also differentiate due to the types of muscles they innervate.
For example, small motor units usually supply red muscle fibers with nerves, and large
motor units supply the pale muscle fibers with nerves. The small motor units are
known as slow motor units and are important for activities that don’t require very
much energy like keeping your posture straight. The larger motor units are known as
fast fatigable motor units since the activities performed with these muscles can easily
cause you fatigue. These are important for things such as running or exercising
(Purves 2001).

6
 3. What movements are involved in the action of standing up? What muscles
need to contract to perform these actions? (Natalie)
The action of standing up is very complex because a lot of leg and abdominal muscles are
required in order for our body to stand upright. While a human stands, the movements
involved are split into 3 phases: bending forward to stand, pushing up to stand, and
then finally standing up. Throughout the movements, the muscles are given different
titles based off of their involvement in the actions they perform. When muscles
contract they are often in antagonist pairs, which is when one muscle contracts and
another muscle relaxes (GCSE N.D). In antagonistic pairs, there are two titles that
muscles are given based on their involvements in contraction. These two titles are the
agonist, which is the muscle that provides the major force to complete the movement,
and the antagonist, typically relax and oppose the agonist. Outside of the antagonist
pairs, there are muscles that are given other titles based on their involvement in
moving the body parts. These titles include the synergist, the muscle that stabilizes a
joint when movement is occurring, and the fixator, the muscle that stabilizes the origin
and the joint the agonist spans around (Muscle 2016). In order for muscles to perform
any types of movements they must contract, but there are different types of
contractions. These different types of contractions include the concentric, eccentric,
and isometric.

Muscles are able to contract due to thick filaments, made of myosin proteins,
and thin filaments, made of actin proteins. The thick filaments are composed of
myosin molecules arranged in a cylinder and the thin filaments resemble two strands
of pearls twisted around each other. When muscles contract, the thin filaments attach
to the thick filaments as a result they form crossbridges. During this process the thick
filaments pull the thin filaments and slides them across their surface in order to shorten
the sarcomere, the most basic unit of the skeletal muscle that is made up of myofibrils
(Editors 2017). Electric impulses signal muscles to contract by causing the thick and
thin filaments to shorten all of the myofibrils in the sarcomere simultaneously, which
results in the movement of the muscle (Freudenrich 2001). During a movement,
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depending on if the muscle shortens or lengthens while contracting determines what
type of contraction has occurred. Concentric contractions occur when any muscle has
shortened under a load of tension. An example of a concentric contraction occurring
can be seen during the lifting phase of a bicep curl (Nichols 2010). Eccentric
contractions occur when muscles lengthen under load or tension. An example of an
eccentric contraction can be seen during the lowering phase of a bicep curl (Ingraham
2007). Isometric contraction occur when muscles do not lengthen or shorten to
develop tension (Muscle N.D). An example of an isometric contraction can be seen in
a human who is carrying anything because the muscles are not contracting.

8
 In preparing to fully stand up, the muscles must first put the body in a bent
forward position bend the body forward. In this process the body uses 6 muscles in
total, 3 muscles moving forward and 3 muscles moving backward. The 3 muscles that
move forward are the internal oblique, the rectus abdominis, and the
sternocleidomastoid. The 3 muscles that move backward are the trapezius, the
latissimus dorsi, and the external oblique. In this case the internal oblique is the
agonist, because it is the muscle that is performing majority of the force in order to to
move the abdomen of the body to a bent forward position. The trapezius acts as the
antagonist, because it opposes the contraction of the internal oblique in order to keep
and balance the movements of the abdomen. The Latissimus Dorsi acts as the
synergist, because it stabilizes the region of the abdomen that is moving. The rectus
abdominis acts as the fixator, because it stabilizes the region of the abdomen that the
internal oblique spans around (Brucker N.D). The external oblique and the
sternocleidomastoid are not given specific titles but they still contract in order to help
the body stand.

While the body is pushing to stand, the body pushes to stand from the bent
position that was in the previous stage. In this phase 6 muscles are also used, 2
muscles are moving forward and 4 muscles are moving back. The 2 muscles that move
forward are the tibialis anterior and the quadriceps. The 4 muscles moving backward
are the hamstrings, gastrocnemius, soleus, and the latissimus dorsi. The agonist in this
phase is the tibialis anterior, because it provides majority of the force in order to allow
the lower leg to push the rest of the body up from the bent over position. The

9
antagonist is the hamstrings, because it opposes the movement of the tibialis anterior
in order to balance the forces of the legs in order to allow the body to push up. The
gastrocnemius and the soleus muscles act as synergist, because it stabilizes the moving
region of the leg. The latissimus dorsi acts as the fixator, because it stabilizes the
region of the abdomen that the tibialis anterior is spanning around (Brucker N.D). The
quadriceps are not given a specific title. After the body has completed all of these
movements it then proceeds to finally stand.

The body uses 8 muscles in the process of finally standing after it bends
forward and pushes to stand. The 3 muscles that move forward throughout this phase
are the tibialis anterior, quadriceps, and the rectus abdominis. The 5 muscles that move
backward are the gluteus maximus, the hamstrings, the gastrocnemius, the soleus, and
the iliopsoas. In this case the gluteus maximus acts as the agonist, because it is
providing majority of the force to allow the body to stand. The hamstrings act as the
antagonist, because it balances the force produced by the gluteus maximus in order to
allow the body to fully stand. The gastrocnemius and the soleus muscles act as the
synergist, because it stabilizes the moving region of the leg. The tibialis anterior acts
as the fixator, because it stabilizes the region of the leg that the gluteus maximus is
spanning around (Brucker N.D). The quadriceps, the rectus abdominis, and the
iliopsoas are not given specific titles.

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 4. What are the different levels of organization of a muscle down to
myofilaments? What is a “sarcomere” and how are the proteins organized?
(Amber)
Muscles are bundles of fibrous tissue, designed to aid the body in movement as
well as other activities through their ability to contract and expand. Muscles and nerve
fibers together allow the body to maintain its position and allow the body to move.
There are about 320 pairs of identical skeletal muscles that are bilateral, meaning they
can be found on either side of the body (Nordqvist 2017). With three types of muscle:
cardiac, smooth, and skeletal, there are about 650 to 800 muscles in the body, which
make up about 40% of our body mass. The total number of muscles, however, cannot
be precisely determined because of the conflicting opinions of researchers. Each
muscle contains a group of parallel fascicles. This group of fascicles is surrounded by
an elastic tissue known as the epimysium (Klijn 2012). The epimysium is very fibrous
tissue made up of dense irregular connective tissue and fully composes these muscle
fascicles and each individual part of the muscle fascicles that make it up (National
Cancer Institute N.D). The main purpose of the epimysium is to reduce friction
between muscles and serve as a protecting outside layer of the muscle cell. The
epimysium also facilitates muscle tension and movement by creating tendons, without
which people would not be able to move properly. Many of the messages sent
throughout the muscles are sent to the epimysium to release tension as a way of
relieving pain. The messages are targeted to this specific part of the muscle because of
its close proximity to other organs making it a good conductor of this energy
(Encyclopedia of Neuroscience N.D). The endomysium is made of collagen fibers and
also contains capillaries as well as the extracellular fluid and nutrients, supplied
throughout the blood and to the muscle tissue, which are used to support the muscle
fiber. Muscles tend to use an abundance of ATP energy and thus create an abundance
of waste as well, because of this it is very important for each part of the muscle to be
highly vascular in order to get rid of waste and bring in the nutrients necessary to
thrive. The collagen fibers also found in the epimysium as well as many of the other
protective layers are the major protein composed in these layers.
The muscle is composed of tightly packed bundles of muscle fibers that can be
compared to the appearance of a can of vienna sausages in that they are individual
cylindrical muscle cells packaged with little space in between each and you can see the
separation between each sausage (Encyclopedia of Otolaryngology 2013). These
tightly packed groups of muscle fibers are called fascicles. The arrangement of these
fascicles vary depending on the type and function of the muscle. The most common
arrangements of the fascicles are circular, parallel, convergent, and pennate (Wallace,
2005). Circular arrangement, generally seen on muscles named sphincters, is a ring
formation and surround external body openings, closing by contracting. Some
examples of this fascicular arrangement include the muscles that surround the mouth
and eyes, known as orbicularis muscles. The arrangement of fascicles can be
considered parallel when the length of the fascicle runs parallel to the length of the
muscle. From here these parallel fascicles can be broken down further into spindle
shaped or straplike. Spindle shaped parallel fascicles can be found in the biceps brachii
muscle of the arm, while straplike parallel fascicles can be found in the sartorius

11
muscle of the thigh. A convergent arrangement of fascicles are fan or triangle in shape,
with its fascicles converging to a single tendon. An example of a convergent
arrangement of fascicles include the pectoralis major muscle of the anterior thorax.
Lastly, in a pennate arrangement, the fascicles are short in size and attach to a tendon
running through either the midline, which is known as bipennate, one side, which is
known as unipennate, or multiple points of the muscle, which is known as
multipennate (Wallace, 2005).

Fascicles have a connective tissue outer layering similar to the epimysium that
surrounds the entire muscle. This connective tissue layer is called the perimysium. The
perimysium surrounds groups of fascicles and breaks them into bundles which contain
muscle fibers. The perimysium contains collagen, blood vessels, and nerves (Klijn
2012). These maintain blood flow and supply the fascicles with nerves. The
perimysium supplies each fascicle with branches of blood vessels and nerves (Klijn
2012). Fascicles contain individual muscle fibers that make up another portion of the
muscle’s anatomy.
Muscle fibers (or muscle cells) are the basic units of muscle tissue, with the
ability to contract, it makes this part of a muscle extremely important because it allows
for movement as well as the production of force (Klijn 2012). Muscle tissue includes
the three types: skeletal muscle, the muscles responsible for bone movement; smooth
muscle, muscle surrounding organs and is involuntary; and cardiac muscle, the muscle
specifically only found in the heart. These muscle fibers are once again surrounded by
a connective tissue sheath used to protect the fibers as well as hold its components

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together. This loose connective tissue layer of reticular fibers containing capillaries,
nerve fibers, and lymphatics is the endomysium (Krstić). This is not to be confused
with the outer membrane of each muscle fiber named the sarcolemma. The
sarcolemma has generally an alike structure as the plasmalemma, or general cell
membrane, however they are considered transverse as the extensions of the
sarcolemma pass across each muscle fiber from side to side (Klijn 2012). These tunnel
like extensions of the sarcolemma are called T-tubules. T-tubules aid in conducting
stimulus into the cell (Highlands 1992). The endomysium encompases both the muscle
fiber as well as it’s cell membrane, of sarcolemma.
Muscle fibers are multinucleated, meaning they have multiple nuclei and
contain an abundance of myofibrils. Myofibrils are cylindrical structures that extend in
columns that are parallel to each other, along the length of the muscle cell. The
myofibril is further composed of thick and thin myofilaments, which is what causes
muscles to take on a ‘striped’ appearance (Irimia 2013). Thick myofilaments are
composed of myosin, or molecules whose shape and structure of the ‘head’ attach to
the binding sites on the action of the thin filaments which all contributes to the process
of muscle contraction. Thin filaments are composed of actin, a protein important for
contraction; troponin, a protein molecule that reacts with tropomyosin in the thin
filaments to form a
helix structure and
control muscle
contraction.

Myofibrils are
surrounded by the
sarcoplasmic reticulum. The sarcoplasmic reticulum is located in the sarcoplasm
(specialized cytoplasm) of the muscle cell. It is similar to the smooth endoplasmic
reticulum as it is a network of membrane enclosed interconnecting tubules that
retrieves, restores and releases calcium ions. The sarcoplasmic reticulum is responsible
for the uptake of calcium from the sarcoplasm as well as releasing it back into the
sarcoplasm to begin muscle contraction and taking it back during relaxation (Klijn
2012). Myofibrils contain structures called sarcomeres. Sarcomeres are the basic
functioning piece of the muscle cell, making them one of the most important parts.

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 Sarcomeres are the groups of microfilaments and the proteins that they
encompass (myosin, actin, troponin, and tropomyosin). The sarcomere is within the
myofibril and continues along the length of the muscle fiber until it attaches to the
sarcolemma at the end. Sarcomeres are very small and can be observed under the
microscope where it can be seen that they are striated as a result of the thick and thin
filaments as mentioned previously. More specifically, the striations are caused by the
alignment of bands created as a result of the placement of proteins (Klijn 2012). There
are 2 types of bands that the most prominent striations are due to. This includes the A
band, which is a term used to describe the central location and area that the sarcomere
is located, which extends along the full length of the thick filaments. These are dark in
appearance as a result of the protein's' ability to polarize light, making them
anisotropic. This dark appearance along with the light appearance of I bands, as a
result of not being able to polarize light, making them ​isotropic, ​create a striped look
with the contrasted colors (Highlands 1992). The second type of band is the I bands.
The I bands are different than that of the A bands as they describe the area within a
sarcomere. The I bands are the regions between the A bands and the sections of the I
bands only include thin filaments and exclude the adjacent thick filaments and A
bands. Within the A band, there is an H zone. This H zone represents a section of the
sarcomere and is seen as a light strip in the sarcomere midsection. The A bands and I
bands relative to the H zone can give us enough information to determine the state of
contraction or relaxation that the muscle is in (Klijn 2012).

At both ends of a sarcomere are z discs. Z discs separate neighboring

sarcomeres and are plate shaped regions are formed by the proteins at the junctions
between sarcomeres. The thin filaments are connected in a zig zagged structure where
the thinner actin filaments are bound creating a boundary of each sarcomere
(Highlands 1992).

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15
 5. Starting from the release of acetylcholine by the motor neuron, what are the
steps in muscle contraction? How is contraction ended? (Amanda)
The process of acetylcholine release must first begin with the synthesis
of acetylcholine itself, which begins inside of mitochondria of the stoma (the cell
body). (Course and Wang 2016) Inside of the motor neuron, acetylcholine is
synthesized from Acetyl Coenzyme A and Choline, which has the byproduct of
Coenzyme A as well. Coenzyme A (CoA) is a product that is derived from ATP, and
is considered a thiol, which are organic sulfur compounds that are responsible for
allowing connections to acetyl groups. (National Center for Biotechnology
Information, 2018) This process is catalyzed by the process of choline
acetyltransferase, which is an enzyme that removes acetyl groups towards choline
groups, which thus allows for the two compounds to fuse together. To do this, the
acetyl group first binds to the enzyme, thus changing the resulting shape. Then, the
choline group bonds to the resulting shape, thus allowing for the bonding of the
molecules. (Zimmerberg, 2000) Since molecules change shape when fused together,
this forces the acetyl group to release the CoA, which results in byproducts of
Acetylcholine and CoA.

It is after this synthesis reaction that acetylcholine is prepped to leave the

neuron. As the acetylcholine (ACh) was created in the soma body of the cell,
transporter proteins were used to move the molecules down the axon terminal and
through the cytoplasm. Called the vesicular ACh transporter (VAChT), this carrier
protein uses secondary active transport to move ACh throughout the cell while
releasing positively charged Hydrogen ions. This process continues until the
acetylcholine reaches the motor endplate, where the resulting ACh is then packaged
into vesicles for storage. (Zimmerberg 2000)
To activate the release of ACh from the neuron, an action potential must first
be sponsored in the cell, which is caused through a change in the concentration
gradient in the neuron, which is the different concentration of ions in the cell. As an
action potential is an electrical reaction, this causes the movement of higher than
average positively charged ions down the axon terminal, which results in the
movement of this electrical signal. These ions are more specifically K+ and Na+,
which trades spots inside of the neuron through the movement of potassium ions
outside of the cell and the movement of the sodium into the cell. This movement of
ions occurs in voltage-activated sodium and potassium gates, which converts these
chemical movements of the potassium and sodium ions into electrical energy. (Khan
Academy 2018) After the voltage inside of the neuron reaches approximately -50 mV,
the action potential threshold is reached, which results in the sponsoring of synaptic
exocytosis, which moves the acetylcholine outside of the cell and into the synaptic

16
cleft. (Freeman and Company, 2000) From this stage, the acetylcholine travels across
the synaptic cleft, where it bonds to both muscarinic ACh receptors (controls smooth
muscle movement), and more importantly, nicotinic ACh receptors (controls the
movement of skeletal muscles). (European Molecular Biology Laboratory, 2018). This
process causes the formation of an action potential in the dendrites of the receiving
neuron, which forms a chain reaction that occurs until the action potential reaches the
desired muscle section. (Freeman and Company, 2000)
This action potential is then sent through the neuron through the activation of
nicotinic receptors in the motor endplate. There, the binding of the ACh releases
sodium ions into the cell, which causes the depolarization of the cell (meaning the
imbalance between Na+ and K+ in the cell), which increases the chance of an action
potential. (Sinauer Associates, 2001) With this release of ACh and the resulting
imbalance of Na+ and Ca²⁺ going into the cell, while more K⁺ leaves the cell, this
results in the movement of electrons down the channel in response to the gradient. As
a result, this ACh causes the formation of an electric signal, which moves across the
surface of the muscle cell. (Rice University, 2018)

Lining the outside of the cell, there is a layer of membranous tissue called the
sarcolemma, which is a lipid bilayer that lines the outside of the muscle cell. Lipid
bilayers act as semiconductors, which allows for the movement of ions across the
membrane after entering the cell. (Wiegand, et. al, 2002) This action potential moves
across the sarcolemma and down through T-tubules (officially known as Transverse
tubules), which are essentially tubes that connect the myofibrils together. (Souza, et.
al, 2011) At the end of these t-tubules, there are voltage calcium pumps present, which
allows for the release of Ca²⁺ in response to the voltage of the action potential.
(Tanford et. al, 1987) These receptors have multiple parts, which are consistent of the
dihydropyridine receptor, the myoplasm, the ryanodine receptor, and finally, the
calsequestrin, which is located inside of the sarcoplasmic reticulum. In the
dihydropyridine receptor, voltage carried through the t-tubules is sensed, which
17
triggers signals to be sent to the ryanodine receptor, a channel that sponsors the release
of Ca²⁺ inside of the sarcoplasmic reticulum. (Araya, et. a., 2003) (Lanner, et. al,
2010) While the ryanodine receptor is activated, the calsequestrin is also activated as
well, which is a Ca²⁺ binding protein. Through this protein, this activates the release of
stored calcium deposits inside of the sarcoplasmic reticulum, which is thus pumped
out of the organelle and into the surrounding myoplasm, or intracellular matrix.
(Beard, Laver, & Dulhunty 2004)

From here, it is important to discuss the physical structure of the muscle cell.
Inside every individual muscle cell, there are myofibrils that are present, which
subdivides the muscle fiber into small units. In this structure, there are sarcomeres,
which are structures present that contracts in the process of muscle contraction. (Feher,

18
2012) From here, the fiber is further divided into multiple sections, with the z-disks
being a point of attachment to other sarcomeres (that is pulled in the process of muscle
contraction), the actin filament, which is covered by the molecules troponin and
tropomyosin, which are bonded together. Troponin is a molecule that is
calcium-loving, which is bonded to the tropomyosin (a long molecule that creates a
protective sheath around the actin chain), which prevents the underlying myosin heads
from bonding to the actin chain. These myosin chains are located underneath and on
top of the actin chains, and are composed of club-like protein heads that are drawn to
the actin molecule (Washington University, 2018)

When
this

19
calcium is released, the troponin binds with the calcium due to its affinity for calcium,
which causes the troponin to move as a result of its shape change. While this occurs,
the tropomyosin moves as well, as troponin and the myosin are attached
(Szent-Györgyi, 1975). This exposes the actin filament to the myosin heads, which
allows for the bonding of myosin and actin together. To complete this, the myosin
goes through ATP hydrolysis (also known as the breaking down of ATP), which
results in the formation of an ADP group and a Phosphorus ion. This process frees the
chemical energy held in the bonds and allows for it to be turned into mechanical
energy, which is used by the myosin to move (Crofts, 1996). As a result, this myosin
head becomes bonded to the actin chain, which simultaneously causes the myosin to
become stuck to the actin strand. As the actin strand is attached to fibers, which are
then attached to the z-discs, the z-discs to move towards the center, thus causing
muscle contraction. This process can happen in multiple sarcomeres at a time, and the
entire sarcomere can be shrunken as well. Called the sliding filament model, this idea
states that the movement of myosin causes the pulling of actin chains and z-discs,
which leads to the shortening of sarcomere and thus the rest of the muscle tissue
(Cooper, 2000). To detach itself from the actin, the myosin releases its ADP group and
phosphorus ion and bonds with a floating ATP molecule, which resets the myosin
back into a ready position and causes the myosin release of the actin, as the protein
changed structural shape. As a result, this action becomes a recurring action of
attaching and releasing from actin, which drives muscle contraction as a continuous
action (Rice University, 2018).

20
 A very similar process shown in muscle contraction is found in muscle
relaxation, with the myosin letting go of the actin filament instead of attaching to it.
This is mediated through the release of the ADP and phosphorus ion from the myosin
through unbonding, which allows for the bonding to a fresh ATP molecule on the
surface of the myosin head. As the structure of proteins change when bonding with
different molecules, this bonding with a fresh ATP group causes the myosin head to
reset to a firing position, as shown in the contraction process. However, there is a halt
in this process, as the myosin will become blocked inside of the cell. During the entire
contraction process, ACh is constantly bonding with the lignated-gate channels, which
creates voltage in the muscle cell by unbalancing the input of calcium into the cell,
thus generating a current. When this ACh flow is halted, this causes the inactivation of
the voltage-gated calcium channels, the end of the electric signal carried in the
t-tubules, and the end of calcium production in the sarcoplasmic reticulum. When this
happens, the excessive Ca²⁺ is pumped back into the sarcoplasmic reticulum using
active transport. As a result, the bonding of troponin to the calcium diminishes, which
causes both the troponin and the tropomyosin to move back into a position covering
the actin, halting the process of myosin-actin bonds. Since the myosin is no longer
able to bond with and pull on the actin filament, the z-discs are no longer becoming
pulled towards the center, thus causing the relaxation of the sarcomere (Rice
University, 2018).

21
6. Are Kathy’s medical problems related to her sensory neurons, motor neurons, or
both? What in kathy’s medical history supports your answer? (Amanda and Faryal)
In Kathy’s case, there was both damage to the sensory and motor neurons, with
initial damage occurring in the sensory neurons. Due to the initial tingling in her feet
and the ringing in her ears, this suggests that Kathy has sensory neuron damage, as the
senses are controlled through sensory input from these neurons.
Out of the symptoms that were felt by the patient, it is the damage that occured
to the inner ear that represents the sensory neuron damage experienced throughout the
rest of Kathy’s body. Inside of the inner ear (more specifically the cochlea) ,
asymmetrical hair bundles are present, which are attached to both sensory and motor
neurons. While these hair bundles are connected to both sensory and motor neurons,
these hairs primarily act to receive sensory signals through sensory neurons (which is
mediated through the movement of stereocilia in the inner ear). Through the
movement of these hair follicles, this causes the pulling of actin like strands, putting
tension in the hair follicles. As a result of this movement, this causes the
depolarization of the sensory neurons, which sends electrical signals down the sensory
neuron and into the peripheral nervous system. Primarily, these neurons are composed
of ganglia (neurons specifically designed to send sensory information from the outside
and to the nervous system, but small muscle fibers are located on the groups of each
sensory neuron that contains motor neurons, thus allowing for the transmitting of
sensory information into the nervous system. (Sienknecht, Köppl, and Fritzsch, 2013)
In Kathy’s case, with hearing loss in her right ear, this suggests that there was an
inhibition of the cochlear nerve, which connects the sensory neurons of the cochlea to
the neurons in the cerebral cortex. As there was no documented ringing in the ear,
called tinnitus, this suggests that there was an inhibition of the junction between
sensory neurons of the inner ear cochlear hairs and between the cochlear nerve, which
points to more of a sensory neuron issue instead of motor neurons. (Alberti, 2013;
Pujol, Puel, and Venail ,2016; Venail & Pujol, 2016)
In the treatment of her hearing loss, Kathy was prescribed steroids to treat her
ailment, which is a practice that is commonly used to treat hearing loss. In the
treatment of hearing loss, patients are given a dose of corticosteroids, which are
produced by the covering of the adrenal gland. More specific to the inner ear, there are
receptors called glucocorticoid receptors, which has the function of metabolizing
lipids, proteins, and carbohydrates. These receptors also transport Na⁺ and K⁺, which
are in creating action potentials in sensory and motor neurons and in regulating the
flow of electrons throughout the nervous system. (Oakley and Cidlowski, 2013). When
steroids are prescribed in the case of hearing loss, this is in an attempt to increase the
levels of glucocorticoid inside
of the inner ear into a threshold
that sponsors activation
potentials, which allows for the
effective sending of action
potentials down through the
cochlear nerve. (Trune and
Canlon, 2012) This made this

22
treatment effective in Kathy’s case, as the prescription of corticosteroids returned
increased the levels of glucocorticoid inside of inner ear, which fixed this issue.
However, as the nervous system damage was larger than in simply the inner ear, as
shown by the tingling in the patient’s feet and in the later motor neuron damage, the
prescription of steroids acted as a temporary solution and had little effect in slowing
the other nerve damage in the body.
Kathy’s paralysis in her right leg was due to damage to her motor neurons.
Motor neurons are surrounded and protected by a white substance composed of fat and
cholesterol known as the myelin sheath. The myelin sheath wraps around the axon of a
neuron and acts as a protective covering against other electrical impulses, and also
helps with speeding up the transmission of of nerve impulses. Nerve cells also contain
tiny gaps known as nodes in between the myelin sheath which allow electricity to
travel through neurons. When a message is being transmitted from the brain to the
spinal cord, the impulses will travel from node to node, but when the myelin sheath of
a neuron is destroyed, these impulses do not have a clear path to travel along which
prevents nerves from passing messages to other parts of the body. (Stoppler, Davis
2018)
Due to the degradation of Kathy’s myelin sheath, communication between her
nerve impulses were not properly directed to the rest of her body, which explains why
she was unable to move her legs. The nervous system sends commands to the muscles
through the motor neurons, but Kathy was barely receiving them or not receiving them
at all in different areas of her legs. Her left leg engaged which meant there was not any
motor neuron damage to that part of her body yet, but she was unable to move her
right leg which showed there was motor damage to that area (Litherland 2017).

23
7.What is myelin and how does it affect the transmission of nerve impulses? Identify
the cells responsible for the formation of myelin. (Allison)
Each neuron in the nervous system is made up of a cell body and an axon. An
axon is a branch off of the cell body that carries messages or signals. Most of the
axons in the central nervous system are wrapped in myelin, a substance rich in lipids
(fatty substances) and proteins. Myelin is a fat-based material that covers, protects, and

insulates nerves, creating an environment where they can quickly gather impulses
between the brain and the others parts of the body (National Multiple Sclerosis
Society). The communication between two neurons happens when the signal from the
first neuron releases neurotransmitters. Neurotransmitters connect to the receptors on
the second neuron
which creates
another signal. The
signal interaction,
also known as
electrical currents,
is the movement of
a positive charge.
Myelin acts as an
insulator for the
positive charge
within the axon and
it increases the distance that the signal can travel (Medicurio 2016).

24
 Nerve cells are coated with sections of myelin, and the tiny spaces between the
sections of myelin sheath are called nodes (Nodes of Ranvier). As the brain sends
directions and signals through the nerves of the spinal cord, the impulses jump from
node to node. The myelin sheath prevents the impulses from slipping away from the
nerve at a point where it is not at the end to transmit the signal (Dangond 2017).
Myelin Sheath is a central part of the Central Nervous System. The
autoimmune disease Multiple Sclerosis only affects the Central Nervous System by
causing deterioration of the myelin sheath. Multiple Sclerosis damages/destroys the
myelin and
oligodendrocytes on the
axon of the neuron.
Oligodendrocytes
provide support for the
axon and provide
nutrients to the neuron.
The damaged areas from
the myelin deterioration
create scars along the
nerve that can be
detected by magnetic
resonance imaging
(MRI). Multiple
Sclerosis also stops or
slows down the nerve signaling (National Multiple Sclerosis Society). The messages
or signals the nerves try to send are delayed or distorted and the messages the brain
receives may be misinterpreted (Dangond 2017).
Each oligodendrocyte can be creating segments of the myelin sheath on the
axons of multiple neurons. The different segments of myelin sheath can be branched
from separate oligodendrocytes from any neuron (Jenson 2014).
When one has
Multiple Sclerosis, their
own immune system
attacks itself because it
thinks that the
oligodendrocytes are
invaders (WebMD).
T-cells from the body's
immune system attack and
diminish the myelin
sheath, concluding in the
nerve cell fibers to be
unprotected. T-cells
completely strip the
myelin off the fibers.
When the nerve cell is

25
unprotected, the signals are not as strong and the orders given may not be accurate
once received in the correct place. Membrane potential is a measure of how positive or
negative the inside of the neuron is compared to the outside of the neuron. When the
neuron is resting, the neuron is more negatively charged inside than outside. The
negatively charged inside creates a negative membrane potential. After the activation
of a neurotransmitter that inserts a positive charge into the neuron, the positive charge
spreads down the axon due to the repulsion within the area of positive charge and
attraction towards the more negative surroundings of the neuron. As the positive
charge moves down the axon, the amount of positive charge decreases as it gets further
away from the starting point of ignition. When there is no myelin sheath to keep the
positive charge inside, some charge naturally leaks out of the neuron while the rest
spreads out. By the time the signal reaches the end of the axon, quantity of positive
charge is small. This situation could be compared to a metal rod being heated at one
end. From the initial heating point of the rod, the heat spreads through the rod the as
the distance between the initial point and the current point increases, the rod loses the
heat (Medicurio 2016).
As a result of the weak Central Nervous System communication, Multiple
Sclerosis can weaken muscles, damage coordination, and in the worst case, could lead
to paralysis depending on which part of the Central Nervous System is damaged
severely (WebMD N.D).

26
8.What are the “scleroses” in Multiple Sclerosis and where do they occur? How does
this influence nerve transmission? (Natalie)
Multiple Sclerosis, also known as MS, is a disorder that
occurs in the brain and the spinal cord, essentially the central
nervous system, and it causes the immune system to attacks the
myelin sheath of our nerve cells in the brain, spinal cord, and
optic nerves. The myelin sheath is the protective coating of a
nerve fiber. The disease is potentially disabling and can cause
nerves to deteriorate and become permanently damaged (Multiple
2017). The effects of Multiple Sclerosis can cause people to have
trouble walking, muscle weakness and spasms, depression,
blurred vision, and many more symptoms (What). Scleroses is
plural for sclerosis and it is the localized hardening of skin,
commonly known as a scar (Definition N.D).
Scleroses, scarred myelin, occur at the previous healthy
myelin sheath. The cells in the immune system that have been
known to attack the myelin sheath, and cause it to become
scarred, due to Multiple Sclerosis are the macrophage, microglia, the T cell, and the B
cell. Scientists believe most of the damage is because of the work done by T and B
cells. Immune cells are not typically found in the nervous system because the
blood-brain barrier protects them from entering, but in the case of a person who has
been diagnosed with Multiple Sclerosis
the blood-brain barrier is compromised.
The dysfunctioning blood-barrier allows
the passage of T and B cells into the
brain and the spinal cord. The
responsibility of the B cells is to
recognize foreign invaders and produce
antibodies. Based on the stage of
development of a B cell determines what
type of B cell is present. In the stages of
development, the B cells have different
types of proteins on their surface. For example, proteins such as CD19, CD20, or
CD27. Due to the types of proteins on the surface of B cell, can distinguish it from
being an Activated B cell, Immature B cell, Memory B cell, and many more. T cells
are responsible for attacking infected cells inside in the body. In order for the B and T
cells to mistakenly attack the myelin sheath they can perform many different actions.
The B cells can recognize the myelin sheath and communicate to the T cells to attack
the myelin sheath, as if it were infected. The T and B cells can cause inflammation, by
releasing chemicals that attract and communicate to other immune system cells. The B
cells can produce antibodies that can communicate to other immune cells to attack the
myelin. Lastly, the T and B cells can reside in the central nervous system permanently
and continue to attack the myelin (Genentech 2014). The harm that the myelin sheath
undergoes because of the attacks caused by T and B cells results in them scarring and
forming scleroses.

27
 Nerve transmission is when the neurons transmit signals in the form of
electrical currents. Neurons usually transmit signals from sensory organs, such as the
tongue or the eyes, to the central nervous system and then from the central nervous
system to effector organs, which is an organ that is capable to respond to a stimulus.
A neuron is composed of the cell body, dendrites, axon, and the
myelin sheath. The function of the myelin sheath is to coat the
axon and insulate the electricity in order to increase the speed of
the electric signal. The axon is used to transport electric signals
out of the cell. In order for nerve transmission to occur and for the
neurons to communicate to other neurons, they must transport
electric signals known as the action potentials. Action potential
occurs due to potential difference and polarization that takes place
within the neuron. To begin the process the neuron, at rest, has
potential difference of approximately -70 mV. A neuron is able to maintain this
voltage because a co-transporter carries 2 potassium ions inside of the axon for every 3
sodium ions that it transports out. Because of this the concentration of potassium
inside of the neuron and the concentration of sodium outside of the neuron is high, but
the concentration of sodium outside of the cell is higher than the concentration of
potassium inside of the cell. As a result of this the
outside of the neuron’s membrane has a higher charge
than the inside. In the process of depolarization inside
of the neuron the sodium channels in the axon of a cell
are sensitive to the action potential, which results in
them opening and allowing sodium ions to enter inside
of the neuron. When a threshold value of -40 mV is
reached in the sodium channels and neuron has
undergone the full process of depolarization, the
potential difference inside of the neuron raises to 40
mV. The raise in voltage, -70 mV to 40 mV, creates the electric charge during
neurotransmission (Bekaboo 2018).
Because the scarred area that results from multiple sclerosis is the myelin, the
myelin is unable to insulate electric signals needed for nerve transmission to different
organs. The reason why victims of Multiple Sclerosis lose their ability to move some
of their body parts, is because it is difficult for the neurons inside of the body to
communicate with other organs if the electric signals are not being transmitted
properly or at all. Without the myelin sheath, the electric charges that are used to
communicate across the cell are virtually useless.

28
9. How do an MRI and spinal tap help confirm the diagnosis of Multiple Sclerosis?
(Natalie, Allison, and Amber)

MRI stands for magnetic resonance imaging and

physicians and doctors use it in order to monitor
and diagnose their patients. A MRI uses the
magnetic field, radio waves and frequency pulses,
and a computer in order to produce detailed
pictures of the body’s internal organs, soft tissues,
bones, and many other internal structures. A MRI
does not use ionizing radiation like X-rays do.
Typically a MRI is used to observe pelvic organs,
organs in the abdomen, blood vessels, and lymph nodes. A physician uses a MRI to
monitor or diagnose tumors in the chest, abdomen, or pelvis, liver diseases, bowel
diseases, blood vessel inflammation and malformations, and a pregnant woman’s fetus
(Radiology N.D). The damaged areas from the myelin, on the axon of the neuron,
deterioration create scars along the nerve that can be detected by magnetic resonance
imaging (National Multiple Sclerosis Society N.D).
MRIs are normally the test of choice along with initial blood tests. The MRI
can detect abnormalities in tissue by evaluating the relative water content in the tissues
through magnetic fields and radio waves (Chavoustie 2018). When conducting an MRI
on a patient who is suspected to have MS, doctors will be looking for two things:
they’ll look for abnormalities that will override the diagnosis of MS, such as a brain
tumor or when this is not applicable, they will look for evidence of demyelination. The
MRI can provide evidence of demyelination if it occurs in the brain or the spinal cord
(Chavoustie 2018).
In addition to diagnosing MS, an MRI can be used to track the progress of the
disease. Doctors may want to bring the patient back in for another MRI after diagnosis
to track how well the medications are working or how the disease is progressing over
time (WebMD N.D). Using an MRI to diagnose MS is very common as it is the most
sensitive and non invasive diagnostic tool for MS, making it most suitable to the
patients (National Multiple Sclerosis Society N.D).
During the MRI, the strong magnetic field causes a portion of the hydrogen
protons in water to line up in the direction of the magnetic field. Once the hydrogen
protons are lined up, it creates a small but noticeable signal for imaging. Radio waves
and weaker magnetic fields then come and take the hydrogen protons out of place,
29
moving them from this previously formed line. Once the radio waves stop, the protons
relax back into the line once again. This relaxation sends signals to a computer which
can then be observed by the doctors to determine whether the patient has MS (National
Multiple Sclerosis Society N.D).
A spinal tap procedure or also known as a lumbar puncture procedure is used
by healthcare professionals in order to evaluate the cerebrospinal fluid of their
patients. Cerebrospinal fluid is a liquid that soaks the brain and the spinal cord. During
the spinal tap procedure, the healthcare professional will attempt to keep the
environment sterile. While wearing sterile gloves, the healthcare professional usually
will position the patient into a fetal position in order to open up the vertebral spaces. In
order to find the correct area to place the needle in the spinal cord, the doctor will
being to feel for the top of the pelvis bone in order to find the fourth and fifth lumbar
space. Before placing the needle inside of the lumbar space to retrieve cerebrospinal
fluid, the healthcare professional injects lidocaine, a numbing medication, into the skin
and the tissues of the lower back (Fell N.D).

30
10. Why did Steroids help alleviate Kathy’s symptoms? (Amanda)
In the treatment of MS, glucocorticoids are often prescribed, which reduces
inflammation inside of the body. In the treatment of her hearing loss, Kathy was
prescribed steroids to treat her ailment, which is a practice that is commonly used to
treat hearing loss. In the treatment of hearing loss, patients are given a dose of
corticosteroids, which are produced by the covering of the adrenal gland. More
specific to the inner ear, there are receptors called glucocorticoid receptors, which has
the function of metabolizing lipids, proteins, and carbohydrates. These receptors also
transport Na⁺ and K⁺, which are in creating action potentials in sensory and motor
neurons and in regulating the flow of electrons throughout the nervous system.
(Oakley and Cidlowski, 2013). When steroids are prescribed in the case of hearing
loss, this is in an attempt to increase the levels of glucocorticoid inside of the inner ear
into a threshold that sponsors activation potentials, which allows for the effective
sending of action potentials down through the cochlear nerve. (Trune and Canlon,
2012) This made this treatment effective in Kathy’s case, as the prescription of
corticosteroids returned increased the levels of glucocorticoid inside of inner ear,
which fixed this issue.
These steroids also have been shown to have both the ability to produce an
anti-inflammatory response and an immunosuppressant function, as MS is considered
an autoimmune disease. In these disorders, the immune system attacks its own cells, as
identifying protein-fused-carbohydrate chains on the surface of the cell (called
glycoproteins) are not recognized by the immune system.(Cooper, 2000). Antibodies
are also made of glycoproteins and contains polypeptide chains, and connect to
substances that do not have a recognized structure on the plasma membrane. (Thermo
Fisher Scientific, n.d) Used as identifying markers of foreign bodies (called antigens;
includes substances such as bacteria, viruses, or parasites), antibodies are used as
labels to simultaneously mark and clump together antigens, which makes destruction
of the antigens possible by other cells, such as the phagocytes (which ingests microbes
and other foreign molecules), macrophages (large cells that ingest antibody-targeted
cells, causing cell death [or apoptosis] through receptor-mediated phagocytosis), and T
lymphocytes (cells that attach to foreign bodies that do not have matching antibodies
on the exterior of the cells, which sponsors a sent signal to the nucleus of the antigen,
sponsoring apoptosis) (McDowall 2016; Institute for Quality and Efficiency in Health
Care, 2016)
It is the t-cells that are involved in the death of the Schwann Cells of the
myelin sheath. In normal conditions, t-cells have a t-cell receptor that can bind to
self-antigens (body cells that pose a threat to the body, such as some cancer cells),
which causes both the death of the cell and the inflammation of surrounding areas.
Called autoimmune encephalomyelitis, this inflammation of nervous system causes
damage to the myelin sheath in some instances due to the enlargement of the
surrounding matrix, while the cells themself, more specifically the Schwann Cells, are
targeted by the T-cells for destruction. Often times, this incorrect immune response by
the T-cells starts in the peripheral nervous system and works its way up through the
nerves into the central nervous system of patients, which results in the movement of
this disease into affecting cognitive function in chronic cases. (Stinissen, Medaer, &

31
Raus 1998) While it is not completely understood the cause behind this initial
activation of MS in patients, it is theorized that the myelin basic protein is involved,
which is the protein that signals the production of Schwann cells in the lining of the
axon of cells, is involved and is targeted by t-cells that tend to destroy viruses due to a
similar molecular structure. (NCBI, 2018) In this confusion, these T-cells signal
apoptosis in the Schwann cells, resulting in the degradation of the myelin sheath. After
becoming aroused by their initial targeting and killing of a Schwann cell, these T-cells
go into overdrive, enlarge, and enter the CNS, where they attack cells at this site, often
after becoming deactivated. (Stinissen, Madaer, & Raus, 1998) Since these T-cells
often become temporarily deactivated when reaching the CNS, the reactivation of
these cells causes relapses in patients, which cycles between immune system targeting
of Schwann Cells and the regrowth (albeit hindered) of the destroyed Schwann Cells.
In the use of glucocorticoids, this reduces inflammation by inhibiting
vasodilation, reducing the ability for substances to enter the blood supply, which has
the function of reducing the access that leukocytes (including t-cells) have to tissues
outside of the blood supply. Additionally, these steroids act as agonists (that is, a
substance that mimics another molecule) in the protein synthesis process inside of
these leukocytes, which reduces the activity of these cells. (Coutinho & Chapman,
2011) In doing this, t-leukocytes are trapped inside of the blood stream through
vasoconstriction and are kept out of the peripheral nervous system, which reduces
damage to the myelin sheath, while these cells are “reprogrammed” to become more
passive, which helps to alleviate the symptoms of both inflammation and
t-leukocyte-mediated apoptosis among Schwann Cells.

32
11. How does copaxone work as treatment for Multiple Sclerosis? How do other
medications differ? (Amber)
Copaxone is a medication specifically prescribed to people that suffer from
Relapsing-Remitting Multiple Sclerosis (RRMS). Relapsing-Remitting Multiple
Sclerosis affects the myelin which is an insulating layer surrounding nerve fibers in the
central nervous system that impulses are conducted through. The myelin, as well as the
nerve fibers are attacked during relapses of Multiple Sclerosis. These attacks cause the
cells of the immune system to activate, causing small areas to be damaged, these areas
differ from person to person. This damage produces the symptoms associated with
Multiple Sclerosis (MS) and since the areas in which the damage is caused vary
between patients, it is rare for multiple people to express the exact same set of
symptoms (​National Multiple Sclerosis Society N.D​).

Following these relapses are periods of recovery which are known as

remissions . The symptoms normally go away during the time of remissions. Some
however, can be permanent (​National Multiple Sclerosis Society N.D​). RRMS can be
categorized into 4 types. This includes active, not active, worsening, or not worsening.
Active RRMS is when the patient suffers from relapses or there is evidence of disease
progression and activity in MRI scans. Non active is the opposite of active, where
there are no relapses nor is there MRI activity. Worsening RRMS can be characterized
as a confirmed increase of the disability over a period of time following a relapse,
while non worsening can be characterized as a stable level or declining of the

33
disability (​National Multiple Sclerosis Society N.D​). This increase in disability in
worsening RRMS is considered confirmed after two or more neurological evaluations,
when the patient shows the same or worsening signs of disability. These neurological
evaluations are normally 6 to 12 months apart.
The medication Copaxone is not used to cure RRMS, but instead used to
reduce the frequency of relapses and reduce the inflammation of the myelin sheath
surrounding nerves caused by the immune system (​Seqirus 2012​). Copaxone is
injected underneath the skin daily and impacts the immune system in order to reduce
the attacks on the myelin sheath of the nerve cells (Seqirus 2012). The part of the
immune system that affects the myelin sheath are the T-cells. T-cells of the immune
system are designed to recognize foreign materials so that the immune system can then
attack these materials and protect the body (​Science Museum 2012​). In the immune
system of a person who suffers from RRMS, the T-cells recognize the myelin sheath
as a foreign invader, attacking it, which causes the symptoms of RRMS such as
numbness, eye pain, dizziness, along with many more symptoms that are associated
with RRMS (​Lava 2017​).
Copaxone is made of a synthetic protein, Glatiramer acetate. Glatiramer acetate
is an immunomodulator which is a chemical that modifies the immune response or the
functioning of the immune system. This synthetic protein is made of synthetic
polypeptides which are further made up of 4 non synthetic amino acids: L- glutamic
acid, L-alanine, L-tyrosine and L-lysine (​Marshall 2015​). Glatiramer acetate works by
simulating the myelin protein that insulates the nerve fibers in the brain as well as the
spinal cord that is the victim of damage from the T-cells (​National Multiple Sclerosis
Society N.D​). By simulating this protein, Copaxone blocks the T-cells that damage the
myelin sheath. The complete function of Glatiramer acetate is still being studied and is
not fully understood because the disease itself still needs further research (Marshall
2015).
Along with Copaxone, there are many medications that work to lessen the
effects of Multiple Sclerosis. There are three categories in which these medications are
placed: injectable medications, oral medications, and infused medications. Copaxone
is an injectable medication as well as Avonex. Avonex uses an interferon called
interferon beta-1a that is produced through recombinant DNA technology. This is
where the interferon beta-1a is made by a cell that has received a gene in their DNA,
which makes it able to produce it (European Medicine Agency 2011). Interferons are
produced by the body and are used to fight against foreign substances in the body such
as an infection. The interferon in Avonex, interferon beta-1a works to help protect the
myelin by blocking the attacks, although the exact way that interferon beta-1a interacts
with the body is not completely known yet (European Medicine Agency 2011).

34
 One of the medications that can be taken orally is Aubagio. Aubagio is an
immunomodulator called teriflunomide in pill form that is taken daily for people
suffering from RRMS. Aubagio has been proven to work differently from other MS
medication in that it reduces the reproduction of the activated T-cells that target the
destruction of the myelin sheath of the nerve cells. By limiting the numbers of these
cells, Aubagio reduces the effects of MS. Specifically, it inhibits dihydroorotate
dehydrogenase (DHODH). DHODH is an enzyme needed by the cells in order for
them to rapidly divide (Aubagio 2017). The enzyme lowers the activation energy
needed for the T-cells to divide, making the cells able to divide faster. By inhibiting
this enzyme, the T-cells will divide slowly and the extreme decrease in these cells will
decrease the attacks on the myelin sheath, ultimately lessening the effects of RRMS.
An example of medication that is infused into IV tubes and given to the patient
through the IV is Novantrone. Novantrone is a cytotoxic immunosuppressive drug
called Mitoxantrone and is currently the only cytotoxic immunosuppressive drug used
for the treatment of multiple sclerosis (​Eden 2016​). Cytotoxic immunosuppressive
drugs like Novantrone are practical in that they are potent drugs that help to reduce
disease activity in skin or internal organs without using other methods of medication
such as steroids that might cause worse effects on the patient (​American Osteopathic
College of Dermatology N.D​). Novantrone, similar to Aubagio, prevents the
reproduction of T-cells, B-cells, and macrophages. Antigen presenting cells are also
killed in this process as well as the migration of activated leukocytes is inhibited
(​Maghzi 2010​). T-cells, B-cells, macrophages and leukocytes are all pieces to the
immune system that collectively work to kill foreign substances in the body, which in
this case, they recognize the myelin sheath as the foreign substance. By killing these
activated cells and inhibiting their reproduction or function, Novantrone reduces
relapses of multiple sclerosis, allowing for the patient to live with minimal attacks
(Mahzi 2010).

35
12.Why did Kathy experience the altered
sensation in her lower body? Was there
something wrong with her skin? Why
couldn’t she stand? Was there something
wrong with the muscles of her right leg?
(Faryal)
Kathy experienced the altered
sensation in her lower body due to the
damage to her motor neurons. Motor
neurons contain a protective covering
composed of lipids and proteins known as
the myelin sheath which wraps around the
axon of a neuron. This sheath not only
protects neurons against other chemical
impulses, but also helps speed up the
transmission of nerve impulses. This is
facilitated through the properties of lipids
as an electrical semiconductors and as an insulator, as the fatty, dry matrix around the
neuron is dry, making the myelin sheath effective at maintaining electric signals. Like
a rubber coating around a wire, this myelin sheath has the function of maximizing
electrical signals inside of the axon, preventing the escape of waywards electrical
signals from inside the axon. By reducing the instance of escaping electrical signals,
this increases the efficiency of ionic-electrical transfer (Rosenberg & Jendrasiak
1968).
When damage occurs to the myelin sheath, your nerves have no way of
communicating or reaching your muscle fibers, which can in turn cause paralysis.
These abnormal sensations, better known as paresthesias, occur because the nerve
impulses are exposed and can now escape the axon they are traveling along. Since
these nerve impulses are not being correctly interpreted, in order to make up for the
loss of feeling, the brain will try to familiarize the body with a sensation it has felt
before such as numbness or tingling like Kathy had experienced. There wasn’t
anything wrong with her skin, it was due to the way her brain was now interpreting the
nerve impulses traveling inside her central nervous system (Multiple Sclerosis Trust
2015).
Kathy was unable to stand because because the nerve impulses in her brain and
spinal cord could not send messages or commands to the muscle fibers in her legs.
Muscle movement occurs in the somatic nervous system through motor neurons, but
since Kathy’s myelin sheath was damaged, there was no way for her neurons to reach
those fibers and cause movement to occur. The initial damage was to her motor
neurons which then caused weakness and eventually paralysis in her right leg. Her
muscles were affected because they were not receiving the nerve impulses they needed
in order to work and move efficiently, leading them to weaken over time until she
could no longer feel them (Wyat 2017).

36
13: Did Kathy’s hearing loss have anything to do with the Multiple Sclerosis? Why/
why not? (All Group Members)
Multiple Sclerosis damages/destroys the myelin and oligodendrocytes on the
axon of the neuron. Oligodendrocytes provide support for the axon and provide
nutrients to the neuron. Multiple Sclerosis also stops or slows down the nerve
signaling (National Multiple Sclerosis Society N.D). The messages or signals the
nerves try to send are delayed or distorted and the messages the brain receives may be
misinterpreted (Dangond 2017). The delayed and distorted signal causes the symptoms
of Multiple Sclerosis. Some symptoms of Multiple Sclerosis include fatigue, walking
(gait) difficulties, numbness or tingling, spasticity, weakness, vision problems,
dizziness and vertigo, bladder problems, sexual problems, bowel problems, pain,
cognitive changes, emotional changes, and depression. Kathy’s hearing impairment is
related to Multiple Sclerosis depending on the part of brain that was directly affected
by the deterioration of the myelin sheath.
Out of the symptoms that were felt by the patient, it is the damage that occured
to the inner ear that represents the sensory neuron damage experienced throughout the
rest of Kathy’s body. Inside of the inner ear (more specifically the cochlea) ,
asymmetrical hair bundles are present, which are attached to both sensory and motor
neurons. While these hair bundles are connected to both sensory and motor neurons,
these hairs primarily act to receive sensory signals through sensory neurons (which is
mediated through the movement of stereocilia in the inner ear). Through the
movement of these hair follicles, this causes the pulling of actin like strands, putting
tension in the hair follicles. As a result of this movement, this causes the
depolarization of the sensory neurons, which sends electrical signals down the sensory
neuron and into the peripheral nervous system. Primarily, these neurons are composed
of ganglia (neurons specifically designed to send sensory information from the outside
and to the nervous system, but small muscle fibers are located on the groups of each
sensory neuron that contains motor neurons, thus allowing for the transmitting of
sensory information into the nervous system. (Sienknecht, Köppl, and Fritzsch, 2013)
In Kathy’s case, with hearing loss in her right ear, this suggests that there was an
inhibition of the cochlear nerve, which connects the sensory neurons of the cochlea to
the neurons in the cerebral cortex. As there was no documented ringing in the ear,
called tinnitus, this suggests that there was an inhibition of the junction between
sensory neurons of the inner ear cochlear hairs and between the cochlear nerve, which
points to more of a sensory neuron issue instead of motor neurons. (Alberti, 2013;
Pujol, Puel, and Venail ,2016; Venail & Pujol, 2016)
Hearing impairment is a very rare symptom of Multiple Sclerosis, but it still
does occur. The auditory nerve, also known as the eighth cranial nerve, connects the

37
ear to the brainstem. Because multiple sclerosis can cause damage to the auditory
nerve, it can lead to the possibility of sensorineural hearing loss. Sensorineural hearing
loss represents how the ear is normal but the nerves inside are damaged and unable to
transmit messages and signals from the ear to the brain(Buxhoeveden 2016). Multiple
Sclerosis inhibits the brain from processing auditory information because the neurons
associated with the auditory nerve are not able to transmit signals and messages
because the myelin coating the axon is scarred.

38
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